MAPK1

Summary: MAPK1/ERK2 localizes to the nucleus after stimulation.

Reason: Nuclear localization is supported, but should be interpreted as stimulus-dependent rather than constitutive.

Summary: MAPK1/ERK2 is cytoplasmic in quiescent cells.

Reason: Cytoplasmic localization is a core supported localization for ERK2.

Summary: MAPK1 functions in intracellular signal transduction downstream of extracellular cues.

Reason: Intracellular signal transduction is a supported core process for MAPK1 as the ERK2 kinase in the canonical MAPK cascade.

Summary: MAPK1/ERK2 is an ATP-dependent protein serine/threonine kinase.

Reason: Serine/threonine protein kinase activity is a core molecular function of MAPK1; the more specific MAP kinase activity term should also be retained where present.

Summary: MAPK1 responds to cell-surface receptor inputs, but its core role is the downstream intracellular ERK/MAPK cascade.

Reason: Cell surface receptor signaling is too broad and upstream-oriented for the MAPK1 core function; ERK/MAPK cascade terms are more specific.

Proposed replacements: ERK1 and ERK2 cascade MAPK cascade

Summary: MAPK1 is a protein kinase, but this term is less specific than the supported serine/threonine MAP kinase terms.

Reason: The generic protein kinase term should be replaced by protein serine/threonine kinase activity and MAP kinase activity, which capture MAPK1 specificity.

Proposed replacements: protein serine/threonine kinase activity MAP kinase activity

Summary: MAPK1/ERK2 has MAP kinase activity.

Reason: MAP kinase activity is the most specific core catalytic function for MAPK1/ERK2.

Summary: MAPK1 binds ATP as the phosphoryl donor for kinase catalysis.

Reason: ATP binding is integral to the active-site chemistry of ERK2 kinase activity.

Summary: MAPK1/ERK2 localizes to the nucleus after stimulation.

Reason: Nuclear localization is supported, but should be interpreted as stimulus-dependent rather than constitutive.

Summary: MAPK1/ERK2 is cytoplasmic in quiescent cells.

Reason: Cytoplasmic localization is a core supported localization for ERK2.

Summary: This early endosome annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the early endosome location is a context-/pathway-specific or high-throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This late endosome annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the late endosome location is a context-/pathway-specific or high- throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This Golgi apparatus annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the Golgi apparatus location is a context-/pathway-specific or high-throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This centrosome annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the centrosome location is a context-/pathway-specific or high- throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This spindle annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the spindle location is a context-/pathway-specific or high- throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This caveola annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the caveola location is a context-/pathway-specific or high- throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This focal adhesion annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the focal adhesion location is a context-/pathway-specific or high-throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: MAPK1 can affect transcriptional programs through downstream substrates, but broad regulation of RNA polymerase II transcription overstates the direct function.

Reason: The direct MAPK1 function is kinase activity and ERK/MAPK cascade signaling; broad transcriptional regulation should not be inferred from pathway membership alone.

Summary: MAPK1 is activated in receptor and growth-factor signaling contexts, but these are stimulus-specific pathway contexts rather than the core conserved ERK2 function.

Reason: Growth-factor and receptor-specific signaling annotations can be retained as non-core contexts; the core MAPK1 process is the intracellular ERK/MAPK cascade.

Summary: This is a context-dependent downstream process linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function.

Summary: Positive regulation of telomere maintenance is inferred from a high-throughput RNAi telomerase screen (PMID:21531765) plus electronic annotation.

Reason: This is a high-throughput screen-derived, indirect pathway outcome rather than a direct MAPK1 function; it should not be elevated to a core ERK2 annotation without direct mechanistic evidence.

Summary: This automated annotation places canonical ERK2 in a stress-activated MAPK cascade context.

Reason: GO:0032872 is a stress-activated MAPK cascade term associated with JNK/p38 signaling, whereas MAPK1/ERK2 is curated here as the canonical ERK/MAPK cascade kinase. The automated inference overstates the evidence.

Summary: This is an amino-acid-starvation response annotation linked to ERK signaling context.

Reason: The starvation-response annotation may be retained as non-core where the source evidence supports this context, but it should not be treated as the core conserved MAPK1 function.

Summary: This synapse annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the synapse location is a context-/pathway-specific or high- throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This automated annotation places canonical ERK2 in the stress-activated MAPK cascade.

Reason: GO:0051403 refers to stress-activated MAPK cascade biology associated with JNK/p38 signaling, not the canonical ERK1/ERK2 cascade. The automated inference should not be retained as a valid non-core MAPK1 annotation.

Summary: This is a context-dependent downstream process (regulation of cytoskeleton organization) linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function, which is ERK2 MAP kinase activity in the ERK/MAPK cascade.

Summary: This is a context-dependent downstream process linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function.

Summary: MAPK1/ERK2 is a central component of the ERK1 and ERK2 cascade.

Reason: ERK1 and ERK2 cascade is a core pathway term for MAPK1 and is more specific than generic signaling process terms.

Summary: MAPK1 is activated in receptor and growth-factor signaling contexts, but these are stimulus-specific pathway contexts rather than the core conserved ERK2 function.

Reason: Growth-factor and receptor-specific signaling annotations can be retained as non-core contexts; the core MAPK1 process is the intracellular ERK/MAPK cascade.

Summary: This is a context-dependent downstream process (caveolin-mediated endocytosis) linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function, which is ERK2 MAP kinase activity in the ERK/MAPK cascade.

Summary: This is a context-dependent downstream process (regulation of Golgi inheritance) linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function, which is ERK2 MAP kinase activity in the ERK/MAPK cascade.

Summary: This ciliary tip annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the ciliary tip location is a context-/pathway-specific or high- throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: MAPK1 can phosphorylate serine residues, but the serine-only term is incomplete for ERK2.

Reason: ERK2 is a proline-directed serine/threonine MAP kinase; GO:0004674 and GO:0004707 better capture the supported activity than a serine-only activity term.

Proposed replacements: protein serine/threonine kinase activity MAP kinase activity

Summary: This is a context-dependent downstream process linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function.

Summary: This is a context-dependent downstream process (regulation of early endosome to late endosome transport) linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function, which is ERK2 MAP kinase activity in the ERK/MAPK cascade.

Summary: ERK2 forms a complex with the tyrosine phosphatase LC-PTP/HePTP (PTPN7; WITH/FROM P35236), which dephosphorylates and inactivates it via a KIM-dependent interaction.

Reason: The cited study shows direct complex formation between ERK2 and the phosphatase HePTP/LC-PTP; 'protein phosphatase binding' is the informative MF for this interaction.

Proposed replacements: protein phosphatase binding

Summary: ERK2 binds the KIM of the receptor-type tyrosine phosphatase PTP-SL (PTPRR; WITH/FROM Q15256), which retains it in the cytoplasm and dephosphorylates it.

Reason: The paper directly characterises KIM-mediated association of ERK1/2 with the phosphatase PTP-SL; replace bare protein binding with 'protein phosphatase binding'.

Proposed replacements: protein phosphatase binding

Summary: Interaction of ERK2 with the tyrosine phosphatase HePTP (PTPN7; WITH/FROM P35236), which regulates ERK2 nuclear translocation.

Reason: The partner is the ERK-directed tyrosine phosphatase HePTP; 'protein phosphatase binding' is the informative MF.

Proposed replacements: protein phosphatase binding

Summary: Interaction of ERK2 with MKP3/DUSP6 (WITH/FROM Q16828), an ERK-directed dual-specificity phosphatase.

Reason: The partner is the MAP kinase phosphatase MKP3/DUSP6, which dephosphorylates p-ERK1/2 in this study; 'protein phosphatase binding' is the informative MF.

Proposed replacements: protein phosphatase binding

Summary: ERK2 binds the KIM of the nuclear dual-specificity phosphatase DUSP5 (WITH/FROM Q16690), which inactivates and anchors ERK2 in the nucleus.

Reason: Direct KIM-dependent binding of ERK2 to the phosphatase DUSP5 is demonstrated; 'protein phosphatase binding' is the informative MF.

Proposed replacements: protein phosphatase binding

Summary: ERK co-precipitates with MAP kinase phosphatase-2 (MKP-2/DUSP4; WITH/FROM Q13115).

Reason: The partner is the dual-specificity phosphatase MKP-2/DUSP4; 'protein phosphatase binding' is the informative MF.

Proposed replacements: protein phosphatase binding

Summary: Active ERK2 docks onto the DEF motif of MKP-1/DUSP1 (WITH/FROM P28562) and phosphorylates it, promoting its SCF(Skp2)-dependent degradation.

Reason: The interaction is ERK2 docking to the phosphatase MKP-1/DUSP1; 'protein phosphatase binding' is the informative MF.

Proposed replacements: protein phosphatase binding

Summary: ERK2 binds the N-terminal domain of the MAPK phosphatase PAC-1/DUSP2 (WITH/FROM Q05922), catalytically activating the phosphatase.

Reason: Direct binding of ERK2 to the phosphatase PAC-1/DUSP2 is shown; 'protein phosphatase binding' is the informative MF.

Proposed replacements: protein phosphatase binding

Summary: Interaction with the Capicua transcriptional repressor (WITH/FROM Q9U1H0) through a MAPK docking site in Capicua.

Reason: The partner is the HMG-box transcriptional repressor Capicua, bound through its MAPK docking site; 'DNA-binding transcription factor binding' is more informative than bare protein binding. The abstract describes the interaction with Drosophila Rolled; the curator's assignment to human ERK2 presumably reflects assays in the full text, which is deferred to.

Proposed replacements: DNA-binding transcription factor binding

Summary: ERK1/2 bind Mxi2, a p38alpha (MAPK14) isoform (WITH/FROM Q16539-3; also MEK1 and PEA-15 listed), which promotes stimulus-independent ERK nuclear import.

Reason: The principal partner studied is the p38alpha kinase isoform Mxi2 (MEK1 also listed); 'protein kinase binding' is the informative MF. GOA now lists this interaction as one row per partner; this row's partner is UniProtKB:Q02750 (Dual specificity mitogen-activated protein kinase kinase 1), so only the protein kinase binding replacement applies to it.

Proposed replacements: protein kinase binding

Summary: This is a generic protein-binding (GO:0005515) interaction annotation for MAPK1/ERK2 from PMID:18060821; ERK2 has many reported interacting partners.

Reason: The generic protein binding term is uninformative for a multi-partner kinase like ERK2 and should not be retained as a bare GO:0005515 assertion. ERK partner recognition is motif/exosite-driven (KIM/D-domain, DEF/FXFP), and specific docking, substrate, scaffold, or phosphatase interactions should be curated with a more informative molecular-function term where the evidence supports one.

Summary: This is a generic protein-binding (GO:0005515) interaction annotation for MAPK1/ERK2 from PMID:18084305; ERK2 has many reported interacting partners.

Reason: The generic protein binding term is uninformative for a multi-partner kinase like ERK2 and should not be retained as a bare GO:0005515 assertion. ERK partner recognition is motif/exosite-driven (KIM/D-domain, DEF/FXFP), and specific docking, substrate, scaffold, or phosphatase interactions should be curated with a more informative molecular-function term where the evidence supports one.

Summary: ERK1/2 bind human biliverdin reductase (BLVRA; WITH/FROM P53004), a dual-function reductase/Ser-Thr-Tyr kinase, via C- and D-box MAPK docking motifs; hBVR activates ERK and serves as an ERK nuclear transporter.

Reason: The partner hBVR is described as a Ser/Thr/Tyr kinase that docks onto ERK; 'protein kinase binding' is the informative MF.

Proposed replacements: protein kinase binding

Summary: This is a generic protein-binding (GO:0005515) interaction annotation for MAPK1/ERK2 from PMID:18616943; ERK2 has many reported interacting partners.

Reason: The generic protein binding term is uninformative for a multi-partner kinase like ERK2 and should not be retained as a bare GO:0005515 assertion. ERK partner recognition is motif/exosite-driven (KIM/D-domain, DEF/FXFP), and specific docking, substrate, scaffold, or phosphatase interactions should be curated with a more informative molecular-function term where the evidence supports one.

Summary: ERK1/2 are direct substrates of, and bind, the receptor tyrosine phosphatase DEP-1/PTPRJ (WITH/FROM Q12913).

Reason: Pulldown and dephosphorylation assays show ERK binds the phosphatase DEP-1; 'protein phosphatase binding' is the informative MF.

Proposed replacements: protein phosphatase binding

Summary: This is a generic protein-binding (GO:0005515) interaction annotation for MAPK1/ERK2 from PMID:21826244; ERK2 has many reported interacting partners.

Reason: The generic protein binding term is uninformative for a multi-partner kinase like ERK2 and should not be retained as a bare GO:0005515 assertion. ERK partner recognition is motif/exosite-driven (KIM/D-domain, DEF/FXFP), and specific docking, substrate, scaffold, or phosphatase interactions should be curated with a more informative molecular-function term where the evidence supports one.

Summary: ERK1/2 bind the kinase interaction motif of MKP-4/DUSP9 (WITH/FROM Q99956), which mediates their inactivation.

Reason: KIM-dependent binding of ERK to the phosphatase DUSP9 is shown; 'protein phosphatase binding' is the informative MF.

Proposed replacements: protein phosphatase binding

Summary: High-throughput yeast two-hybrid interaction between ERK2 and RSK2/RPS6KA3 (WITH/FROM P51812) in the human liver interactome.

Reason: The IntAct-derived WITH/FROM partner(s) for this high-throughput interactome study are protein kinases (RPS6KA3/RSK2). The binding itself is the experimental observation, so the more informative 'protein kinase binding' captures it; the partners are well-known ERK docking-motif (D-motif) containing downstream kinases/substrates.

Proposed replacements: protein kinase binding

Summary: ERK2 forms a complex with ETS1 and with Mxi2, the p38alpha (MAPK14) isoform (WITH/FROM Q16539-3), in renal proximal tubule cells.

Reason: The GOA partner is the p38alpha kinase isoform Mxi2; 'protein kinase binding' is the informative MF.

Proposed replacements: protein kinase binding

Summary: Interaction of ERK with its upstream activating kinase MEK1/MAP2K1 (WITH/FROM Q02750) in a study of MEK1-dependent Golgi fragmentation.

Reason: The partner is the MAP kinase kinase MEK1; 'mitogen-activated protein kinase kinase binding' is the specific informative MF.

Proposed replacements: mitogen-activated protein kinase kinase binding

Summary: AP-MS interaction between ERK2 and RSK1/RPS6KA1 (WITH/FROM Q15418) in a standardized kinase interactome study.

Reason: The IntAct-derived WITH/FROM partner(s) for this high-throughput interactome study are protein kinases (RPS6KA1/RSK1). The binding itself is the experimental observation, so the more informative 'protein kinase binding' captures it; the partners are well-known ERK docking-motif (D-motif) containing downstream kinases/substrates.

Proposed replacements: protein kinase binding

Summary: Crystal structures of ERK2 bound to docking peptides, including the reverse D-motif of RSK1/RPS6KA1 (WITH/FROM Q15418).

Reason: The partner is the D-motif of the downstream kinase RSK1 bound to the ERK2 docking groove; 'protein kinase binding' is the informative MF.

Proposed replacements: protein kinase binding

Summary: ERK is directly dephosphorylated by, and bound by, the metal-dependent phosphatase PPM1A (WITH/FROM P35813).

Reason: The partner is the Ser/Thr phosphatase PPM1A acting on ERK; 'protein phosphatase binding' is the informative MF.

Proposed replacements: protein phosphatase binding

Summary: Crystal structures of ERK2 bound to the scaffolding protein PEA-15 (WITH/FROM Q15121), which occupies two ERK2 docking sites.

Reason: PEA-15 is explicitly described as a scaffolding protein that directly binds ERK1/2; 'scaffold protein binding' is the informative MF.

Proposed replacements: scaffold protein binding

Summary: This is a generic protein-binding (GO:0005515) interaction annotation for MAPK1/ERK2 from PMID:23584453; ERK2 has many reported interacting partners.

Reason: The generic protein binding term is uninformative for a multi-partner kinase like ERK2 and should not be retained as a bare GO:0005515 assertion. ERK partner recognition is motif/exosite-driven (KIM/D-domain, DEF/FXFP), and specific docking, substrate, scaffold, or phosphatase interactions should be curated with a more informative molecular-function term where the evidence supports one.

Summary: AP-MS interaction of ERK2 with RSK2/RPS6KA3 and RSK3/RPS6KA2 (WITH/FROM P51812, Q15349) in the CMGC kinase interaction landscape.

Reason: The IntAct-derived WITH/FROM partner(s) for this high-throughput interactome study are protein kinases (RPS6KA3/RSK2, RPS6KA2/RSK3). The binding itself is the experimental observation, so the more informative 'protein kinase binding' captures it; the partners are well-known ERK docking-motif (D-motif) containing downstream kinases/substrates. GOA now lists this interaction as one row per partner; this row's partner is UniProtKB:P51812 (Ribosomal protein S6 kinase alpha-3), so only the protein kinase binding replacement applies to it.

Proposed replacements: protein kinase binding

Summary: Endogenous in situ proximity ligation detection of ERK2 with RSK2/RPS6KA3 and the phosphatases HePTP/PTPN7 and PTP-SL/PTPRR (WITH/FROM P51812, P35236, Q15256).

Reason: The partners are a protein kinase (RSK2) and ERK-directed tyrosine phosphatases (HePTP, PTPRR); 'protein kinase binding' and 'protein phosphatase binding' capture these interactions more informatively. GOA now lists this interaction as one row per partner; this row's partner is UniProtKB:P35236 (Tyrosine-protein phosphatase non-receptor type 7), so only the protein phosphatase binding replacement applies to it.

Proposed replacements: protein phosphatase binding

Summary: Interaction of ERK2 with RSK3/RPS6KA2 (WITH/FROM Q15349) in a kinase interaction network analysis.

Reason: The IntAct-derived WITH/FROM partner(s) for this high-throughput interactome study are protein kinases (RPS6KA2/RSK3). The binding itself is the experimental observation, so the more informative 'protein kinase binding' captures it; the partners are well-known ERK docking-motif (D-motif) containing downstream kinases/substrates.

Proposed replacements: protein kinase binding

Summary: This is a generic protein-binding (GO:0005515) interaction annotation for MAPK1/ERK2 from PMID:26267535; ERK2 has many reported interacting partners.

Reason: The generic protein binding term is uninformative for a multi-partner kinase like ERK2 and should not be retained as a bare GO:0005515 assertion. ERK partner recognition is motif/exosite-driven (KIM/D-domain, DEF/FXFP), and specific docking, substrate, scaffold, or phosphatase interactions should be curated with a more informative molecular-function term where the evidence supports one.

Summary: This is a generic protein-binding (GO:0005515) interaction annotation for MAPK1/ERK2 from PMID:26733474; ERK2 has many reported interacting partners.

Reason: The generic protein binding term is uninformative for a multi-partner kinase like ERK2 and should not be retained as a bare GO:0005515 assertion. ERK partner recognition is motif/exosite-driven (KIM/D-domain, DEF/FXFP), and specific docking, substrate, scaffold, or phosphatase interactions should be curated with a more informative molecular-function term where the evidence supports one.

Summary: Interaction of ERK2 with the MAPK phosphatases DUSP4, DUSP6 and DUSP9 (WITH/FROM Q13115, Q16828, Q99956) in systematic phosphatase interaction profiling.

Reason: All partners are ERK-directed dual-specificity phosphatases; 'protein phosphatase binding' is the informative MF. GOA now lists this interaction as one row per partner; this row's partner is UniProtKB:Q13115 (Dual specificity protein phosphatase 4), so only the protein phosphatase binding replacement applies to it.

Proposed replacements: protein phosphatase binding

Summary: LuTHy two-hybrid interaction between ERK2 and RSK1/RPS6KA1 (WITH/FROM Q15418).

Reason: The IntAct-derived WITH/FROM partner(s) for this high-throughput interactome study are protein kinases (RPS6KA1/RSK1). The binding itself is the experimental observation, so the more informative 'protein kinase binding' captures it; the partners are well-known ERK docking-motif (D-motif) containing downstream kinases/substrates.

Proposed replacements: protein kinase binding

Summary: AP-MS interactions of ERK2 in colorectal cancer cells with RSK1/2, MKNK1 and the phosphatases DUSP4, DUSP6 and DUSP9 (WITH/FROM P51812, Q15418, Q9BUB5, Q13115, Q16828, Q99956, Q9BRK4).

Reason: Most partners are protein kinases (RSK1, RSK2, MNK1) or ERK-directed phosphatases (DUSP4/6/9); 'protein kinase binding' and 'protein phosphatase binding' capture these interactions more informatively. GOA now lists this interaction as one row per partner; this row's partner is UniProtKB:P51812 (Ribosomal protein S6 kinase alpha-3), so only the protein kinase binding replacement applies to it.

Proposed replacements: protein kinase binding

Summary: This is a generic protein-binding (GO:0005515) interaction annotation for MAPK1/ERK2 from PMID:32296183; ERK2 has many reported interacting partners.

Reason: The generic protein binding term is uninformative for a multi-partner kinase like ERK2 and should not be retained as a bare GO:0005515 assertion. ERK partner recognition is motif/exosite-driven (KIM/D-domain, DEF/FXFP), and specific docking, substrate, scaffold, or phosphatase interactions should be curated with a more informative molecular-function term where the evidence supports one.

Summary: Kinase interaction network interactions of ERK2 with RSK2, RSK3 and MNK1 (WITH/FROM P51812, Q15349, Q9BUB5).

Reason: The IntAct-derived WITH/FROM partner(s) for this high-throughput interactome study are protein kinases (RPS6KA3/RSK2, RPS6KA2/RSK3, MKNK1). The binding itself is the experimental observation, so the more informative 'protein kinase binding' captures it; the partners are well-known ERK docking-motif (D-motif) containing downstream kinases/substrates. GOA now lists this interaction as one row per partner; this row's partner is UniProtKB:P51812 (Ribosomal protein S6 kinase alpha-3), so only the protein kinase binding replacement applies to it.

Proposed replacements: protein kinase binding

Summary: This is a generic protein-binding (GO:0005515) interaction annotation for MAPK1/ERK2 from PMID:32814053; ERK2 has many reported interacting partners.

Reason: The generic protein binding term is uninformative for a multi-partner kinase like ERK2 and should not be retained as a bare GO:0005515 assertion. ERK partner recognition is motif/exosite-driven (KIM/D-domain, DEF/FXFP), and specific docking, substrate, scaffold, or phosphatase interactions should be curated with a more informative molecular-function term where the evidence supports one.

Summary: This is a generic protein-binding (GO:0005515) interaction annotation for MAPK1/ERK2 from PMID:33961781; ERK2 has many reported interacting partners.

Reason: The generic protein binding term is uninformative for a multi-partner kinase like ERK2 and should not be retained as a bare GO:0005515 assertion. ERK partner recognition is motif/exosite-driven (KIM/D-domain, DEF/FXFP), and specific docking, substrate, scaffold, or phosphatase interactions should be curated with a more informative molecular-function term where the evidence supports one.

Summary: AP-MS interactions of ERK2 with RSK1, RSK2 and RSK3 (WITH/FROM Q15418, P51812, Q15349) in a head and neck cancer protein network.

Reason: The IntAct-derived WITH/FROM partner(s) for this high-throughput interactome study are protein kinases (RPS6KA1/2/3 (RSK1-3)). The binding itself is the experimental observation, so the more informative 'protein kinase binding' captures it; the partners are well-known ERK docking-motif (D-motif) containing downstream kinases/substrates. GOA now lists this interaction as one row per partner; this row's partner is UniProtKB:P51812 (Ribosomal protein S6 kinase alpha-3), so only the protein kinase binding replacement applies to it.

Proposed replacements: protein kinase binding

Summary: OpenCell endogenous-tagging interaction between ERK2 and RSK3/RPS6KA2 (WITH/FROM Q15349).

Reason: The IntAct-derived WITH/FROM partner(s) for this high-throughput interactome study are protein kinases (RPS6KA2/RSK3). The binding itself is the experimental observation, so the more informative 'protein kinase binding' captures it; the partners are well-known ERK docking-motif (D-motif) containing downstream kinases/substrates.

Proposed replacements: protein kinase binding

Summary: HaloTag-enrichment mass spectrometry interaction between ERK2 and STAT3 (WITH/FROM P40763) in adipocytes.

Reason: The partner STAT3 is a DNA-binding transcription factor and a known ERK phosphorylation target; 'DNA-binding transcription factor binding' is more informative than bare protein binding. The partner identity is taken from the GOA WITH/FROM field of this high-throughput study.

Proposed replacements: DNA-binding transcription factor binding

Summary: Multimodal cell map interaction between ERK2 and the scaffold protein PEA-15 (WITH/FROM Q15121).

Reason: The partner PEA-15 is a well-characterised ERK scaffolding/anchoring protein (see PMID:23575685); 'scaffold protein binding' is the informative MF.

Proposed replacements: scaffold protein binding

Summary: This is a generic protein-binding (GO:0005515) interaction annotation for MAPK1/ERK2 from PMID:9632734; ERK2 has many reported interacting partners.

Reason: The generic protein binding term is uninformative for a multi-partner kinase like ERK2 and should not be retained as a bare GO:0005515 assertion. ERK partner recognition is motif/exosite-driven (KIM/D-domain, DEF/FXFP), and specific docking, substrate, scaffold, or phosphatase interactions should be curated with a more informative molecular-function term where the evidence supports one.

Summary: ERK2 is a preferred substrate of, and binds, the cytosolic dual-specificity MAP kinase phosphatase Pyst2/MKP-X (DUSP7; WITH/FROM Q16829), which it catalytically activates.

Reason: The partner is the ERK-selective phosphatase DUSP7; 'protein phosphatase binding' is the informative MF.

Proposed replacements: protein phosphatase binding

Summary: MAPK1/ERK2 self-associates (homodimerizes); identical protein binding is supported by PMID:16627622.

Reason: ERK2 dimerization is a documented property relevant to its cytoplasmic retention and scaffold interactions, but it is a regulatory/structural property rather than the core catalytic MAP kinase function.

Summary: MAPK1/ERK2 self-associates (homodimerizes); identical protein binding is supported by PMID:26267534.

Reason: ERK2 dimerization is a documented property relevant to its cytoplasmic retention and scaffold interactions, but it is a regulatory/structural property rather than the core catalytic MAP kinase function.

Summary: This term assigns phosphotyrosine residue binding to ERK2.

Reason: ERK2 substrate and partner recognition is mediated by D-domain/KIM and DEF/FXFP docking motifs rather than by a dedicated phosphotyrosine-binding module; this automated assignment is not supported as a core ERK2 molecular function.

Summary: MAPK1/ERK2 is an ATP-dependent protein serine/threonine kinase.

Reason: Serine/threonine protein kinase activity is a core molecular function of MAPK1; the more specific MAP kinase activity term should also be retained where present.

Summary: Ensembl ortholog projection of mitochondrion from mouse Mapk1; a minor, stimulus-dependent ERK2 pool at mitochondria is supported by primary studies.

Reason: ORGANELLES check (2026-11-03), previously MARK_AS_OVER_ANNOTATED. The projection source is mouse Mapk1 (P63085), whose mitochondrion row in QuickGO is an MGI IDA on PMID:11884367 (ERKs co-localised with cardiac mitochondria by immunoblotting and immunofluorescence; abstract-only, so the fraction's ER control cannot be checked), so the projection is not circular. Independent primary studies agree that a minor ERK pool enters or associates with mitochondria: in mouse LP07 tumour cells, mitochondrial subfractionation placed ERK1/2 with MEK1/2 in the outer-membrane and intermembrane-space fractions, and an ERK2 Cys214 mutant that cannot bind MEK1/2 was retained in mitochondria (PMID:18545666); ERK1/2 were found active in the outer membrane/intermembrane space fraction of rat brain mitochondria (PMID:15030409, abstract-only); and in HeLa cells the paralog ERK1 was shown in purified mitochondria checked for ER contamination by 5'-nucleotidase and glucose-6-phosphatase (PMID:19847302). The organelle claim therefore holds as a minor, stimulus-dependent signalling pool, which is non-core next to the cytoplasmic and nuclear ERK2 pools; the earlier MARK_AS_OVER_ANNOTATED read the term as a core-location claim. Stays at the root: ERK2 has no transit peptide or membrane anchor, the pool is transient trafficking rather than residence (TRAF3/BRAF precedent), and the sub-mitochondrial data split between outer membrane and IMS (with only antibodies that do not separate ERK1 from ERK2), so no sub-compartment row is added.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment.

Reason: Cytosolic localization is consistent with ERK2 being predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation.

Summary: MAPK1 is activated in receptor and growth-factor signaling contexts, but these are stimulus-specific pathway contexts rather than the core conserved ERK2 function.

Reason: Growth-factor and receptor-specific signaling annotations can be retained as non-core contexts; the core MAPK1 process is the intracellular ERK/MAPK cascade.

Summary: This term assigns RNA polymerase II CTD heptapeptide repeat kinase activity to ERK2.

Reason: ERK2 is a proline-directed Ser/Thr MAP kinase; while it phosphorylates Ser/Thr-Pro motifs, dedicated RNA Pol II CTD kinase activity is not a core supported ERK2 function and this ISS/IEA assignment overstates substrate specificity. The supported catalytic terms are MAP kinase activity and protein serine/threonine kinase activity.

Summary: This is a distal or cell-type-specific outcome rather than a core MAPK1 function.

Reason: The available synthesis supports ERK/MAPK cascade membership as core, but warns against promoting broad developmental or disease-associated outcomes to core MAPK1 functions without direct MAPK1-specific evidence.

Summary: MAPK1 is a kinase, but this term is too broad for ERK2.

Reason: The broad kinase activity annotation should use the more informative serine/threonine MAP kinase terms.

Proposed replacements: protein serine/threonine kinase activity MAP kinase activity

Summary: MAPK1 binds MAP kinase phosphatases such as DUSP6/MKP-3.

Reason: Phosphatase binding is a supported regulatory interaction, but it is not the primary catalytic function of MAPK1.

Summary: This pseudopodium annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the pseudopodium location is a context-/pathway-specific or high- throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This is a context-dependent downstream process (response to nicotine) linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function, which is ERK2 MAP kinase activity in the ERK/MAPK cascade.

Summary: MAPK1 is activated in receptor and growth-factor signaling contexts, but these are stimulus-specific pathway contexts rather than the core conserved ERK2 function.

Reason: Growth-factor and receptor-specific signaling annotations can be retained as non-core contexts; the core MAPK1 process is the intracellular ERK/MAPK cascade.

Summary: This is a distal or cell-type-specific outcome rather than a core MAPK1 function.

Reason: The available synthesis supports ERK/MAPK cascade membership as core, but warns against promoting broad developmental or disease-associated outcomes to core MAPK1 functions without direct MAPK1-specific evidence.

Summary: MAPK1/ERK2 self-associates (homodimerizes); identical protein binding is supported by GO_REF:0000107.

Reason: ERK2 dimerization is a documented property relevant to its cytoplasmic retention and scaffold interactions, but it is a regulatory/structural property rather than the core catalytic MAP kinase function.

Summary: This is a distal or cell-type-specific outcome rather than a core MAPK1 function.

Reason: The available synthesis supports ERK/MAPK cascade membership as core, but warns against promoting broad developmental or disease-associated outcomes to core MAPK1 functions without direct MAPK1-specific evidence.

Summary: MAPK1 is activated in receptor and growth-factor signaling contexts, but these are stimulus-specific pathway contexts rather than the core conserved ERK2 function.

Reason: Growth-factor and receptor-specific signaling annotations can be retained as non-core contexts; the core MAPK1 process is the intracellular ERK/MAPK cascade.

Summary: This is a distal or cell-type-specific outcome rather than a core MAPK1 function.

Reason: The available synthesis supports ERK/MAPK cascade membership as core, but warns against promoting broad developmental or disease-associated outcomes to core MAPK1 functions without direct MAPK1-specific evidence.

Summary: MAPK1/ERK2 has MAP kinase activity.

Reason: MAP kinase activity is the most specific core catalytic function for MAPK1/ERK2.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment.

Reason: Cytosolic localization is consistent with ERK2 being predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation.

Summary: This is a distal or cell-type-specific outcome rather than a core MAPK1 function.

Reason: The available synthesis supports ERK/MAPK cascade membership as core, but warns against promoting broad developmental or disease-associated outcomes to core MAPK1 functions without direct MAPK1-specific evidence.

Summary: MAPK1 can phosphorylate serine residues, but the serine-only term is incomplete for ERK2.

Reason: ERK2 is a proline-directed serine/threonine MAP kinase; GO:0004674 and GO:0004707 better capture the supported activity than a serine-only activity term.

Proposed replacements: protein serine/threonine kinase activity MAP kinase activity

Summary: MAPK1/ERK2 is an ATP-dependent protein serine/threonine kinase.

Reason: Serine/threonine protein kinase activity is a core molecular function of MAPK1; the more specific MAP kinase activity term should also be retained where present.

Summary: ERK2 phosphorylation of GLI1 links MAPK1 to Smoothened/Hedgehog pathway output in this specific context.

Reason: This is a supported pathway-specific downstream role from PMID:35831023, but the core MAPK1 function remains ERK2 serine/threonine MAP kinase activity in the ERK/MAPK cascade.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment.

Reason: Cytosolic localization is consistent with ERK2 being predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation.

Summary: MAPK1/ERK2 has MAP kinase activity.

Reason: MAP kinase activity is the most specific core catalytic function for MAPK1/ERK2.

Summary: MAPK1/ERK2 has MAP kinase activity.

Reason: MAP kinase activity is the most specific core catalytic function for MAPK1/ERK2.

Summary: MAPK1/ERK2 is an ATP-dependent protein serine/threonine kinase.

Reason: Serine/threonine protein kinase activity is a core molecular function of MAPK1; the more specific MAP kinase activity term should also be retained where present.

Summary: MAPK1/ERK2 is a central component of the ERK1 and ERK2 cascade.

Reason: ERK1 and ERK2 cascade is a core pathway term for MAPK1 and is more specific than generic signaling process terms.

Summary: This is a distal or cell-type-specific outcome rather than a core MAPK1 function.

Reason: The available synthesis supports ERK/MAPK cascade membership as core, but warns against promoting broad developmental or disease-associated outcomes to core MAPK1 functions without direct MAPK1-specific evidence.

Summary: MAPK1/ERK2 has MAP kinase activity.

Reason: MAP kinase activity is the most specific core catalytic function for MAPK1/ERK2.

Summary: This is a context-dependent downstream process (chemokine-mediated signaling pathway) linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function, which is ERK2 MAP kinase activity in the ERK/MAPK cascade.

Summary: MAPK1/ERK2 functions in the canonical MAPK cascade.

Reason: MAPK cascade membership is a core biological process for ERK2, downstream of Ras-RAF-MEK signaling.

Summary: This is a context-dependent downstream process linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function.

Summary: MAPK1/ERK2 functions in the canonical MAPK cascade.

Reason: MAPK cascade membership is a core biological process for ERK2, downstream of Ras-RAF-MEK signaling.

Summary: MAPK1 is activated in receptor and growth-factor signaling contexts, but these are stimulus-specific pathway contexts rather than the core conserved ERK2 function.

Reason: Growth-factor and receptor-specific signaling annotations can be retained as non-core contexts; the core MAPK1 process is the intracellular ERK/MAPK cascade.

Summary: ERK1/2 bind and phosphorylate PGK1 (WITH/FROM P00558) at S203, promoting its mitochondrial translocation where PGK1 acts as a protein kinase.

Reason: The partner PGK1 is shown in this paper to function as a protein kinase (phosphorylating PDHK1); 'protein kinase binding' is more informative than bare protein binding.

Proposed replacements: protein kinase binding

Summary: Positive regulation of telomere maintenance is inferred from a high-throughput RNAi telomerase screen (PMID:21531765) plus electronic annotation.

Reason: This is a high-throughput screen-derived, indirect pathway outcome rather than a direct MAPK1 function; it should not be elevated to a core ERK2 annotation without direct mechanistic evidence.

Summary: Positive regulation of cholesterol biosynthesis is an ERK2-linked downstream metabolic outcome reported in PMID:38503280.

Reason: This is a context-dependent downstream metabolic process mediated via ERK signaling rather than a core conserved MAPK1 molecular function; retained as non-core.

Summary: Interaction of ERK2 with the MAPK phosphatase MKP-7/DUSP16 (WITH/FROM Q9BY84).

Reason: The partner is the dual-specificity MAP kinase phosphatase MKP-7/DUSP16; 'protein phosphatase binding' is the informative MF.

Proposed replacements: protein phosphatase binding

Summary: RASopathy-associated MAPK1 variants alter ERK2 interaction with MEK1 (WITH/FROM Q02750) and MKP3/DUSP6 (WITH/FROM Q16828).

Reason: The partners are the upstream MAP kinase kinase MEK1 and the ERK phosphatase MKP3/DUSP6; 'mitogen-activated protein kinase kinase binding' and 'protein phosphatase binding' are the informative MFs. GOA now lists this interaction as one row per partner; this row's partner is UniProtKB:Q02750 (Dual specificity mitogen-activated protein kinase kinase 1), so only the mitogen-activated protein kinase kinase binding replacement applies to it.

Proposed replacements: mitogen-activated protein kinase kinase binding

Summary: MAPK1/ERK2 localizes to the nucleus after stimulation.

Reason: Nuclear localization is supported, but should be interpreted as stimulus-dependent rather than constitutive.

Summary: MAPK1/ERK2 is cytoplasmic in quiescent cells.

Reason: Cytoplasmic localization is a core supported localization for ERK2.

Summary: Activated ERK2 binds the zinc-finger transcriptional repressor ZNF263 (WITH/FROM O14978) through a D-domain, promoting SIX3 silencing in glioblastoma.

Reason: ZNF263 is a DNA-binding transcriptional repressor (binds the SIX3 promoter) that docks onto ERK2; 'DNA-binding transcription factor binding' is the informative MF.

Proposed replacements: DNA-binding transcription factor binding

Summary: MAPK1/ERK2 is an ATP-dependent protein serine/threonine kinase.

Reason: Serine/threonine protein kinase activity is a core molecular function of MAPK1; the more specific MAP kinase activity term should also be retained where present.

Summary: This is a context-dependent downstream process linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function.

Summary: This is a context-dependent downstream process linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function.

Summary: Activated ERKs interact with the major vault protein (MVP; WITH/FROM Q14764), described as a scaffold protein in EGF signaling that also complexes with SHP-2.

Reason: The partner MVP is described as a scaffold protein for EGF/ERK signaling; 'scaffold protein binding' is the informative MF.

Proposed replacements: scaffold protein binding

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: This is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization; secretory or granule-lumen locations are likely pathway-context over-annotations for soluble ERK2.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is an ATP-dependent protein serine/threonine kinase.

Reason: Serine/threonine protein kinase activity is a core molecular function of MAPK1; the more specific MAP kinase activity term should also be retained where present.

Summary: This plasma membrane annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the plasma membrane location is a context-/pathway-specific or high-throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This caveola annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the caveola location is a context-/pathway-specific or high- throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This is a context-dependent downstream process linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function.

Summary: This is a context-dependent downstream process (response to nicotine) linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function, which is ERK2 MAP kinase activity in the ERK/MAPK cascade.

Summary: This is an amino-acid-starvation response annotation linked to ERK signaling context.

Reason: The starvation-response annotation may be retained as non-core where the source evidence supports this context, but it should not be treated as the core conserved MAPK1 function.

Summary: This stress-activated MAPK cascade annotation on MAPK1/ERK2 derives from a paper focused on ASK1/JNK stress signaling, not the canonical ERK cascade.

Reason: GO:0051403 (stress-activated MAPK cascade) is associated with JNK/p38 (SAPK) signaling. PMID:11096076 concerns the Gln-dependent interaction of glutaminyl-tRNA synthetase with apoptosis signal-regulating kinase 1 (ASK1) and JNK/SAPK, not ERK2; assigning the stress-activated MAPK cascade to canonical ERK2 over-annotates MAPK1.

Summary: This is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization; secretory or granule-lumen locations are likely pathway-context over-annotations for soluble ERK2.

Summary: This is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization; secretory or granule-lumen locations are likely pathway-context over-annotations for soluble ERK2.

Summary: This is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization; secretory or granule-lumen locations are likely pathway-context over-annotations for soluble ERK2.

Summary: This is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization; secretory or granule-lumen locations are likely pathway-context over-annotations for soluble ERK2.

Summary: ERK2 interacts with MFAP3L (WITH/FROM O75121), reported as a nuclear protein kinase that phosphorylates ERK2 downstream of nuclear EGFR.

Reason: The partner MFAP3L is reported in this paper to act as a protein kinase that phosphorylates ERK2; 'protein kinase binding' is the informative MF.

Proposed replacements: protein kinase binding

Summary: MAPK1 directly phosphorylates protein substrates.

Reason: Protein phosphorylation is the direct biochemical output of the MAPK1 kinase activity.

Summary: MAPK1/ERK2 localizes to the nucleus after stimulation.

Reason: Nuclear localization is supported, but should be interpreted as stimulus-dependent rather than constitutive.

Summary: MAPK1/ERK2 is cytoplasmic in quiescent cells.

Reason: Cytoplasmic localization is a core supported localization for ERK2.

Summary: MAPK1/ERK2 is cytoplasmic in quiescent cells.

Reason: Cytoplasmic localization is a core supported localization for ERK2.

Summary: This mitotic spindle annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the mitotic spindle location is a context-/pathway-specific or high-throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This is a generic protein-binding (GO:0005515) interaction annotation for MAPK1/ERK2 from PMID:23847209; ERK2 has many reported interacting partners.

Reason: The generic protein binding term is uninformative for a multi-partner kinase like ERK2 and should not be retained as a bare GO:0005515 assertion. ERK partner recognition is motif/exosite-driven (KIM/D-domain, DEF/FXFP), and specific docking, substrate, scaffold, or phosphatase interactions should be curated with a more informative molecular-function term where the evidence supports one.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation; this is one of several Reactome reaction-level annotations placing ERK2 in the nucleoplasm.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2. The repeated Reactome nucleoplasm rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation; this is one of several Reactome reaction-level annotations placing ERK2 in the nucleoplasm.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2. The repeated Reactome nucleoplasm rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation; this is one of several Reactome reaction-level annotations placing ERK2 in the nucleoplasm.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2. The repeated Reactome nucleoplasm rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation; this is one of several Reactome reaction-level annotations placing ERK2 in the nucleoplasm.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2. The repeated Reactome nucleoplasm rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation; this is one of several Reactome reaction-level annotations placing ERK2 in the nucleoplasm.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2. The repeated Reactome nucleoplasm rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation; this is one of several Reactome reaction-level annotations placing ERK2 in the nucleoplasm.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2. The repeated Reactome nucleoplasm rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation; this is one of several Reactome reaction-level annotations placing ERK2 in the nucleoplasm.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2. The repeated Reactome nucleoplasm rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation; this is one of several Reactome reaction-level annotations placing ERK2 in the nucleoplasm.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2. The repeated Reactome nucleoplasm rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation; this is one of several Reactome reaction-level annotations placing ERK2 in the nucleoplasm.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2. The repeated Reactome nucleoplasm rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation; this is one of several Reactome reaction-level annotations placing ERK2 in the nucleoplasm.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2. The repeated Reactome nucleoplasm rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation; this is one of several Reactome reaction-level annotations placing ERK2 in the nucleoplasm.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2. The repeated Reactome nucleoplasm rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation; this is one of several Reactome reaction-level annotations placing ERK2 in the nucleoplasm.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2. The repeated Reactome nucleoplasm rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation; this is one of several Reactome reaction-level annotations placing ERK2 in the nucleoplasm.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2. The repeated Reactome nucleoplasm rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation; this is one of several Reactome reaction-level annotations placing ERK2 in the nucleoplasm.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2. The repeated Reactome nucleoplasm rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 can accumulate in the nuclear compartment after stimulation; this is one of several Reactome reaction-level annotations placing ERK2 in the nucleoplasm.

Reason: Nucleoplasmic localization is compatible with the supported stimulus-dependent nuclear accumulation of ERK2. The repeated Reactome nucleoplasm rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment; this is one of many Reactome reaction-level annotations placing ERK2 in the cytosol.

Reason: Cytosolic localization is a core supported localization for ERK2, which is predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation. The numerous Reactome cytosol rows are group-accepted as consistent with this core localization.

Summary: MAPK1 is activated in receptor and growth-factor signaling contexts, but these are stimulus-specific pathway contexts rather than the core conserved ERK2 function.

Reason: Growth-factor and receptor-specific signaling annotations can be retained as non-core contexts; the core MAPK1 process is the intracellular ERK/MAPK cascade.

Summary: MAPK1/ERK2 is an ATP-dependent protein serine/threonine kinase.

Reason: Serine/threonine protein kinase activity is a core molecular function of MAPK1; the more specific MAP kinase activity term should also be retained where present.

Summary: This is a generic protein-binding (GO:0005515) interaction annotation for MAPK1/ERK2 from PMID:18794356; ERK2 has many reported interacting partners.

Reason: The generic protein binding term is uninformative for a multi-partner kinase like ERK2 and should not be retained as a bare GO:0005515 assertion. ERK partner recognition is motif/exosite-driven (KIM/D-domain, DEF/FXFP), and specific docking, substrate, scaffold, or phosphatase interactions should be curated with a more informative molecular-function term where the evidence supports one.

Summary: MAPK1/ERK2 localizes to the nucleus after stimulation.

Reason: Nuclear localization is supported, but should be interpreted as stimulus-dependent rather than constitutive.

Summary: MAPK1/ERK2 is cytoplasmic in quiescent cells.

Reason: Cytoplasmic localization is a core supported localization for ERK2.

Summary: MAPK1 is activated in receptor and growth-factor signaling contexts, but these are stimulus-specific pathway contexts rather than the core conserved ERK2 function.

Reason: Growth-factor and receptor-specific signaling annotations can be retained as non-core contexts; the core MAPK1 process is the intracellular ERK/MAPK cascade.

Summary: This is a generic protein-binding (GO:0005515) interaction annotation for MAPK1/ERK2 from PMID:22253824; ERK2 has many reported interacting partners.

Reason: The generic protein binding term is uninformative for a multi-partner kinase like ERK2 and should not be retained as a bare GO:0005515 assertion. ERK partner recognition is motif/exosite-driven (KIM/D-domain, DEF/FXFP), and specific docking, substrate, scaffold, or phosphatase interactions should be curated with a more informative molecular-function term where the evidence supports one.

Summary: MAPK1/ERK2 is an ATP-dependent protein serine/threonine kinase.

Reason: Serine/threonine protein kinase activity is a core molecular function of MAPK1; the more specific MAP kinase activity term should also be retained where present.

Summary: MAPK1/ERK2 localizes to the nucleus after stimulation.

Reason: Nuclear localization is supported, but should be interpreted as stimulus-dependent rather than constitutive.

Summary: Mitochondrion (TAS) from the Yao and Seger review of ERK-cascade compartments; a minor, stimulus-dependent ERK2 pool at mitochondria is supported by primary studies.

Reason: ORGANELLES check (2026-11-03), previously MARK_AS_OVER_ANNOTATED. The TAS source PMID:19565474 is a review whose cached text is abstract-only and does not name the mitochondrion, so the row is judged on primary papers. Independent primary studies agree that a minor ERK pool enters or associates with mitochondria: in mouse LP07 tumour cells, mitochondrial subfractionation placed ERK1/2 with MEK1/2 in the outer-membrane and intermembrane-space fractions, and an ERK2 Cys214 mutant that cannot bind MEK1/2 was retained in mitochondria (PMID:18545666); ERK1/2 were found active in the outer membrane/intermembrane space fraction of rat brain mitochondria (PMID:15030409, abstract-only); and in HeLa cells the paralog ERK1 was shown in purified mitochondria checked for ER contamination by 5'-nucleotidase and glucose-6-phosphatase (PMID:19847302). The organelle claim therefore holds as a minor, stimulus-dependent signalling pool, which is non-core next to the cytoplasmic and nuclear ERK2 pools; the earlier MARK_AS_OVER_ANNOTATED read the term as a core-location claim. Stays at the root: ERK2 has no transit peptide or membrane anchor, the pool is transient trafficking rather than residence (TRAF3/BRAF precedent), and the sub-mitochondrial data split between outer membrane and IMS (with only antibodies that do not separate ERK1 from ERK2), so no sub-compartment row is added.

Summary: This early endosome annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the early endosome location is a context-/pathway-specific or high-throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This late endosome annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the late endosome location is a context-/pathway-specific or high- throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This Golgi apparatus annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the Golgi apparatus location is a context-/pathway-specific or high-throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: MAPK1/ERK2 is present in the cytosolic/cytoplasmic compartment.

Reason: Cytosolic localization is consistent with ERK2 being predominantly cytoplasmic in quiescent cells before stimulus-dependent nuclear accumulation.

Summary: This cytoskeleton annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the cytoskeleton location is a context-/pathway-specific or high- throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This caveola annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the caveola location is a context-/pathway-specific or high- throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This focal adhesion annotation is not a supported core MAPK1 localization in this review.

Reason: Falcon synthesis supports cytoplasmic/cytosolic and stimulus-dependent nuclear localization as core; the focal adhesion location is a context-/pathway-specific or high-throughput-derived assignment that should not be promoted to a core ERK2 localization without direct MAPK1-specific evidence in that compartment.

Summary: This TAS annotation assigns regulation of the stress-activated MAPK cascade to MAPK1/ERK2, citing a general ERK compartmentalization review.

Reason: GO:0032872 (regulation of stress-activated MAPK cascade) is associated with JNK/p38 (SAPK) biology rather than the canonical ERK cascade. PMID:19565474 is a review of ERK signaling across subcellular compartments and does not establish ERK2 as a regulator of the stress-activated (JNK/p38) MAPK cascade; this is an over-annotation for canonical ERK2, consistent with the corresponding IEA row.

Summary: This is a context-dependent downstream process (regulation of cytoskeleton organization) linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function, which is ERK2 MAP kinase activity in the ERK/MAPK cascade.

Summary: This is a context-dependent downstream process (caveolin-mediated endocytosis) linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function, which is ERK2 MAP kinase activity in the ERK/MAPK cascade.

Summary: This is a context-dependent downstream process (regulation of Golgi inheritance) linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function, which is ERK2 MAP kinase activity in the ERK/MAPK cascade.

Summary: This is a context-dependent downstream process (regulation of early endosome to late endosome transport) linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function, which is ERK2 MAP kinase activity in the ERK/MAPK cascade.

Summary: MAPK1 can increase phosphorylation of downstream threonine-containing protein substrates.

Reason: The term is consistent with ERK2 substrate phosphorylation, but it is less central than the direct kinase activity and ERK/MAPK cascade annotations.

Summary: MAPK1/ERK2 is a central component of the ERK1 and ERK2 cascade.

Reason: ERK1 and ERK2 cascade is a core pathway term for MAPK1 and is more specific than generic signaling process terms.

Summary: MAPK1 binds MAP kinase phosphatases such as DUSP6/MKP-3.

Reason: Phosphatase binding is a supported regulatory interaction, but it is not the primary catalytic function of MAPK1.

Summary: This term assigns RNA polymerase II CTD heptapeptide repeat kinase activity to ERK2.

Reason: ERK2 is a proline-directed Ser/Thr MAP kinase; while it phosphorylates Ser/Thr-Pro motifs, dedicated RNA Pol II CTD kinase activity is not a core supported ERK2 function and this ISS/IEA assignment overstates substrate specificity. The supported catalytic terms are MAP kinase activity and protein serine/threonine kinase activity.

Summary: MAPK1/ERK2 has MAP kinase activity.

Reason: MAP kinase activity is the most specific core catalytic function for MAPK1/ERK2.

Summary: This is a context-dependent downstream process linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function.

Summary: This is a context-dependent downstream process linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function.

Summary: MAPK1 participates in signal transduction, but the generic term should be replaced by more specific intracellular MAPK/ERK signaling terms.

Reason: Generic signal transduction underspecifies MAPK1; intracellular signal transduction and ERK/MAPK cascade terms capture the supported biology more accurately.

Proposed replacements: intracellular signal transduction ERK1 and ERK2 cascade

Summary: This is a context-dependent downstream process linked to ERK signaling.

Reason: The process may be retained as non-core where the source evidence supports a specific context, but it should not be treated as the core conserved MAPK1 function.

Summary: This is a generic protein-binding assertion for MAPK1/ERK2 from PMID:17255949.

Reason: GO:0005515 is uninformative for a multi-partner MAP kinase. This row does not distinguish substrate recognition, scaffold docking, phosphatase binding, or another specific MAPK1 regulatory interaction, so it should be replaced only if later source-specific curation can capture a mechanistically informative binding activity.

Summary: ERK1/2 bind Mxi2, a p38alpha (MAPK14) isoform (WITH/FROM Q16539-3; also MEK1 and PEA-15 listed), which promotes stimulus-independent ERK nuclear import.

Reason: The principal partner studied is the p38alpha kinase isoform Mxi2 (MEK1 also listed); 'protein kinase binding' is the informative MF. GOA now lists this interaction as one row per partner; this row's partner is UniProtKB:Q16539-3 (Mitogen-activated protein kinase 14), so only the protein kinase binding replacement applies to it.

Proposed replacements: protein kinase binding

Summary: This is a generic protein-binding assertion for MAPK1/ERK2 from PMID:18060821.

Reason: GO:0005515 is uninformative for a multi-partner MAP kinase. This row does not distinguish substrate recognition, scaffold docking, phosphatase binding, or another specific MAPK1 regulatory interaction, so it should be replaced only if later source-specific curation can capture a mechanistically informative binding activity.

Summary: This is a generic protein-binding assertion for MAPK1/ERK2 from PMID:18060821.

Reason: GO:0005515 is uninformative for a multi-partner MAP kinase. This row does not distinguish substrate recognition, scaffold docking, phosphatase binding, or another specific MAPK1 regulatory interaction, so it should be replaced only if later source-specific curation can capture a mechanistically informative binding activity.

Summary: This is a generic protein-binding assertion for MAPK1/ERK2 from PMID:18616943.

Reason: GO:0005515 is uninformative for a multi-partner MAP kinase. This row does not distinguish substrate recognition, scaffold docking, phosphatase binding, or another specific MAPK1 regulatory interaction, so it should be replaced only if later source-specific curation can capture a mechanistically informative binding activity.

Summary: AP-MS interaction of ERK2 with RSK2/RPS6KA3 and RSK3/RPS6KA2 (WITH/FROM P51812, Q15349) in the CMGC kinase interaction landscape.

Reason: The IntAct-derived WITH/FROM partner(s) for this high-throughput interactome study are protein kinases (RPS6KA3/RSK2, RPS6KA2/RSK3). The binding itself is the experimental observation, so the more informative 'protein kinase binding' captures it; the partners are well-known ERK docking-motif (D-motif) containing downstream kinases/substrates. GOA now lists this interaction as one row per partner; this row's partner is UniProtKB:Q15349 (Ribosomal protein S6 kinase alpha-2), so only the protein kinase binding replacement applies to it.

Proposed replacements: protein kinase binding

Summary: Endogenous in situ proximity ligation detection of ERK2 with RSK2/RPS6KA3 and the phosphatases HePTP/PTPN7 and PTP-SL/PTPRR (WITH/FROM P51812, P35236, Q15256).

Reason: The partners are a protein kinase (RSK2) and ERK-directed tyrosine phosphatases (HePTP, PTPRR); 'protein kinase binding' and 'protein phosphatase binding' capture these interactions more informatively. GOA now lists this interaction as one row per partner; this row's partner is UniProtKB:P51812 (Ribosomal protein S6 kinase alpha-3), so only the protein kinase binding replacement applies to it.

Proposed replacements: protein kinase binding

Summary: Endogenous in situ proximity ligation detection of ERK2 with RSK2/RPS6KA3 and the phosphatases HePTP/PTPN7 and PTP-SL/PTPRR (WITH/FROM P51812, P35236, Q15256).

Reason: The partners are a protein kinase (RSK2) and ERK-directed tyrosine phosphatases (HePTP, PTPRR); 'protein kinase binding' and 'protein phosphatase binding' capture these interactions more informatively. GOA now lists this interaction as one row per partner; this row's partner is UniProtKB:Q15256 (Receptor-type tyrosine-protein phosphatase R), so only the protein phosphatase binding replacement applies to it.

Proposed replacements: protein phosphatase binding

Summary: Interaction of ERK2 with the MAPK phosphatases DUSP4, DUSP6 and DUSP9 (WITH/FROM Q13115, Q16828, Q99956) in systematic phosphatase interaction profiling.

Reason: All partners are ERK-directed dual-specificity phosphatases; 'protein phosphatase binding' is the informative MF. GOA now lists this interaction as one row per partner; this row's partner is UniProtKB:Q16828 (Dual specificity protein phosphatase 6), so only the protein phosphatase binding replacement applies to it.

Proposed replacements: protein phosphatase binding