Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Automatic Gene Ontology annotation based on Rhea mapping
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Kinase suppressor of Ras forms a multiprotein signaling complex and modulates MEK localization.
The CXC chemokine stromal cell-derived factor activates a Gi-coupled phosphoinositide 3-kinase in T lymphocytes.
Hepatitis C virus core protein interacts with 14-3-3 protein and activates the kinase Raf-1.
PV1 is a key structural component for the formation of the stomatal and fenestral diaphragms.
Human tribbles, a protein family controlling mitogen-activated protein kinase cascades.
Interaction with MEK causes nuclear export and downregulation of peroxisome proliferator-activated receptor gamma.
An antiapoptotic protein, c-FLIPL, directly binds to MKK7 and inhibits the JNK pathway.
Mxi2 promotes stimulus-independent ERK nuclear translocation.
Spatial regulation of Raf kinase signaling by RKTG.
A novel tandem affinity purification strategy for the efficient isolation and characterisation of native protein complexes.
Final stages of cytokinesis and midbody ring formation are controlled by BRUCE.
Regulation of human myoblast differentiation by PEBP4.
The ERK signaling cascade--views from different subcellular compartments.
The prolyl isomerase Pin1 enhances HER-2 expression and cellular transformation via its interaction with mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1.
Pseudorabies virus tegument protein Us2 recruits the mitogen-activated protein kinase extracellular-regulated kinase (ERK) to membranes through interaction with the ERK common docking domain.
VRK2 inhibits mitogen-activated protein kinase signaling and inversely correlates with ErbB2 in human breast cancer.
Mutation that blocks ATP binding creates a pseudokinase stabilizing the scaffolding function of kinase suppressor of Ras, CRAF and BRAF.
Sensitive detection of idiotypic platelet-reactive alloantibodies by an electrical protein chip.
VRK2 anchors KSR1-MEK1 to endoplasmic reticulum forming a macromolecular complex that compartmentalizes MAPK signaling.
MEK1 inactivates Myt1 to regulate Golgi membrane fragmentation and mitotic entry in mammalian cells.
Mechanism of MEK inhibition determines efficacy in mutant KRAS- versus BRAF-driven cancers.
MEK1 promotes YAP and their interaction is critical for tumorigenesis in liver cancer.
MiR-92a mediates AZD6244 induced apoptosis and G1-phase arrest of lymphoma cells by targeting Bim.
Disruption of CRAF-mediated MEK activation is required for effective MEK inhibition in KRAS mutant tumors.
Structure of the BRAF-MEK complex reveals a kinase activity independent role for BRAF in MAPK signaling.
A proteome-scale map of the human interactome network.
Crystal structure of a BRAF kinase domain monomer explains basis for allosteric regulation.
Tunable-combinatorial mechanisms of acquired resistance limit the efficacy of BRAF/MEK cotargeting but result in melanoma drug addiction.
A human interactome in three quantitative dimensions organized by stoichiometries and abundances.
Divergent effects of intrinsically active MEK variants on developmental Ras signaling.
MEK drives BRAF activation through allosteric control of KSR proteins.
Extensive rewiring of the EGFR network in colorectal cancer cells expressing transforming levels of KRAS(G13D).
A reference map of the human binary protein interactome.
Kinase Interaction Network Expands Functional and Disease Roles of Human Kinases.
Enhanced MAPK1 Function Causes a Neurodevelopmental Disorder within the RASopathy Clinical Spectrum.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Biallelic mutations in MOS cause female infertility characterized by human early embryonic arrest and fragmentation.
OpenCell: Endogenous tagging for the cartography of human cellular organization.
Systematic discovery of mutation-directed neo-protein-protein interactions in cancer.
Cloning and characterization of two distinct human extracellular signal-regulated kinase activator kinases, MEK1 and MEK2.
Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling.
MAP2K1 phosphorylates MAPK3
Dissociation of p-T,Y-MAPK3:MAP2K1
Inactivation of MAP2K1 by CDK1
Anthrax lef cleaves target cell MAP2K1 (MEK1)
MAP2Ks and MAPKs bind to the activated RAF complex
MAP2Ks phosphorylate MAPKs
RAF phosphorylates MAP2K dimer
Dissociation of RAS:RAF complex
MAP2Ks and MAPKs are phosphorylated at the endosome membrane
WDR83:LAMTOR2:LAMTOR3 binds MAPK components
IL17RD binds p-2S MAP2Ks and MAPKs
MAP2Ks phosphorylate MAPK at the Golgi membrane
Activated MAPKs phosphorylate MAP2K1
Activated MAP2Ks phosphorylate MAPKs downstream of high kinase activity BRAF mutants
High kinase activity BRAF complexes phosphorylate MAP2Ks
High kinase activity BRAF mutants bind MAP2Ks and MAPKs
RAS:GTP:moderate kinase activity p-RAF complexes bind MAP2Ks and MAPKs
Activated MAP2Ks phosphorylate MAPKs downstream of inactive BRAF mutants
RAS:GTP:moderate kinase activity p-RAF complexes phosphorylate MAP2Ks
Activated MAP2Ks phosphorylate MAPKs downstream of moderate kinase activity BRAF mutants
Activated MAP2Ks phosphorylate MAPKs downstream of oncogenic RAS
Mutant RAS:p-RAF complexes bind MAP2Ks and MAPKs
Mutant RAS:p-RAF complexes phosphorylate MAP2Ks
Dissociation of BRAF/RAF fusion complex
p-BRAF and RAF fusion dimers phosphorylate MAP2Ks
p-BRAF and RAF fusion dimers bind MAP2Ks and MAPKs
MAPKs are phosphorylated downstream of BRAF and RAF fusion dimers
RAS:GTP:p-RAF complexes paradoxically bind MAP2Ks and MAPKs
RAS:GTP:inactive p-RAF complexes phosphorylate MAP2Ks
Dissociation of high activity BRAF complexes
Dissociation of moderate activity BRAF complexes
Dissociation of oncogenic RAS:RAF complex
Dissociation of paradoxically activated RAS:BRAF complexes
Activated BRAF recruits MAP2Ks and MAPKs to the endosome
Activated BRAF phosphorylates MAP2K dimers downstream of RAP1 and NGF
Dissociation of phosphorylated MAP2Ks and MAPKs
MAP2Ks phosphorylate MAPKs downstream of BRAF and NGF
MAP2K mutants constitutively phosphorylate MAPKs
Dissociation of RAS:RAF1 mutant complex
MAP2Ks and MAPKs bind to the activated mutant RAF1 complex
MAP2Ks phosphorylate MAPKs downstream of RAF1 mutants
RAF1 mutant complexes phosphorylate MAP2K dimer
Dual mechanism MAP2K inhibitors bind MAP2Ks
Dual mechanism MAPK inhibitors bind MAPKs
Single mechanism MAP2K inhibitors bind phosphorylated MAP2Ks
Single mechanism MAPK inhibitors bind phosphorylated MAPK
UniProt entry Q02750 (MP2K1_HUMAN)
Deep research report on MAP2K1 (falcon)