GRIA1 encodes GluA1, a pore-forming subunit of tetrameric AMPA glutamate receptors. These receptors mediate excitatory postsynaptic currents; subunit composition determines calcium permeability. GluA1 binds receptor-organizing proteins and occupies synaptic and trafficking membrane pools. Pathogenic variants can alter channel function and cause neurodevelopmental disease.
Curated functional classes representing distinct biological activities. These may be splice variants, cleavage products, or other forms with different functions.
GRIA1_FLOPGRIA1_FLIP| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0001540 amyloid-beta binding | IEA GO_REF:0000107 | UNDECIDED | Reason: Retain uncertainty about the GluA1 contribution to amyloid-associated receptor complexes. The accessible abstract foregrounds GluR2; this does not negate the positive rat curator assertion. Supporting Evidence: |
| GO:0001540 amyloid-beta binding | ISS GO_REF:0000024 | UNDECIDED | Reason: The rat curator supports amyloid-complex binding in hippocampal pyramidal neurons. Accessible text emphasizes GluR2-containing complexes; the GluR1 contribution remains unverified. Retain uncertainty without denying the positive interaction. Supporting Evidence: |
| GO:0001666 response to hypoxia | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Reason: Hypoxia changes rat GluA1 abundance and phosphorylation. This establishes a receptor readout of hypoxic stress, but does not establish GluA1 participation in the hypoxia-response machinery. Supporting Evidence: |
| GO:0001919 regulation of receptor recycling | IEA GO_REF:0000107 | UNDECIDED | Reason: The authentic abstract distinguishes plasticity-associated GluR1/GluR2 delivery from continuous GluR2/GluR3 replacement. The full original remains inaccessible, so the specific receptor-recycling regulatory inference cannot be independently adjudicated. Supporting Evidence: |
| GO:0001965 G-protein alpha-subunit binding | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Rat forebrain coimmunoprecipitation supports association with G-alpha-s in a receptor signaling complex; retain this non-core interaction without asserting direct contact. Supporting Evidence: |
| GO:0004970 glutamate-gated receptor activity | IEA GO_REF:0000120 | TOO GENERAL | Reason: The matched ARBA rule and orthology branches support glutamate-receptor function. Retained AMPA glutamate receptor activity supplies the more specific function for this same unextended product. Supporting Evidence: GO_REF:0000120 |
| GO:0004971 AMPA glutamate receptor activity | IBA GO_REF:0000033 | ACCEPT | Reason: Retain the inherited AMPA activity placed at AN396/PTN000438081 (original IBD.gaf line45401). The verified GRIA1 leaf descends from that node; target self-inclusion is legitimate experimental descendant evidence, not circular support. Supporting Evidence: GO_REF:0000033 file:human/GRIA1/GRIA1-phylogeny.json |
| GO:0004971 AMPA glutamate receptor activity | IDA PMID:1311100 Molecular cloning, chromosomal mapping, and functional expre... | ACCEPT | Reason: Human HBGR1 flop cRNA produced agonist-gated currents in Xenopus oocytes. The historical kainate/AMPA terminology and steady-state recording limitation do not contradict the established AMPA receptor identity. Supporting Evidence: |
| GO:0004971 AMPA glutamate receptor activity | IDA PMID:20805473 Functional comparison of the effects of TARPs and cornichons... | ACCEPT | Reason: GluA1 expressed in HEK cells generated glutamate-evoked currents with auxiliary-subunit-dependent kinetics. This supports receptor activity; the accessible main paper does not establish the recombinant GluA1 species or splice identity. Supporting Evidence: |
| GO:0004971 AMPA glutamate receptor activity | IDA PMID:21172611 Hippocampal AMPA receptor gating controlled by both TARP and... | ACCEPT | Reason: Human GluA1, flip unless indicated, generated agonist-evoked currents in HEK293T cells. TARP and cornichon coexpression altered channel kinetics; these modulators remain distinct from the pore-forming receptor. Supporting Evidence: |
| GO:0004971 AMPA glutamate receptor activity | IEA GO_REF:0000107 | ACCEPT | Reason: AMPA receptor activity is the conserved channel function. The rat donor study concerns native receptor complexes and auxiliary-subunit effects on gating. Supporting Evidence: |
| GO:0004971 AMPA glutamate receptor activity | IMP PMID:28628100 Hotspots of missense mutation identify neurodevelopmental di... | ACCEPT | Reason: Synthesized human WT and A636T GluA1 were tested in HEK293 cells. Glutamate responses verified channel expression, while NBQX-sensitive constitutive current distinguished the mutant. This supports receptor function without assigning mutant leak behavior to WT. Supporting Evidence: |
| GO:0004971 AMPA glutamate receptor activity | IMP PMID:35675825 Identification and functional evaluation of GRIA1 missense a... | ACCEPT | Reason: Human disease variants were modeled in rat flip GluA1, with glutamate-evoked currents measured in Xenopus oocytes. WT controls and variant effects support the conserved receptor activity; this is not a direct human-construct assay or the separate tadpole knockout experiment. Supporting Evidence: |
| GO:0005216 monoatomic ion channel activity | IEA GO_REF:0000002 | TOO GENERAL | Reason: IPR001508 supports an ion-channel assignment; the retained AMPA receptor activity specifies both its ligand and receptor class for the same product. Supporting Evidence: GO_REF:0000002 |
| GO:0005515 protein binding | IPI PMID:20805473 Functional comparison of the effects of TARPs and cornichons... | REMOVE | Reason: Positive GluA1βCNIH2 coimmunoprecipitation is retained as complex-association evidence. Generic protein binding adds no informative receptor function and does not make GluA1 the auxiliary regulator; AMPA receptor activity is already represented. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:20805473 Functional comparison of the effects of TARPs and cornichons... | REMOVE | Reason: GluA1 coimmunoprecipitated with TARP gamma-2/CACNG2. Preserve that positive association, but remove generic protein binding: GluA1 supplies receptor/channel function, whereas the auxiliary protein modulates it; the assay does not establish purified binary affinity. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32814053 Interactome Mapping Provides a Network of Neurodegenerative ... | REMOVE | Reason: The BECN1 interaction is positive; the generic binding label adds no functional information. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32814053 Interactome Mapping Provides a Network of Neurodegenerative ... | MODIFY | Reason: Human GRIA1 binds RAB11B in the NN1.0 yeast two-hybrid screen. Small-GTPase binding describes this interaction without asserting Rab regulation or nucleotide-state specificity. Proposed replacements: small GTPase binding Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32814053 Interactome Mapping Provides a Network of Neurodegenerative ... | REMOVE | Reason: Retain the ASCL4 interaction as evidence; remove the uninformative generic binding annotation. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32814053 Interactome Mapping Provides a Network of Neurodegenerative ... | REMOVE | Reason: Retain the KLF15 interaction as evidence; remove the uninformative generic binding annotation. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:32814053 Interactome Mapping Provides a Network of Neurodegenerative ... | REMOVE | Reason: Retain the ZNF232 interaction as evidence; remove the uninformative generic binding annotation. Supporting Evidence: |
| GO:0005769 early endosome | IEA GO_REF:0000107 | TOO GENERAL | Reason: Retained early-endosome membrane localization supplies more precise coverage of this positive trafficking compartment. Supporting Evidence: |
| GO:0005789 endoplasmic reticulum membrane | IEA GO_REF:0000120 | KEEP AS NON CORE | Reason: Endogenous human ER fractionation supports this non-core pool, independently of the synthesis source. Supporting Evidence: GO_REF:0000120 PMID:22720072 We examined the expression of the AMPA receptor subunits, GluR 1β4, in the ER fraction (Figure 4). |
| GO:0005789 endoplasmic reticulum membrane | ISS GO_REF:0000024 | KEEP AS NON CORE | Reason: Endogenous human ER fractionation supports this non-core pool, independently of the synthesis source. The original-reference ER assay used transfected COS1 cells. |
| GO:0005789 endoplasmic reticulum membrane | TAS Reactome:R-HSA-203973 | KEEP AS NON CORE | Reason: Endogenous human ER fractionation supports this non-core pool, independently of the synthesis source. |
| GO:0005789 endoplasmic reticulum membrane | TAS Reactome:R-HSA-204008 | KEEP AS NON CORE | Reason: Endogenous human ER fractionation supports this non-core pool, independently of the synthesis source. |
| GO:0005789 endoplasmic reticulum membrane | TAS Reactome:R-HSA-5694417 | KEEP AS NON CORE | Reason: Endogenous human ER fractionation supports this non-core pool, independently of the synthesis source. |
| GO:0005789 endoplasmic reticulum membrane | TAS Reactome:R-HSA-5694442 | KEEP AS NON CORE | Reason: Endogenous human ER fractionation supports this non-core pool, independently of the synthesis source. |
| GO:0005789 endoplasmic reticulum membrane | TAS Reactome:R-HSA-5694522 | KEEP AS NON CORE | Reason: Endogenous human ER fractionation supports this non-core pool, independently of the synthesis source. |
| GO:0005789 endoplasmic reticulum membrane | TAS Reactome:R-HSA-5694527 | KEEP AS NON CORE | Reason: Endogenous human ER fractionation supports this non-core pool, independently of the synthesis source. |
| GO:0005829 cytosol | IEA GO_REF:0000107 | UNDECIDED | Reason: GluA1 was detected in an operational cytosolic fraction of rat central amygdala. The inspected separation does not resolve whether this represents the organelle-excluding cytosol defined by GO. Supporting Evidence: |
| GO:0005886 plasma membrane | EXP PMID:23739980 A eukaryotic specific transmembrane segment is required for ... | ACCEPT | Reason: Rat flip-receptor surface assays support this membrane location; retain the positive general compartment alongside synaptic specializations. Supporting Evidence: |
| GO:0005886 plasma membrane | IBA GO_REF:0000033 | ACCEPT | Reason: Retain plasma-membrane activity inherited from AN1/PTN000437926 (IBD.gaf line 11513), alongside specialized synaptic compartments. Both literal donor snapshots and the target lineage are preserved. Supporting Evidence: GO_REF:0000033 file:human/GRIA1/GRIA1-phylogeny.json |
| GO:0005886 plasma membrane | IEA GO_REF:0000120 | ACCEPT | Reason: Retain the physiological plasma-membrane location; the combined electronic sources remain distinct from the more specialized synaptic annotations. Supporting Evidence: GO_REF:0000120 |
| GO:0005886 plasma membrane | ISS GO_REF:0000024 | ACCEPT | Reason: Retain the curator-supported hippocampal membrane location as a physiological receptor compartment. The anatomical extension is preserved; its detailed original assay was not independently inspected. Supporting Evidence: |
| GO:0005886 plasma membrane | TAS PMID:1311100 Molecular cloning, chromosomal mapping, and functional expre... | ACCEPT | Reason: Human HBGR1 oocyte currents support the membrane receptor location. Supporting Evidence: |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-399711 | ACCEPT | Reason: The event-specific P42261 leaf is in the plasma membrane. Retain this positive receptor location; the modeled trafficking event does not make GluA1 the trafficking machinery. Supporting Evidence: Reactome:R-HSA-399711 |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-399712 | ACCEPT | Reason: The event-specific P42261 leaf is in the plasma membrane. Retain this positive receptor location; the modeled trafficking event does not make GluA1 the trafficking machinery. Supporting Evidence: Reactome:R-HSA-399712 |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-416320 | ACCEPT | Reason: The event-specific P42261 leaf is in the plasma membrane. Retain this positive receptor location; the modeled trafficking event does not make GluA1 the trafficking machinery. Supporting Evidence: Reactome:R-HSA-416320 |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-416639 | ACCEPT | Reason: The event-specific P42261 leaf is in the plasma membrane. Retain this positive receptor location; the modeled trafficking event does not make GluA1 the trafficking machinery. Supporting Evidence: Reactome:R-HSA-416639 |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-416985 | ACCEPT | Reason: The event-specific P42261 leaf is in the plasma membrane. Retain this positive receptor location; the modeled trafficking event does not make GluA1 the trafficking machinery. Supporting Evidence: Reactome:R-HSA-416985 |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-420975 | ACCEPT | Reason: The event-specific P42261 leaf is in the plasma membrane. Retain this positive receptor location; the modeled trafficking event does not make GluA1 the trafficking machinery. Supporting Evidence: Reactome:R-HSA-420975 |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-420977 | ACCEPT | Reason: The event-specific P42261 leaf is in the plasma membrane. Retain this positive receptor location; the modeled trafficking event does not make GluA1 the trafficking machinery. Supporting Evidence: Reactome:R-HSA-420977 |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-420980 | ACCEPT | Reason: The event-specific P42261 leaf is in the plasma membrane. Retain this positive receptor location; the modeled trafficking event does not make GluA1 the trafficking machinery. Supporting Evidence: Reactome:R-HSA-420980 |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-421007 | ACCEPT | Reason: The event-specific P42261 leaf is in the plasma membrane. Retain this positive receptor location; the modeled trafficking event does not make GluA1 the trafficking machinery. Supporting Evidence: Reactome:R-HSA-421007 |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-438037 | ACCEPT | Reason: The event-specific P42261 leaf is in the plasma membrane. Retain this positive receptor location; the modeled trafficking event does not make GluA1 the trafficking machinery. Supporting Evidence: Reactome:R-HSA-438037 |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-8849881 | ACCEPT | Reason: The event-specific P42261 leaf is in the plasma membrane. Retain this positive receptor location; the modeled trafficking event does not make GluA1 the trafficking machinery. Supporting Evidence: Reactome:R-HSA-8849881 |
| GO:0005911 cell-cell junction | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Retain GluA1 accumulation at IgSF11-mediated contacts in transfected cells as a non-core adhesion-associated pool. Supporting Evidence: |
| GO:0006811 monoatomic ion transport | IEA GO_REF:0000002 | TOO GENERAL | Reason: Retained monoatomic ion transmembrane transport describes the channel-mediated movement more precisely than this unextended ion-transport annotation. Supporting Evidence: GO_REF:0000002 |
| GO:0007165 signal transduction | TAS PMID:1311100 Molecular cloning, chromosomal mapping, and functional expre... | TOO GENERAL | Reason: Signal transduction is broadly correct; existing involved_in GO:0035235 supplies the more specific glutamate-receptor signaling process through an is_a descendant. Supporting Evidence: |
| GO:0007268 chemical synaptic transmission | TAS PMID:1311100 Molecular cloning, chromosomal mapping, and functional expre... | TOO GENERAL | Reason: The broad involved_in chemical synaptic transmission assertion is supported; existing GO:0035249 provides the more specific glutamatergic transmission is_a descendant. Supporting Evidence: |
| GO:0007416 synapse assembly | ISS GO_REF:0000024 | KEEP AS NON CORE | Reason: GluR1 recruitment accompanies functional synaptic unsilencing under AKAP perturbation. Retain this synaptic-maturation context as non-core. Supporting Evidence: |
| GO:0007616 long-term memory | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Rat hippocampal GluR1 antisense impairs inhibitory-avoidance retention, with scrambled controls and preserved GluR2. Retain the established memory association as a behavioral consequence of synaptic receptor function. Supporting Evidence: |
| GO:0008179 adenylate cyclase binding | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Retain adenylyl-cyclase association within the GluA1 signaling complex as non-core; pairwise contact was not established. Supporting Evidence: |
| GO:0009410 response to xenobiotic stimulus | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Reason: Cannabidiol normalizes rat GluR1 expression alongside reduced heroin seeking. The measured expression change alone does not establish GluA1 as a participant in the xenobiotic response. Supporting Evidence: |
| GO:0009636 response to toxic substance | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Alloxan potentiates recombinant GluR1 currents, with loss of potentiation in S831A receptors, and changes hippocampal transmission. Retain this bounded pharmacological response without assigning toxicant recognition. Supporting Evidence: |
| GO:0009744 response to sucrose | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Reason: Sucrose intake increases rat nucleus-accumbens PSD GluR1. The study leaves the functional consequences unresolved; altered receptor delivery alone does not establish participation in the sucrose response. Supporting Evidence: |
| GO:0009897 external side of plasma membrane | IEA GO_REF:0000107 | ACCEPT | Reason: Rat neuronal surface GluR1 was detected through its extracellular region. The term explicitly includes embedded proteins, so it accommodates the membrane receptor rather than asserting an entirely extracellular protein. Supporting Evidence: PMID:12390532 extracellular portion of GluR1 and fluorescence microscopy. |
| GO:0009986 cell surface | IEA GO_REF:0000107 | TOO GENERAL | Reason: External-side plasma-membrane localization provides more precise same-context coverage of the positive cell-surface assignment. Supporting Evidence: |
| GO:0009986 cell surface | ISS GO_REF:0000024 | TOO GENERAL | Reason: External-side plasma membrane localization entails this unextended cell-surface term; the original surface-labeling evidence remains positive. Supporting Evidence: |
| GO:0010226 response to lithium ion | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Reason: Lithium changes rat GluR1 phosphorylation and surface abundance. These receptor readouts do not by themselves establish a GluA1-mediated lithium response; the positive trafficking measurements remain valid. Supporting Evidence: |
| GO:0010628 positive regulation of gene expression | IEA GO_REF:0000107 | UNDECIDED | Reason: GluR1 knockdown and tail decoys reduce SAP97 accumulation, supporting reciprocal protein stabilization. The original leaves synthesis versus degradation unresolved; conversion of coding sequence into mature product is not established. Supporting Evidence: |
| GO:0012507 ER to Golgi transport vesicle membrane | TAS Reactome:R-HSA-203973 | KEEP AS NON CORE | Reason: The budding output carries CNIH-associated P42261 in the ER-to-Golgi vesicle membrane. Retain this receptor transport pool without assigning vesicle budding machinery activity to GRIA1. Supporting Evidence: Reactome:R-HSA-203973 |
| GO:0012507 ER to Golgi transport vesicle membrane | TAS Reactome:R-HSA-5694409 | KEEP AS NON CORE | Reason: The RAB1 activation input contains P42261 in the COPII cargo vesicle membrane. This is transport-pool localization; nucleotide exchange is performed by the associated machinery. Supporting Evidence: Reactome:R-HSA-5694409 |
| GO:0012507 ER to Golgi transport vesicle membrane | TAS Reactome:R-HSA-5694418 | KEEP AS NON CORE | Reason: The tethering input retains P42261 in the ER-to-Golgi vesicle membrane. The larger tethered assemblyβs ERGIC label does not replace the GRIA1 memberβs own vesicle compartment. Supporting Evidence: Reactome:R-HSA-5694418 |
| GO:0012507 ER to Golgi transport vesicle membrane | TAS Reactome:R-HSA-5694439 | KEEP AS NON CORE | Reason: The TRAPP recruitment input contains the exact P42261 cargo branch in an ER-to-Golgi vesicle membrane. Retain the transient transport compartment as non-core. Supporting Evidence: Reactome:R-HSA-5694439 |
| GO:0012507 ER to Golgi transport vesicle membrane | TAS Reactome:R-HSA-5694441 | KEEP AS NON CORE | Reason: Following modeled SEC23 phosphorylation, the GRIA1 leaf remains in the vesicle-membrane cargo branch, although the larger assembly is labeled ERGIC. Retain that member-specific transport location. Supporting Evidence: Reactome:R-HSA-5694441 |
| GO:0012507 ER to Golgi transport vesicle membrane | TAS Reactome:R-HSA-5694446 | KEEP AS NON CORE | Reason: Before SNARE-mediated fusion, the P42261 cargo leaf is explicitly in the ER-to-Golgi vesicle membrane. This supports a transport pool, not fusion-catalytic activity by GRIA1. Supporting Evidence: Reactome:R-HSA-5694446 |
| GO:0014069 postsynaptic density | IEA GO_REF:0000107 | ACCEPT | Reason: Retain the physiological postsynaptic-density pool supported by rodent receptor fractionation. Supporting Evidence: |
| GO:0014069 postsynaptic density | ISS GO_REF:0000024 | ACCEPT | Reason: Retain the curator-supported postsynaptic-density pool, with the mouse donor provenance preserved. Supporting Evidence: |
| GO:0014069 postsynaptic density | ISS GO_REF:0000024 | ACCEPT | Reason: Retain the curated brain-specific postsynaptic-density location. The unextended membrane row does not replace this anatomical context; exact donor experiments remain uninspected. Supporting Evidence: |
| GO:0015276 ligand-gated monoatomic ion channel activity | IEA GO_REF:0000002 | TOO GENERAL | Reason: The two matched InterPro entries support ligand-gated channel activity. Retained AMPA receptor activity provides the more specific molecular function. Supporting Evidence: GO_REF:0000002 |
| GO:0016020 membrane | IEA GO_REF:0000002 | TOO GENERAL | Reason: The matched InterPro membrane assignment is valid but less specific than the retained membrane compartments for the same product and located_in relation. Supporting Evidence: GO_REF:0000002 |
| GO:0019228 neuronal action potential | IEA GO_REF:0000107 | UNDECIDED | Reason: The original demonstrates recombinant GluR1 trafficking, EPSCs and LTP in rat hippocampal slices. A GluR1-specific neuronal action-potential assay was not identified; retain that unresolved scope rather than infer contradiction. Supporting Evidence: |
| GO:0019722 calcium-mediated signaling | IEA GO_REF:0000108 | KEEP AS NON CORE | Reason: GluA1-containing channels conduct calcium depending on receptor subunit composition. Supporting Evidence: GO_REF:0000108 |
| GO:0019865 immunoglobulin binding | IEA GO_REF:0000107 | REMOVE | Reason: The identified partner is IgSF11, an immunoglobulin-superfamily adhesion protein, rather than an immunoglobulin. Preserve the positive association; this electronic transfer assigns the wrong partner class. Supporting Evidence: |
| GO:0019901 protein kinase binding | IEA GO_REF:0000107 | UNDECIDED | Reason: The accessible rat study abstract does not resolve the protein-kinase interaction assay underlying this transfer. Preserve uncertainty without rejecting the curator's uninspected full-text evidence. Supporting Evidence: |
| GO:0019904 protein domain specific binding | IEA GO_REF:0000107 | TOO GENERAL | Reason: Retained PDZ domain binding provides a more precise domain-specific activity. Preserve the positive rat association evidence. |
| GO:0021510 spinal cord development | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Rat phrenic-motoneuron GluR1 expression declines across P2, P7 and P35. Retain the developmental IEP context without converting abundance correlations into an instructive spinal-patterning mechanism. Supporting Evidence: |
| GO:0021987 cerebral cortex development | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Developing rat cortex shows coordinated GluR1 and scaffolding-protein accumulation. Preserve this developmental expression association as non-core, distinct from a demonstrated cortical-patterning activity. Supporting Evidence: |
| GO:0022849 glutamate-gated calcium ion channel activity | IEA GO_REF:0000107 | ACCEPT | Reason: GluA1 supports calcium-permeable channels in appropriate subunit combinations. Retain the conserved activity with its composition dependence; edited GluA2-containing receptors need not share this permeability. |
| GO:0022849 glutamate-gated calcium ion channel activity | ISS GO_REF:0000024 | ACCEPT | Reason: Rat GluA1 channel assays establish calcium permeability for compatible subunit compositions. Retain this activity without implying that GluA1 makes every heteromer calcium-permeable. |
| GO:0030165 PDZ domain binding | IEA GO_REF:0000107 | ACCEPT | Reason: Terminal-peptide assays support PDZ binding. Retain the interaction without inferring that oxidizing disulfide capture describes its physiological mechanism. Supporting Evidence: |
| GO:0030165 PDZ domain binding | ISS GO_REF:0000024 | ACCEPT | Reason: The GluA1 terminal peptide binds PDZ domains in the rat donor evidence underlying the mouse transfer. Retain informative domain binding without assuming a physiological oxidizing mechanism. Supporting Evidence: |
| GO:0030425 dendrite | IEA GO_REF:0000120 | TOO GENERAL | Reason: Accepted dendritic-spine membrane localization lies within a dendritic spine and dendrite. This unextended located_in annotation adds no distinct compartment. Supporting Evidence: GO_REF:0000120 |
| GO:0030425 dendrite | ISS GO_REF:0000024 | TOO GENERAL | Reason: The positive dendritic assignment is entailed by accepted spine localization with the same cell extension. Supporting Evidence: |
| GO:0030425 dendrite | ISS GO_REF:0000024 | TOO GENERAL | Reason: Accepted dendritic-spine localization entails this broader dendritic assignment. Supporting Evidence: |
| GO:0030666 endocytic vesicle membrane | IEA GO_REF:0000117 | KEEP AS NON CORE | Reason: The matching ARBA branch supports an endocytic-vesicle membrane pool; retain this trafficking localization as non-core to synaptic channel activity. Supporting Evidence: GO_REF:0000117 |
| GO:0030666 endocytic vesicle membrane | TAS Reactome:R-HSA-416320 | KEEP AS NON CORE | Reason: The insertion input includes exact P42261 in an endocytic-vesicle AMPA receptor branch. Retain the intracellular trafficking pool separately from the surface receptor location. Supporting Evidence: Reactome:R-HSA-416320 |
| GO:0030666 endocytic vesicle membrane | TAS Reactome:R-HSA-416639 | KEEP AS NON CORE | Reason: The recycling input contains P42261 in the GRIA1/GRIA2 endocytic-vesicle receptor branch. Retain this trafficking pool without inferring that the receptor performs the recycling machineryβs activity. Supporting Evidence: Reactome:R-HSA-416639 |
| GO:0030666 endocytic vesicle membrane | TAS Reactome:R-HSA-421007 | KEEP AS NON CORE | Reason: The endocytosis output contains a P42261/GRIA2 receptor in the endocytic vesicle membrane. This supports an internalized receptor pool rather than a separate core channel location. Supporting Evidence: Reactome:R-HSA-421007 |
| GO:0031267 small GTPase binding | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Rat GluR1 coimmunoprecipitation with Rab4A supports a non-core trafficking association. This does not make GluA1 a GTPase regulator. Supporting Evidence: |
| GO:0031489 myosin V binding | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Retain the reported GluR1βmyosin-Vb association as a non-core trafficking interaction. The receptor is cargo; no motor activity is assigned to it. Supporting Evidence: |
| GO:0031594 neuromuscular junction | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: GluR1 clusters at reinnervated adult rat motor endplates after a nerve-grafting procedure. Retain this positive specialized localization as non-core. Supporting Evidence: |
| GO:0031623 receptor internalization | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Endogenous rat neuronal GluR1 is internalized after ligand or insulin treatment. Preserve receptor trafficking as context; dynamin/clathrin machinery performs endocytosis, and the tested tail deletion belongs to GluR2. Supporting Evidence: |
| GO:0031667 response to nutrient levels | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Reason: Food restriction changes synaptic GluR1 abundance. The proposed nutritional consequences are not demonstrated as GluA1-mediated outputs, so this transfer exceeds the expression evidence. Supporting Evidence: |
| GO:0031681 G-protein beta-subunit binding | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Retain G-beta association in the receptor signaling complex as non-core, without converting coimmunoprecipitation into a purified binary-binding result. Supporting Evidence: |
| GO:0031698 beta-2 adrenergic receptor binding | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Retain beta2-adrenoceptor association as non-core. PSD95 and stargazin connect the complex; GluA1 is not established as its adrenergic ligand. |
| GO:0031901 early endosome membrane | IEA GO_REF:0000120 | KEEP AS NON CORE | Reason: Retain the early-endosome membrane pool as non-core receptor trafficking. Supporting Evidence: GO_REF:0000120 |
| GO:0031901 early endosome membrane | ISS GO_REF:0000024 | KEEP AS NON CORE | Reason: Retain the curated early-endosome membrane trafficking pool as non-core. Supporting Evidence: |
| GO:0032279 asymmetric synapse | IEA GO_REF:0000107 | TOO GENERAL | Reason: Accepted postsynaptic-density membrane localization entails the broader asymmetric-synapse compartment in this unextended context. Supporting Evidence: |
| GO:0032281 AMPA glutamate receptor complex | IBA GO_REF:0000033 | ACCEPT | Reason: Retain the AMPA receptor-complex membership placed at AN396/PTN000438081 (original IBD.gaf line26021). The verified GRIA1 leaf inherits this part_of assertion; target self-inclusion among descendant evidence is legitimate. Supporting Evidence: GO_REF:0000033 file:human/GRIA1/GRIA1-phylogeny.json |
| GO:0032281 AMPA glutamate receptor complex | IDA PMID:23739980 A eukaryotic specific transmembrane segment is required for ... | ACCEPT | Reason: Blue-native PAGE and fluorescence size-exclusion assays support GluA1-containing tetramers. Rat flip constructs, homomeric and GluA1/GluA2 assemblies, and engineered M4 perturbations are distinguished; this supports conserved membership in the AMPA receptor complex. Supporting Evidence: PMID:23739980 required for the critical dimer-to-tetramer transition. |
| GO:0032281 AMPA glutamate receptor complex | IEA GO_REF:0000107 | ACCEPT | Reason: Retain AMPA-receptor complex membership, supported by the rat GluA1-containing receptor assembly. Supporting Evidence: |
| GO:0032281 AMPA glutamate receptor complex | ISS GO_REF:0000024 | ACCEPT | Reason: Purified functional rat GluA1/GluA2 heterotetramers support conserved AMPA-receptor complex membership. Supporting Evidence: |
| GO:0032281 AMPA glutamate receptor complex | NAS PMID:30872532 Architecture of the heteromeric GluA1/2 AMPA receptor in com... | ACCEPT | Reason: Rat GluA1 was purified within functional GluA1/2βΞ³8 heteromers, supporting the conserved AMPA-receptor complex membership. Supporting Evidence: |
| GO:0032355 response to estradiol | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Reason: Estradiol and estrogen-receptor agonists increase rat hippocampal GluR1. This downstream expression measurement does not establish a GluA1 contribution to the estradiol-response mechanism. Supporting Evidence: |
| GO:0032590 dendrite membrane | IEA GO_REF:0000107 | TOO GENERAL | Reason: Accepted dendritic-spine membrane localization entails this broader dendrite-membrane assignment with the same relation and product. Supporting Evidence: |
| GO:0032591 dendritic spine membrane | IDA PMID:20434989 Syntaxin-4 defines a domain for activity-dependent exocytosi... | ACCEPT | Reason: Endogenous rat neuronal GluR1 recycling and separate SEP-GluR1 insertion into spine plasma membrane support this conserved localization. Supporting Evidence: |
| GO:0032591 dendritic spine membrane | ISS GO_REF:0000024 | ACCEPT | Reason: Surface GluR1 and synaptic-current assays support receptor activity at the spine membrane; retain the human orthology transfer. Supporting Evidence: |
| GO:0032809 neuronal cell body membrane | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Retain the curator-supported somatic membrane receptor pool as a non-core localization. Supporting Evidence: |
| GO:0032991 protein-containing complex | IEA GO_REF:0000107 | TOO GENERAL | Reason: Accepted AMPA-receptor complex membership entails this broader protein-containing-complex assignment with the same part_of relation. Supporting Evidence: |
| GO:0033116 endoplasmic reticulum-Golgi intermediate compartment membrane | TAS Reactome:R-HSA-5694446 | KEEP AS NON CORE | Reason: The fusion output explicitly contains CNIH-associated P42261 in the ERGIC membrane. Retain this biosynthetic transport intermediate; GRIA1 is cargo rather than the membrane-fusion machinery. Supporting Evidence: Reactome:R-HSA-5694446 |
| GO:0034220 monoatomic ion transmembrane transport | IEA GO_REF:0000120 | ACCEPT | Reason: GRIA1 channel conductance directly transports ions; preserve the combined electronic provenance. Supporting Evidence: GO_REF:0000120 |
| GO:0034765 regulation of monoatomic ion transmembrane transport | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Rat VTA GluR1 overexpression changes AMPA-evoked membrane rectification. Retain the channel-regulation context without interpreting GluA1 as a general regulator of unrelated ion transporters. Supporting Evidence: |
| GO:0035235 ionotropic glutamate receptor signaling pathway | NAS PMID:30872532 Architecture of the heteromeric GluA1/2 AMPA receptor in com... | ACCEPT | Reason: GRIA1 contributes the ligand-gated channel step of ionotropic glutamate receptor signaling; rat GluA1/2βΞ³8 complexes produced glutamate-evoked currents. Supporting Evidence: |
| GO:0035249 synaptic transmission, glutamatergic | IBA GO_REF:0000033 | ACCEPT | Reason: Retain the glutamatergic transmission assertion at AN72/PTN001826301 (original IBD.gaf line45768). Postsynaptic receptor gating performs part of the defined transmission process, and the verified GRIA1 lineage inherits this assertion. Supporting Evidence: GO_REF:0000033 file:human/GRIA1/GRIA1-phylogeny.json |
| GO:0035254 glutamate receptor binding | IEA GO_REF:0000107 | MODIFY | Reason: Purified rat GluA1 and GluA2 amino-terminal domains associate. Ionotropic glutamate receptor binding specifies the demonstrated partner class more precisely. Proposed replacements: ionotropic glutamate receptor binding Supporting Evidence: |
| GO:0038023 signaling receptor activity | IEA GO_REF:0000002 | TOO GENERAL | Reason: The InterPro receptor assignment is compatible with GRIA1; retained AMPA receptor activity specifies its signaling mechanism more precisely. Supporting Evidence: GO_REF:0000002 |
| GO:0042220 response to cocaine | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: VTA GluR1 manipulation changes cocaine reinforcement, beyond the accompanying expression measurements. Retain this contextual receptor-mediated response without assigning cocaine binding to GluA1. |
| GO:0042734 presynaptic membrane | IEA GO_REF:0000107 | UNDECIDED | Reason: Rat GluR1 is present in presynaptic fractions, but compartmental fractionation does not resolve receptor activity there. Preserve the positive localization and curator assertion while leaving this activity-location relation unresolved. Supporting Evidence: |
| GO:0042802 identical protein binding | IEA GO_REF:0000107 | MODIFY | Reason: Rat GluA1 amino-terminal domains form homodimers in solution and crystals. Protein homodimerization activity captures this assembly interaction more precisely than identical-protein binding. Proposed replacements: protein homodimerization activity |
| GO:0043005 neuron projection | IEA GO_REF:0000107 | TOO GENERAL | Reason: Accepted dendritic-spine membrane localization supplies more precise coverage of this unextended neuron-projection assignment. Supporting Evidence: |
| GO:0043025 neuronal cell body | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Retain the somatic receptor pool as non-core; exact source-specific localization remains incompletely inspected. Supporting Evidence: |
| GO:0043025 neuronal cell body | ISS GO_REF:0000024 | KEEP AS NON CORE | Reason: Retain the curator's somatic pool as non-core; the specific original localization assay remains uninspected. Supporting Evidence: |
| GO:0043025 neuronal cell body | ISS GO_REF:0000024 | KEEP AS NON CORE | Reason: Retain somatic GluA1 association and localization as a non-core receptor pool. Supporting Evidence: |
| GO:0043197 dendritic spine | IBA GO_REF:0000033 | ACCEPT | Reason: Retain the dendritic-spine activity context at AN396/PTN000438081 (original IBD.gaf line17230). The accepted postsynaptic density membrane term does not entail a dendritic-spine context in the ontology, so this assertion adds location information. Supporting Evidence: GO_REF:0000033 file:human/GRIA1/GRIA1-phylogeny.json |
| GO:0043197 dendritic spine | IEA GO_REF:0000120 | ACCEPT | Reason: Retain the physiological spine location, preserving the combined electronic provenance alongside the specialized membrane context. Supporting Evidence: GO_REF:0000120 |
| GO:0043197 dendritic spine | ISS GO_REF:0000024 | ACCEPT | Reason: Retain the curator-supported spine location and hippocampal pyramidal-cell extension as a physiological receptor site. Supporting Evidence: |
| GO:0043197 dendritic spine | ISS GO_REF:0000024 | ACCEPT | Reason: Retain the curated spine location, corroborated by neuronal GluA1 colocalization. Supporting Evidence: |
| GO:0043198 dendritic shaft | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Retain the positive dendritic-shaft receptor pool as non-core, with the combined GluR1/2/3 antibody scope preserved. Supporting Evidence: |
| GO:0043278 response to morphine | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: GluA1 phosphorylation perturbation alters morphine sensitization, and CeA knockdown alters withdrawal-associated seeking. Retain this contextual response; the sensitization experiments used mice despite the literal rat donor. |
| GO:0043434 response to peptide hormone | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: MCH changes GluR1 phosphorylation, surface abundance and AMPA-mediated synaptic currents. Retain the receptor-mediated component of this hormonal response without assigning MCH recognition to GluA1. Supporting Evidence: |
| GO:0044309 neuron spine | IEA GO_REF:0000107 | TOO GENERAL | Reason: Accepted dendritic-spine membrane localization entails this broader unextended neuron-spine assignment. Supporting Evidence: |
| GO:0044309 neuron spine | ISS GO_REF:0000024 | TOO GENERAL | Reason: Preserve positive spine localization; the accepted dendritic-spine assignment supplies more precise coverage in this unextended donor context. Supporting Evidence: |
| GO:0045202 synapse | IEA GO_REF:0000120 | TOO GENERAL | Reason: Accepted postsynaptic-density membrane localization entails synapse for the same unextended located_in context. The broader term adds no distinct localization. Supporting Evidence: GO_REF:0000120 |
| GO:0045202 synapse | ISS GO_REF:0000024 | TOO GENERAL | Reason: Mouse synaptosomal GluA1 measurements support synaptic localization; accepted postsynaptic-density membrane localization supplies more precise core coverage. Supporting Evidence: |
| GO:0045211 postsynaptic membrane | IDA PMID:23739980 A eukaryotic specific transmembrane segment is required for ... | ACCEPT | Reason: Accept the established postsynaptic location; this cited rat/HEK study establishes surface expression and assembly, not an identified postsynaptic assay. |
| GO:0045211 postsynaptic membrane | IEA GO_REF:0000120 | ACCEPT | Reason: Retain the physiological postsynaptic-membrane location and its combined electronic provenance alongside the specialized density membrane. Supporting Evidence: GO_REF:0000120 |
| GO:0045211 postsynaptic membrane | NAS PMID:17506699 The cell biology of synaptic plasticity: AMPA receptor traff... | ACCEPT | Reason: Retain the established postsynaptic receptor location supported by the review synthesis; this is not a new localization experiment. Supporting Evidence: |
| GO:0045471 response to ethanol | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Reason: Alcohol exposure changes rodent GluR1 expression, while the mechanistic interventions target mTORC1 or prenatal exposure. These readouts alone do not establish GluA1 participation in the ethanol response. |
| GO:0045838 positive regulation of membrane potential | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Alloxan-sensitive GluR1 currents and rat hippocampal synaptic potentiation support a membrane-excitability context. Keep the transferred claim non-core without treating phosphorylation-dependent modulation as a distinct universal voltage-control role. Supporting Evidence: |
| GO:0046685 response to arsenic-containing substance | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Reason: Rat hippocampal GluR1 mRNA was quantified after dimethylarsenic-acid exposure. This expression assay does not establish a GluA1-mediated arsenic response; it is not evidence of arsenic binding or detoxification. Supporting Evidence: |
| GO:0048167 regulation of synaptic plasticity | IEA GO_REF:0000107 | TOO GENERAL | Reason: Accepted long-term synaptic potentiation (GO:0060291) is an is_a descendant of this term and supplies the more specific positive process assertion under the same involved_in relation. Supporting Evidence: |
| GO:0048266 behavioral response to pain | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Reason: The demonstrated GluA1 knockdown endpoint is morphine seeking in rats with persistent pain. This does not establish a GluA1-dependent behavioral response to the pain stimulus itself. Supporting Evidence: |
| GO:0048787 presynaptic active zone membrane | IEA GO_REF:0000107 | UNDECIDED | Reason: The rat donor has positive presynaptic GluR1 immunogold evidence. Presynaptic channel activity was not independently established from the accessible source; retain uncertainty about is_active_in without denying localization. Supporting Evidence: |
| GO:0050804 modulation of chemical synaptic transmission | IBA GO_REF:0000033 | TOO GENERAL | Reason: The GRIA1 lineage inherits modulation at AN72/PTN001826301 (original IBD.gaf line39841). Retained long-term synaptic potentiation is an is_a descendant specifying this positive modulation function. Supporting Evidence: GO_REF:0000033 file:human/GRIA1/GRIA1-phylogeny.json |
| GO:0050804 modulation of chemical synaptic transmission | IEA GO_REF:0000107 | TOO GENERAL | Reason: Accepted long-term synaptic potentiation (GO:0060291) is an is_a descendant of modulation of chemical synaptic transmission under the same involved_in relation. The specific positive process is retained. Supporting Evidence: |
| GO:0050806 positive regulation of synaptic transmission | IEA GO_REF:0000107 | TOO GENERAL | Reason: Accepted long-term synaptic potentiation (GO:0060291) is an is_a descendant of positive regulation of synaptic transmission under the same involved_in relation. Retain that more specific process assertion. Supporting Evidence: |
| GO:0051018 protein kinase A binding | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Retain PKA association as non-core, with AKAP/SAP97-mediated tethering; GluA1 itself is not assigned kinase or anchoring activity. Supporting Evidence: |
| GO:0051428 peptide hormone receptor binding | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Rat brain GluA1 coimmunoprecipitates with the oxytocin receptor. Retain this non-core receptor association without asserting that GluA1 binds oxytocin itself. Supporting Evidence: |
| GO:0051602 response to electrical stimulus | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Reason: Electrical stimulation changes regional rat GluR1 abundance, with upstream interventions on other signaling components. The measured expression changes do not establish GluA1 participation in the electrical-stimulus response. |
| GO:0055037 recycling endosome | IDA PMID:20434989 Syntaxin-4 defines a domain for activity-dependent exocytosi... | TOO GENERAL | Reason: Retained recycling-endosome membrane localization entails this broader recycling-endosome location; positive trafficking evidence remains noncore. Supporting Evidence: |
| GO:0055038 recycling endosome membrane | IEA GO_REF:0000120 | KEEP AS NON CORE | Reason: Retain recycling-endosome membrane localization as non-core trafficking, without assigning local channel activity. Supporting Evidence: GO_REF:0000120 |
| GO:0055038 recycling endosome membrane | ISS GO_REF:0000024 | KEEP AS NON CORE | Reason: Retain the curated recycling-endosome membrane trafficking pool as non-core. Supporting Evidence: |
| GO:0060076 excitatory synapse | IEA GO_REF:0000107 | ACCEPT | Reason: GluR1 was directly examined as a postsynaptic marker in rat excitatory synapses. Retain this physiological receptor compartment. Supporting Evidence: |
| GO:0060078 regulation of postsynaptic membrane potential | IEA GO_REF:0000108 | ACCEPT | Reason: The retained postsynaptic transmitter-gated channel activity directly changes postsynaptic membrane potential. Preserve the ontology-derived provenance; it is not an additional experiment. Supporting Evidence: GO_REF:0000108 |
| GO:0060291 long-term synaptic potentiation | IEA GO_REF:0000107 | ACCEPT | Reason: Rat chemical-LTP experiments recruit endogenous GluA1 to PSD fractions; recombinant GluR1 S845A also reduces hippocampal LTP. Receptor-mediated postsynaptic conductance supplies the functional contribution, with rodent-to-human transfer explicit. |
| GO:0060992 response to fungicide | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Reason: Tributyltin reduces rat GluR1 mRNA, whereas the functional vulnerability analysis centers on GluR2 loss. The GluR1 expression readout alone does not establish a fungicide-response role. Supporting Evidence: |
| GO:0071230 cellular response to amino acid stimulus | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Retain the amino-acid response through GluA1's established glutamate-gated activity. |
| GO:0071345 cellular response to cytokine stimulus | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Reason: IL-10 alters hypoxia-associated rat GluA1 abundance and phosphorylation. The measured receptor response does not establish GluA1 participation in cytokine-response machinery. Supporting Evidence: |
| GO:0071359 cellular response to dsRNA | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Reason: Double-stranded miR-132 transfection increases GluR1 expression through a regulatory intervention. This does not establish GluA1 participation in the cellular response to double-stranded RNA. Supporting Evidence: |
| GO:0071363 cellular response to growth factor stimulus | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Retain the contextual growth-factor response, supported by the specific BDNF-dependent receptor/scaffold interaction evidence. The miR-132 experiment measures downstream expression rather than direct growth-factor recognition. |
| GO:0071375 cellular response to peptide hormone stimulus | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Leptin changes GluR1 surface delivery and excitatory synaptic strength through NMDAR/PTEN signaling. Retain the downstream receptor-mediated component without assigning leptin binding or PTEN activity. Supporting Evidence: |
| GO:0071418 cellular response to amine stimulus | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Reason: Repeated dopamine increases rat GluR1 surface abundance and occludes synaptic scaling. These observations do not isolate a GluA1-dependent amine-response mechanism from regulation of the receptor itself. Supporting Evidence: |
| GO:0090326 positive regulation of locomotion involved in locomotory behavior | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: VTA GluR1 overexpression potentiates AMPA-evoked locomotion in rats. Retain the circuit-level behavioral consequence as non-core rather than a separate locomotor molecular function. Supporting Evidence: |
| GO:0097060 synaptic membrane | IEA GO_REF:0000107 | ACCEPT | Reason: Retain synaptic-membrane localization supported by the rat neuronal receptor-trafficking experiments. Supporting Evidence: |
| GO:0097060 synaptic membrane | ISS GO_REF:0000024 | ACCEPT | Reason: Retain the curator-supported synaptic membrane location in hippocampal pyramidal neurons. Positive surface-AMPAR evidence corroborates localization; the exact original cell-specific assay remains uninspected. Supporting Evidence: |
| GO:0097110 scaffold protein binding | IEA GO_REF:0000107 | ACCEPT | Reason: GluA1 associates with the SAP97 scaffold through its terminal interaction region. Retain scaffold binding as an informative receptor-organizing function. |
| GO:0098685 Schaffer collateral - CA1 synapse | NAS PMID:30872532 Architecture of the heteromeric GluA1/2 AMPA receptor in com... | ACCEPT | Reason: The original introduction explicitly places GluA1/2βΞ³8 receptors at Schaffer collateralβCA1 synapses; retain the curated NAS localization. Supporting Evidence: |
| GO:0098793 presynapse | IEA GO_REF:0000044 | KEEP AS NON CORE | Reason: Retain the mouse-supported presynaptic pool as non-core. Forebrain fractionation detects GluR1 in S3; this localization does not establish presynaptic channel activity. |
| GO:0098793 presynapse | ISS GO_REF:0000024 | KEEP AS NON CORE | Reason: Mouse forebrain fractionation detects a presynaptic-enriched GluR1 pool. Retain non-core localization with the fraction-purity limitation, without inferring presynaptic channel activity. Supporting Evidence: |
| GO:0098839 postsynaptic density membrane | IBA GO_REF:0000033 | ACCEPT | Reason: Retain the postsynaptic density membrane activity context placed at AN72/PTN001826301 (original IBD.gaf line46207) on the verified GRIA1 lineage. Preserve is_active_in separately from the located_in records. Supporting Evidence: GO_REF:0000033 file:human/GRIA1/GRIA1-phylogeny.json |
| GO:0098839 postsynaptic density membrane | IEA GO_REF:0000120 | ACCEPT | Reason: The combined localization sources support postsynaptic-density membrane, a specific site of receptor signaling. Preserve the original electronic inference and its donor context. Supporting Evidence: GO_REF:0000120 |
| GO:0098839 postsynaptic density membrane | ISS GO_REF:0000024 | ACCEPT | Reason: Accept the membrane compartment of the postsynaptic receptor pool. Supporting Evidence: |
| GO:0098978 glutamatergic synapse | IEA GO_REF:0000107 | ACCEPT | Reason: Retain activity at glutamatergic synapses. Rat GluR1-dependent synaptic delivery and electrophysiological evidence support this physiological receptor site. Supporting Evidence: |
| GO:0099092 postsynaptic density, intracellular component | IEA GO_REF:0000107 | ACCEPT | Reason: Rat GluA1 occurs in detergent-insoluble PSD fractions and PSD95-colocalized puncta. Retain the curated intracellular PSD association; the GO definition explicitly includes neurotransmitter receptors. Supporting Evidence: |
| GO:0099505 regulation of presynaptic membrane potential | IEA GO_REF:0000108 | UNDECIDED | Reason: This logical propagation depends on presynaptic channel activity. The underlying functional records do not yet establish a presynaptic membrane context; localization alone does not resolve that requirement. Supporting Evidence: GO_REF:0000108 |
| GO:0099507 ligand-gated monoatomic ion channel activity involved in regulation of presynaptic membrane potential | IDA PMID:8824304 AMPA receptor flip/flop mutants affecting deactivation, dese... | UNDECIDED | Reason: Recombinant currents and surface staining are positive, but the cited original does not identify a presynaptic experiment. Both precise ECO assertions remain unresolved. Supporting Evidence: |
| GO:0099507 ligand-gated monoatomic ion channel activity involved in regulation of presynaptic membrane potential | IMP PMID:8824304 AMPA receptor flip/flop mutants affecting deactivation, dese... | UNDECIDED | Reason: S750 mutations alter recombinant channel gating and modulator responses. Their presynaptic physiological scope was not established in the original experiments. Supporting Evidence: |
| GO:0099507 ligand-gated monoatomic ion channel activity involved in regulation of presynaptic membrane potential | NAS PMID:8824304 AMPA receptor flip/flop mutants affecting deactivation, dese... | UNDECIDED | Reason: The paper establishes recombinant GluA1 channel gating. The presynaptic membrane context required by this NAS assertion remains unverified. Supporting Evidence: |
| GO:0099604 ligand-gated calcium channel activity | IEA GO_REF:0000107 | TOO GENERAL | Reason: Retained glutamate-gated calcium ion channel activity is a child of this ligand-gated term and supplies the same unextended function more precisely. |
| GO:1904315 transmitter-gated monoatomic ion channel activity involved in regulation of postsynaptic membrane potential | IBA GO_REF:0000033 | ACCEPT | Reason: Retain the physiological channel context placed at AN72/PTN001826301 (original IBD.gaf line12651). This term and AMPA receptor activity specify different aspects of the channel function; neither is an ontology ancestor of the other. Supporting Evidence: GO_REF:0000033 file:human/GRIA1/GRIA1-phylogeny.json |
| GO:1904315 transmitter-gated monoatomic ion channel activity involved in regulation of postsynaptic membrane potential | IEA GO_REF:0000107 | ACCEPT | Reason: Synaptic delivery of tagged GluR1 receptors in rat neurons supports the postsynaptic channel role. Retain the conserved function without inferring construct species from neuronal host species. Supporting Evidence: |
| GO:1904315 transmitter-gated monoatomic ion channel activity involved in regulation of postsynaptic membrane potential | ISS GO_REF:0000024 | UNDECIDED | Reason: Retain uncertainty about this narrower conjunction; the unextended channel activity is established. |
| GO:1905232 cellular response to L-glutamate | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Retain the cognate glutamate response, including the measured surface-receptor adaptation. |
| GO:1905430 cellular response to glycine | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: After glycine-induced LTP, GluA1-containing calcium-permeable receptors contribute to the subsequent receptor-composition switch. Retain this contextual response without implying direct glycine binding by GluA1. |
| GO:1990416 cellular response to brain-derived neurotrophic factor stimulus | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: BDNF-dependent GluR1/scaffold interactions contribute to receptor stabilization. Retain this contextual response, preserving preparation- and duration-dependent trafficking effects without assigning BDNF recognition. |
| GO:1990635 proximal dendrite | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Surface GluA1 was measured along proximal dendritic segments of rat hippocampal neurons. Retain this regional receptor pool as non-core. Supporting Evidence: |
| GO:1990708 conditioned place preference | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: Rat CeA GluA1 manipulation changes morphine-conditioned place preference. Retain the behavioral association as non-core; knockdown also lowers GluA2, limiting attribution of that arm to GluA1 alone. Supporting Evidence: |
| GO:1990911 response to psychosocial stress | IEA GO_REF:0000107 | KEEP AS NON CORE | Reason: GluA1 manipulation changes stress-induced psychostimulant cross-sensitization but not social avoidance. Retain this experimentally bounded stress-response contribution rather than all psychosocial outcomes. Supporting Evidence: |
| GO:2000463 positive regulation of excitatory postsynaptic potential | IEA GO_REF:0000107 | ACCEPT | Reason: Rat GluA1 overexpression increases the AMPA/NMDA current ratio and GluA2-lacking current contribution without changing paired-pulse ratio. The GO definition explicitly connects EPSCs to excitatory postsynaptic potential; retain the conserved receptor contribution. Supporting Evidence: |
Loading supporting contentβ¦
Download this section (compressed HTML)Q: Which native experiments resolve the source-specific presynaptic activity and localization assertions retained as uncertain?
Q: Does the operational cytosolic GluA1 fraction contain membrane-associated receptor rather than freely soluble protein?
Loading supporting contentβ¦
Download this section (compressed HTML)Loading supporting contentβ¦
Download this section (compressed HTML)Loading supporting contentβ¦
Download this section (compressed HTML)