GRIN2A — Glutamate ionotropic receptor NMDA type subunit 2A
GRIN2A belongs to a gene co-expression module in 1 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.
GRIN2A's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| Fibroblasts | Lamina Propria ECM ECM production | ADAMTS7, ADGRL4, ANGPTL6, BMP2, CBLN2, CYTL1, DHRS7C, FAM135B +14 more | View in SCUBA |
About the gene
| Synonyms | GluN2A, NMDAR2A |
|---|---|
| Chromosome | 16: 9753404-10182928 |
| Predicted location | Intracellular, Membrane |
| Essential gene | No |
| Protein class | Cancer-related genes, Disease related genes, FDA approved drug targets, Human disease related genes, Plasma proteins, Predicted intracellular proteins, Predicted membrane proteins, RAS pathway related proteins, Transporters |
| Molecular function | Ion channel, Ligand-gated ion channel, Receptor |
| Biological process | Ion transport, Transport |
Function
Component of N-methyl-D-aspartate (NMDA) receptors (NMDARs) that function as heterotetrameric, ligand-gated cation channels with high calcium permeability and voltage-dependent block by Mg(2+). NMDARs participate in synaptic plasticity for learning and memory formation by contributing to the slow phase of excitatory postsynaptic current, long-term synaptic potentiation, and learning (By similarity). Channel activation requires binding of the neurotransmitter L-glutamate to the GluN2 subunit, glycine or D-serine binding to the GluN1 subunit, plus membrane depolarization to eliminate channel inhibition by Mg(2+). NMDARs mediate simultaneously the potasium efflux and the influx of calcium and sodium (By similarity). Each GluN2 subunit confers differential attributes to channel properties, including activation, deactivation and desensitization kinetics, pH sensitivity, Ca2(+) permeability, and binding to allosteric modulators. Participates in the synaptic plasticity regulation through activation by the L- glutamate releaseed by BEST1, into the synaptic cleft, upon F2R/PAR-1 activation in astrocyte (By similarity).
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.