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+) (PubMed:24272827, PubMed:24863970, PubMed:26875626, PubMed:26919761, PubMed:27839871, PubMed:28095420, PubMed:28126851, PubMed:38538865, PubMed:8768735). Participates in synaptic plasticity for learning and memory formation by contributing to the long-term depression (LTD) of hippocampus membrane currents (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+) (PubMed:24272827, PubMed:24863970, PubMed:26875626, PubMed:26919761, PubMed:27839871, PubMed:28095420, PubMed:28126851, PubMed:38538865, PubMed:8768735).
NMDARs mediate simultaneously the potassium 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 (PubMed:26875626, PubMed:28095420, PubMed:28126851, PubMed:38538865, PubMed:8768735). In concert with DAPK1 at extrasynaptic sites, acts as a central mediator for stroke damage.
Its phosphorylation at Ser-1303 by DAPK1 enhances synaptic NMDA receptor channel activity inducing injurious Ca2+ influx through them, resulting in an irreversible neuronal death (By similarity)
Heterotetramer (PubMed:34321660). Forms heterotetrameric channels composed of two GluN1/zeta subunits (GRIN1), and two identical GluN2/epsilon subunits (GRIN2A, GRIN2B, GRIN2C or GRIN2D) or GluN3 subunits (GRIN3A or GRIN3B) (in vitro) (PubMed:26875626, PubMed:26912815, PubMed:26919761, PubMed:28126851, PubMed:34321660, PubMed:8768735). Can also form heterotetrameric channels that contain at least two GluN1 subunits and at least two different GluN2 subunits (or a combination of one GluN2 and one GluN3 subunits) (in vitro) (By similarity).
In vivo, the subunit composition may depend on the expression levels of the different subunits (Probable). Found in a complex with GRIN1 and GRIN3B. Found in a complex with GRIN1, GRIN3A and PPP2CB.
Interacts with PDZ domains of PATJ, DLG3 and DLG4. Interacts with HIP1 and NETO1 (By similarity). Interacts with MAGI3 (PubMed:10748157).
Interacts with DAPK1 (By similarity). Found in a complex with GRIN1 and PRR7 (PubMed:27458189). Interacts with PRR7 (PubMed:27458189).
Interacts with CAMK2A (PubMed:28130356). Interacts with ARC; preventing ARC oligomerization (By similarity). Interacts with TMEM25 (By similarity).
Interacts (via the extreme C-terminus) with FRMPD2 (via the second PDZ domain); the interaction is direct and is likely to promote NMDAR-mediated neural signal transmission (By similarity). Interacts with FAM81A; the interaction facilitates condensate formation via liquid-liquid phase separation (By similarity)
Primarily found in the fronto-parieto-temporal cortex and hippocampus pyramidal cells, lower expression in the basal ganglia
The extracellular N-terminal domain (NTD) endows NMDARs with a unique capacity for allosteric modulation, harboring several binding sites for small molecule ligands that act as subunit-specific allosteric modulators of ion channel activity
A hydrophobic region that gives rise to the prediction of a transmembrane span does not cross the membrane, but is part of a discontinuously helical region that dips into the membrane and is probably part of the pore and of the selectivity filter
A disorder characterized by significantly below average general intellectual functioning associated with impairments in adaptive behavior and manifested during the developmental period. MRD6 additional features may include seizures, hypotonia, abnormal movements, such as dystonia, and autistic features.
A form of epileptic encephalopathy, a heterogeneous group of severe early-onset epilepsies characterized by refractory seizures, neurodevelopmental impairment, and poor prognosis. Development is normal prior to seizure onset, after which cognitive and motor delays become apparent.
No mutation information available.
Genes with an experimentally identified or computationally predicted synthetic-lethal relationship to GRIN2B, aggregated across our SSL data sources. Click any partner node to view that gene’s page.
Nodes and edges are coloured by the SSL data source. Partners appearing in more than one source are shown in grey.
Total Trials Found: 28
| NCT ID | Condition | Brief Title | Phase | Status |
|---|---|---|---|---|
| NCT00472576 | Major Depression | Antidepressant Effects of NR2B in Major Depression | PHASE1 | COMPLETED |
| NCT07377032 | GRIN-related Disorders, GRIN1, GRIN2A, GRIN2B, GRIN2D, Epilepsy, Neurodevelopmental Disorder (Diagnosis) | TAP-GRIN: Interventional Study on Patients With GRIN-related Neurodevelopmental Disorders | PHASE3 | RECRUITING |
| NCT05818943 | GRIN-related Disorders | Honeycomb: Evaluation of Radiprodil in Children with GRIN-related Disorder | PHASE1 | ACTIVE_NOT_RECRUITING |
| NCT07224581 | GRIN-related Neurodevelopmental Disorder | Beeline: A Phase 3 Study in GRIN-related Neurodevelopmental Disorder | PHASE3 | RECRUITING |
| NCT00163085 | Parkinson's Disease | The Effects of an NR2B NMDA Antagonist, CP-101,606, in Patients With Parkinson's Disease | PHASE2 | COMPLETED |
| NCT01238250 | 16P11.2 Deletion Syndrome, 16p11.2 Duplications, 1Q21.1 Deletion, 1Q21.1 Microduplication Syndrome (Disorder), ACTL6B, ADNP, AHDC1, ANK2, ANKRD11, ARID1B, ASH1L, BCL11A, CHAMP1, CHD2, CHD8, CSNK2A1, CTBP1, CTNNB1 Gene Mutation, CUL3, DDX3X, DNMT3A, DSCAM, DYRK1A, FOXP1, GRIN2A, GRIN2B, HIVEP2-Related Intellectual Disability, HNRNPH2, KATNAL2, KDM5B, KDM6B, KMT2C Gene Mutation, KMT2E, KMT5B, MBD5, MED13L, PACS1, PPP2R5D-Related Intellectual Disability, PTCHD1, REST, SCN2A Encephalopathy, SETBP1 Gene Mutation, SETD5, SMARCA4 Gene Mutation, SMARCC2, STXBP1 Encephalopathy With Epilepsy, SYNGAP1-Related Intellectual Disability, TBR1, ARHGEF9, HNRNPU, PPP3CA, PPP2R1A, SLC6A1, 2p16.3 Deletions, 5q35 Deletions, 5q35 Duplications, 7q11.23 Duplications, 15Q13.3 Deletion Syndrome, 16p11.2 Triplications, 16P12.2 Microdeletion, 16P13.11 Microdeletion Syndrome (Disorder), 17Q12 Microdeletion Syndrome (Disorder), 17Q12 Duplication Syndrome, 17Q21.31 Deletion Syndrome, 17q21.3 Duplications, ACTB, ADSL, AFF2, ALDH5A1, ANK3, ARX, ATRX Gene Mutation, AUTS2 Syndrome, BCKDK, BRSK2, CACNA1C, CAPRIN1, CASK, CASZ1, CHD3, CIC, CNOT3, CREBBP Gene Mutation, CSDE1, CTCF, DEAF1, DHCR7, DLG4, EBF3, EHMT1, EP300 Gene Mutation, GIGYF1, GRIN1, GRIN2D, IQSEC2-Related Syndromic Intellectual Disability, IRF2BPL, KANSL1, KCNB1, KDM3B, NEXMIF, KMT2A, MBOAT7, MEIS2, MYT1L, NAA15, NBEA, NCKAP1, NIPBL, NLGN2, NLGN3, NLGN4X, NR4A2, NRXN1, NRXN2, NSD1 Gene Mutation, PHF21A, PHF3, PHIP, POMGNT1, PSMD12, RELN, RERE, RFX3, RIMS1, RORB, SCN1A, SETD2 Gene Mutation, SHANK2, SIN3A, SLC9A6, SON, SOX5, SPAST, SRCAP, TAOK1, TANC2, TCF20, TLK2, TRIO, TRIP12, UPF3B, USP9X, VPS13B, WAC, WDFY3, ZBTB20, ZNF292, ZNF462, 2Q37 Deletion Syndrome, 9q34 Duplications, 15q15 Deletions, 15Q24 Deletion, NR3C2, SYNCRIP, 2q34 Duplication, 2q37.3 Deletion, 6q16 Deletion, 15q11.2 BP1-BP2 Deletion, 16p13.3 Deletion, 17Q11.2 Microduplication Syndrome (Disorder), 17p13.3, Xq28 Duplication, CLCN4, CSNK2B, DYNC1H1, EIF3F, GNB1, MED13, MEF2C, RALGAPB, SCN1B, YY1, Xp11.22 Duplication, PACS2, MAOA, MAOB, HNRNPC, HNRNPD, HNRNPK, HNRNPR, HNRNPUL2, 5P Deletion Syndrome, TCF7L2 Gene Mutation, HECW2 | Online Study of People Who Have Genetic Changes and Features of Autism: Simons Searchlight | N/A | RECRUITING |
| NCT05666687 | Major Depressive Disorder | An Open-label, Adaptive Design, Positron Emission Tomography Study in Healthy Male Participants to Characterize Receptor Occupancy by MIJ821 in the Brain | PHASE1 | COMPLETED |
| NCT00526968 | Human Volunteers | The Effects of a Novel NMDA NR2B-Subtype Selective Antagonist, EVT 101, on Brain Function | PHASE1 | COMPLETED |