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Symbol GRIN2B contributors: mct - updated : 08-10-2015
HGNC name glutamate receptor, ionotropic, N-methyl D-aspartate 2B
HGNC id 4586
Corresponding disease
EIEE27 epileptic encephalopathy, early infantile, 27
MRD6 mental retardation, autosomal dominant 6
Location 12p13.1      Physical location : 13.714.409 - 14.133.022
Synonym name
  • N-methyl-D-aspartate receptor subunit 3
  • glutamate [NMDA] receptor subunit epsilon-2
  • Synonym symbol(s) NMDAR2B, NR2B, NME2, MGC142180, NR3, MGC142178, EIEE27, GluN2B, MRD6, hNR3, GLURE2
    TYPE functioning gene
    STRUCTURE 418.61 kb     13 Exon(s)
    10 Kb 5' upstream gene genomic sequence study
    MAPPING cloned Y linked N status confirmed
    TRANSCRIPTS type messenger
    identificationnb exonstypebpproduct
    ProteinkDaAAspecific expressionYearPubmed
    13 - 5941 - 1484 - 2001 11400170
    Type restricted
       expressed in (based on citations)
    SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
    Nervousbrainbasal nuclei  lowly
     brainforebraincerebral cortexfrontal 
     brainforebraincerebral cortexparietal 
     brainforebraincerebral cortextemporal 
     braindiencephalonhypothalamussuprachiasmatic nuclei  Homo sapiens
     nervecranial nerve   
    SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
    SystemCellPubmedSpeciesStageRna symbol
    Lymphoid/ImmuneT cell
    Nervousneuron Homo sapiens
    cell lineage
    cell lines
    at STAGE
    physiological period fetal, neonatal
    Text hippocampus, forebrain, brain
  • a large intracellular C terminal domain
  • four transmembrane segments (4TM)
  • conjugated GlycoP
    mono polymer heteromer , dimer
    interspecies homolog to murine Grin2b
  • glutamate-regulated family of ion channels
  • CATEGORY receptor membrane , transport channel
    SUBCELLULAR LOCALIZATION     plasma membrane
  • post synaptic membrane
  • predominant at asymmetrical synapses of non-GABAergic neurons
  • basic FUNCTION
  • involved in excitatory neurotransmission, in neuronal cell death and in the epileptic hyperexcitability of dysplastic cortical regions
  • involved in controlling T cell activation
  • ligand-gated ion channel (Ca2+) transporting, when bound to glutamate and Mg2+ released
  • playing a central role in long potentiation memory, and cognitive function
  • with GRIA2, GRIA3, GRIA1, mediate fast synaptic transmission in the brain
  • GRIN2B, GRIN2D play counteractive roles in temporal development and maturation of somatosensory maps without affecting the magnitude of critical period plasticity
  • GRIN2B expressed at glutamatergic synapses on glutamatergic projection neurons facilitates refinement of ascending pathway synapses directly, whereas GRIN2D expressed at glutamatergic synapses on GABAergic interneurons delays it indirectly
  • CELLULAR PROCESS cell life, cell death/apoptosis
    PHYSIOLOGICAL PROCESS development , nervous system
    text small molecule transport
    signaling neurotransmission
    glutamate signaling pathway/excitatory neurotransmission
    a component
  • N-methyl D-aspartate receptor 2, epsilon 2 subunit glutamate receptor
  • heterodimers composed of the key receptor subunit GRIN1 and one or more of the four NMDAR2 subunits (GRIN2A, GRIN 2B, GRIN 2C, GRIN2D)
  • dimer of GRIN1-GRIN2B heterodimers with the twofold symmetry axis running through the entire molecule composed of an amino terminal domain (ATD), a ligand-binding domain (LBD), and a transmembrane domain (TMD)
    small molecule metal binding,
  • Mg2+
  • protein
  • NRF1 co-regulates oxidative enzymes that generate energy and neurochemicals that consume energy related to glutamatergic neurotransmission, such as KIF17, GRIN1, and GRIN2B, thereby ensuring that energy production matches energy utilization at the molecular and cellular levels
  • KIF17 differentially maintains the levels of GRIN2A and GRIN2B, and, when synapses are stimulated, the GRIN2B/KIF17 complex is upregulated on demand through CREB activity
  • stable interaction between the PH domain of KALRN and the juxtamembrane region of GRIN2B preceding its cytosolic C-terminal domain
  • novel and functionally important interaction between the NR2B subunit of the NMDA receptor and KALRNn, proteins known to be essential for normal synaptic plasticity
  • DLG4 associated with NMDA receptors GRIN2A, GRIN2B via their PDZ1 and PDZ2 domains
  • TSPYL2 regulated the expression of GRIN2A and GRIN2B
  • both ARF6 activation through GRIN2B-IQSEC2 during early development and the transition from IQSEC2- to IQSEC1-dependent ARF6 signaling induced by the GRIN2B subunit switch are critical for the development of mature glutamatergic synapses
  • interaction with FRMPD2,through second PDZ (PDZ2) domain binding to the C-terminus of GRIN2A and GRIN2B, two subunits of NMDA receptors
  • cell & other
    activated by selectively activated by the artificial glutamate analog N-methyl D-aspartate
    Other regulated by complex TBR1/CASK/TAF9 (transcriptional complex regulating expression of the GRIN2B)
    corresponding disease(s) MRD6 , EIEE27
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional germinal mutation      
    in a schizophrenia-like syndrome produced by NMDA receptor antagonists
    constitutional germinal mutation      
    in individuals with mental retardation
    constitutional germinal mutation      
    sporadic autistic disorder
    constitutional       loss of function
    GRIN2B and GRIN2D-deficiency protected retinal ganglion cells (RGCs) from NMDA-induced excitotoxic retinal cell death
    Susceptibility to schizophrenia
    Variant & Polymorphism other polymorphism G1001C of GRIN1 asssociated to allele T4197C and T5988C of GRIN2B increasing the risk of schizophrenia
    Candidate gene for bipolar disorder in Ashkenazim
    Therapy target
    GRIN2B and GRIN2D activity is a potential therapeutic strategy for the treatment of several retinal diseases
  • Nmdar 2b knock out mice
  • mutant mice expressing the Nmdar 2b gene without the large intracellular C terminal domain
  • transgenic mice overexpressing the Nmdar 2b gene
  • phenotype of Grin2b-deficient mice is more severe, as they die perinatally due to severe developmental brain defects