|Institutional Source||Beutler Lab|
|Gene Name||glutamate receptor, ionotropic, NMDA2B (epsilon 2)|
|Synonyms||GluRepsilon2, NMDAR2B, GluN2B, Nmdar2b, NR2B|
|Is this an essential gene?||Essential (E-score: 1.000)|
|Stock #||R0164 (G1)|
|Chromosomal Location||135713233-136173511 bp(-) (GRCm38)|
|Type of Mutation||splice site|
|DNA Base Change (assembly)||A to G at 135778648 bp (GRCm38)|
|Amino Acid Change|
|Ref Sequence||ENSEMBL: ENSMUSP00000107536 (fasta)|
|Gene Model||predicted gene model for transcript(s): [ENSMUST00000053880] [ENSMUST00000111905]|
|AlphaFold||no structure available at present|
|Coding Region Coverage||
|Validation Efficiency||98% (85/87)|
FUNCTION: [Summary is not available for the mouse gene. This summary is for the human ortholog.] N-methyl-D-aspartate (NMDA) receptors are a class of ionotropic glutamate receptors. NMDA receptor channel has been shown to be involved in long-term potentiation, an activity-dependent increase in the efficiency of synaptic transmission thought to underlie certain kinds of memory and learning. NMDA receptor channels are heteromers composed of three different subunits: NR1 (GRIN1), NR2 (GRIN2A, GRIN2B, GRIN2C, or GRIN2D) and NR3 (GRIN3A or GRIN3B). The NR2 subunit acts as the agonist binding site for glutamate. This receptor is the predominant excitatory neurotransmitter receptor in the mammalian brain. [provided by RefSeq, Jul 2008]
PHENOTYPE: Homozygotes for targeted null mutations exhibit impairments in suckling, in hippocampal long term depression, and in pattern formation of trigeminal nucleus sensory afferent terminals. Mutants die shortly after birth. [provided by MGI curators]
|Allele List at MGI|
|Other mutations in this stock||
|Other mutations in Grin2b||
(F):5'- GGCTTCTGATGACCATTCAGGCAG -3'
(R):5'- GGGTATTCATGGTGCCCAAGTTACG -3'
(F):5'- CTGATGACCATTCAGGCAGTATTTG -3'
(R):5'- ATGGACCTGTCTTCCAGAATG -3'