|Institutional Source||Beutler Lab|
|Gene Name||glutamate receptor, ionotropic, AMPA2 (alpha 2)|
|Synonyms||Glur2, Glur-2, GluR-B, GluA2, GluR2|
|Is this an essential gene?||Possibly non essential (E-score: 0.482)|
|Stock #||R7225 (G1)|
|Chromosomal Location||80681450-80802835 bp(-) (GRCm38)|
|Type of Mutation||unclassified|
|DNA Base Change (assembly)||T to A at 80802631 bp (GRCm38)|
|Amino Acid Change|
|Ref Sequence||ENSEMBL: ENSMUSP00000141447 (fasta)|
|Gene Model||predicted gene model for transcript(s): [ENSMUST00000075316] [ENSMUST00000107745] [ENSMUST00000192463]|
|AlphaFold||no structure available at present|
|Coding Region Coverage||
|Validation Efficiency||98% (62/63)|
FUNCTION: Glutamate receptors are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes. This gene product belongs to a family of glutamate receptors that are sensitive to alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), and function as ligand-activated cation channels. These channels are assembled from 4 related subunits, Gria1-4. The subunit encoded by this gene (Gria2) is subject to RNA editing (CAG->CGG; Q->R) within the second transmembrane domain, which is thought to render the channel impermeable to Ca(2+). Alternative splicing, resulting in transcript variants encoding different isoforms, (including the flip and flop isoforms that vary in their signal transduction properties), has been noted for this gene. [provided by RefSeq, Jul 2008]
PHENOTYPE: Homozygotes for targeted null mutations exhibit epilepsy, deficient dendritic architecture, altered exploratory behavior, impaired motor and learning performance, and increased mortality. [provided by MGI curators]
|Allele List at MGI|
|Other mutations in this stock||
|Other mutations in Gria2||
(F):5'- CCTCAGCAAATTAGATCCTCTGC -3'
(R):5'- AGGTCTCTAAGAGGCACCAG -3'
(F):5'- CTGCATTTTGAGGTCGAAATTTAGC -3'
(R):5'- AGAAGCTGCCAGGGCTGTG -3'