|Institutional Source||Beutler Lab|
|Gene Name||G protein-coupled receptor 132|
|Synonyms||G2a, G2 accumulation|
|Is this an essential gene?||Non essential (E-score: 0.000)|
|Stock #||R1786 (G1)|
|Chromosomal Location||112850873-112868228 bp(-) (GRCm38)|
|Type of Mutation||missense|
|DNA Base Change (assembly)||A to G at 112852403 bp|
|Amino Acid Change||Serine to Proline at position 268 (S268P)|
|Ref Sequence||ENSEMBL: ENSMUSP00000021729 (fasta)|
|Gene Model||predicted gene model for transcript(s): [ENSMUST00000021729] [ENSMUST00000222776]|
|Predicted Effect||probably damaging
AA Change: S268P
PolyPhen 2 Score 0.996 (Sensitivity: 0.55; Specificity: 0.98)
AA Change: S268P
|Predicted Effect||probably benign
|Meta Mutation Damage Score||0.3187|
|Coding Region Coverage||
|Validation Efficiency||97% (98/101)|
FUNCTION: [Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a member of the guanine nucleotide-binding protein (G protein)-coupled receptor (GPCR) superfamily. The receptors are seven-pass transmembrane proteins that respond to extracellular cues and activate intracellular signal transduction pathways. This protein was reported to be a receptor for lysophosphatidylcholine action, but PubMedID: 15653487 retracts this finding and instead suggests this protein to be an effector of lysophosphatidylcholine action. This protein may have proton-sensing activity and may be a receptor for oxidized free fatty acids. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jul 2013]
PHENOTYPE: Mice homozygous for disruptions in this gene display a generally normal phenotype but eventually develop a "late onset lymphoproliferative autoimmune syndrome" [provided by MGI curators]
|Allele List at MGI|
|Other mutations in this stock||
|Other mutations in Gpr132||
(F):5'- CAAGTGTGTCTCCTCAGAGTC -3'
(R):5'- CATCCTGGCGTTCACCAATC -3'
(F):5'- CTCAGAGTCCTTTGAGCATGTAAC -3'
(R):5'- TCACCAGATCTTCCGGAGC -3'