|Institutional Source||Beutler Lab|
|Gene Name||sphingosine-1-phosphate receptor 5|
|Synonyms||S1P5, Edg8, lpB4|
|Is this an essential gene?||Possibly non essential (E-score: 0.365)|
|Stock #||R3430 (G1)|
|Chromosomal Location||21242912-21248443 bp(-) (GRCm38)|
|Type of Mutation||missense|
|DNA Base Change (assembly)||A to G at 21245082 bp|
|Amino Acid Change||Valine to Alanine at position 16 (V16A)|
|Ref Sequence||ENSEMBL: ENSMUSP00000113843 (fasta)|
|Gene Model||predicted gene model for transcript(s): [ENSMUST00000122088]|
|Predicted Effect||probably benign
AA Change: V16A
PolyPhen 2 Score 0.003 (Sensitivity: 0.98; Specificity: 0.44)
AA Change: V16A
|Predicted Effect||noncoding transcript
|Meta Mutation Damage Score||0.0599|
|Coding Region Coverage||
|Validation Efficiency||100% (67/67)|
FUNCTION: [Summary is not available for the mouse gene. This summary is for the human ortholog.] The lysosphingolipid sphingosine 1-phosphate (S1P) regulates cell proliferation, apoptosis, motility, and neurite retraction. Its actions may be both intracellular as a second messenger and extracellular as a receptor ligand. S1P and the structurally related lysolipid mediator lysophosphatidic acid (LPA) signal cells through a set of G protein-coupled receptors known as EDG receptors. Some EDG receptors (e.g., EDG1; MIM 601974) are S1P receptors; others (e.g., EDG2; MIM 602282) are LPA receptors.[supplied by OMIM, Mar 2008]
PHENOTYPE: Bone marrow from mice homozygous for a knock-out allele induces impaired NK cell egression from the lymph nodes and bone marrow. [provided by MGI curators]
|Allele List at MGI|
|Other mutations in this stock||
|Other mutations in S1pr5||
(F):5'- GTAAGGTGGCGCTCTAAAGC -3'
(R):5'- ACCTTCTCAAGTCCTCAGGG -3'
(F):5'- TCCGACAAAGTGAGGCTGC -3'
(R):5'- AAGTCCTCAGGGGGCGTG -3'