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|Institutional Source||Beutler Lab|
|Gene Name||interleukin 17 receptor A|
|Is this an essential gene?||Probably non essential (E-score: 0.080)|
|Stock #||R8213 (G1)|
|Chromosomal Location||120463247-120487559 bp(+) (GRCm38)|
|Type of Mutation||missense|
|DNA Base Change (assembly)||T to C at 120473034 bp|
|Amino Acid Change||Valine to Alanine at position 91 (V91A)|
|Ref Sequence||ENSEMBL: ENSMUSP00000002976 (fasta)|
|Gene Model||predicted gene model for transcript(s): [ENSMUST00000002976]|
|Predicted Effect||probably benign
AA Change: V91A
PolyPhen 2 Score 0.394 (Sensitivity: 0.90; Specificity: 0.89)
AA Change: V91A
|Coding Region Coverage||
|Validation Efficiency||98% (65/66)|
FUNCTION: [Summary is not available for the mouse gene. This summary is for the human ortholog.] Interleukin 17A (IL17A) is a proinflammatory cytokine secreted by activated T-lymphocytes. It is a potent inducer of the maturation of CD34-positive hematopoietic precursors into neutrophils. The transmembrane protein encoded by this gene (interleukin 17A receptor; IL17RA) is a ubiquitous type I membrane glycoprotein that binds with low affinity to interleukin 17A. Interleukin 17A and its receptor play a pathogenic role in many inflammatory and autoimmune diseases such as rheumatoid arthritis. Like other cytokine receptors, this receptor likely has a multimeric structure. Alternative splicing results in multiple transcript variants encoding different isoforms. [provided by RefSeq, Feb 2014]
PHENOTYPE: Homozygotes for a targeted null mutation exhibit delayed neutrophil recruitment and enhanced susceptibility to intranasal infection by Klibsiella pneumoniae. Mice homozygous for a different knock-out allele exhibit delayed and milder IMQ-induced psoriasis. [provided by MGI curators]
|Allele List at MGI|
|Other mutations in this stock||
|Other mutations in Il17ra||
(F):5'- AACTCATAGCAGGTCTCTGGAC -3'
(R):5'- TGATGCAAGGGAAGGCCTTTC -3'
(F):5'- GTCTCTGGACCCTCTAAGCAG -3'
(R):5'- GGCCTTTCATAAAGACAGTGTG -3'