|Institutional Source||Beutler Lab|
|Gene Name||interleukin 17 receptor A|
|Essential gene?||Probably non essential (E-score: 0.078)|
|Stock #||R4192 (G1)|
|Chromosomal Location||120463247-120487559 bp(+) (GRCm38)|
|Type of Mutation||missense|
|DNA Base Change (assembly)||A to G at 120481511 bp (GRCm38)|
|Amino Acid Change||Aspartic acid to Glycine at position 541 (D541G)|
|Ref Sequence||ENSEMBL: ENSMUSP00000002976 (fasta)|
|Gene Model||predicted gene model for transcript(s): [ENSMUST00000002976]|
AA Change: D541G
PolyPhen 2 Score 0.999 (Sensitivity: 0.14; Specificity: 0.99)
AA Change: D541G
|Meta Mutation Damage Score||0.4970|
|Coding Region Coverage||
|Validation Efficiency||100% (40/40)|
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'- CTTTTCACTGCAGCCATGAAC -3'
(R):5'- GCAGTGGGTCTTCAAACACTTC -3'
(F):5'- TGCAGCCATGAACATGATCCTG -3'
(R):5'- CTTCTTCATCCAGGGAGGGAAGATC -3'