|Institutional Source||Beutler Lab|
|Gene Name||interleukin 17 receptor C|
|Synonyms||1110025H02Rik, IL17-RL, Il17rl|
|Essential gene?||Probably non essential (E-score: 0.066)|
|Stock #||R7010 (G1)|
|Chromosomal Location||113471427-113483140 bp(+) (GRCm38)|
|Type of Mutation||missense|
|DNA Base Change (assembly)||A to G at 113479288 bp (GRCm38)|
|Amino Acid Change||Asparagine to Serine at position 338 (N338S)|
|Ref Sequence||ENSEMBL: ENSMUSP00000055343 (fasta)|
|Gene Model||predicted gene model for transcript(s): [ENSMUST00000032422] [ENSMUST00000058300]|
|AlphaFold||no structure available at present|
AA Change: N338S
PolyPhen 2 Score 0.861 (Sensitivity: 0.83; Specificity: 0.93)
AA Change: N338S
|Coding Region Coverage||
FUNCTION: [Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a single-pass type I membrane protein that shares similarity with the interleukin-17 receptor (IL-17RA). Unlike IL-17RA, which is predominantly expressed in hemopoietic cells, and binds with high affinity to only IL-17A, this protein is expressed in nonhemopoietic tissues, and binds both IL-17A and IL-17F with similar affinities. The proinflammatory cytokines, IL-17A and IL-17F, have been implicated in the progression of inflammatory and autoimmune diseases. Multiple alternatively spliced transcript variants encoding different isoforms have been detected for this gene, and it has been proposed that soluble, secreted proteins lacking transmembrane and intracellular domains may function as extracellular antagonists to cytokine signaling. [provided by RefSeq, Feb 2011]
PHENOTYPE: Mice homozygous for a reporter allele exhibit increased interleukin-17 secretion, reduced chemokine expression, and decreased susceptibility to experimental autoimmune encephalomyelitis. [provided by MGI curators]
|Allele List at MGI|
|Other mutations in this stock||
|Other mutations in Il17rc||
(F):5'- AGGTAACACTGTGCTGGCAG -3'
(R):5'- CGTTAACATGCGTCCTTAAAGCAC -3'
(F):5'- GCAGGCACCAGACCAGAGTC -3'
(R):5'- AACAGTATCGTGCTGTAGCC -3'