| First Author | Zhou H | Year | 2016 |
| Journal | Genes Immun | Volume | 17 |
| Issue | 4 | Pages | 220-7 |
| PubMed ID | 27009487 | Mgi Jnum | J:252471 |
| Mgi Id | MGI:6107666 | Doi | 10.1038/gene.2016.13 |
| Citation | Zhou H, et al. (2016) Alternative splicing directs two IL-20R2 isoforms and is responsible for the incomplete gene knockout via the exon I ablation. Genes Immun 17(4):220-7 |
| abstractText | Two heterodimeric receptors consisting of interleukin (IL)-20R2 are shared by three of the IL-20 family of cytokines, IL-19, IL-20 and IL-24. Along with IL-22, these cytokines are downstream effectors of IL-23 and have been implicated in keratinocyte functions and the pathogenesis of psoriasis. Surprisingly, whereas knocking out either the IL-23 or IL-22 gene abolished imiquimod-induced psoriatic phenotypes in mice, similar attempt for IL-20R2 had little effect. Here, we report that the apparent disparity may result from a new IL-20R2 isoform encoded by an alternatively spliced transcript which survived the previous attempt for IL-20R2 gene knockout via the exon I deletion. |
