AI Article Synopsis
- IL-17 is a proinflammatory cytokine that enhances the expression of various cytokines and chemokines by promoting gene transcription and stabilizing mRNAs.
- The study reveals that IL-17 increases the half-life of Zc3h12a mRNA through an interaction between the adaptor protein CIKS and the DEAD box protein DDX3X, requiring the helicase domain of DDX3X.
- Knockdown of DDX3X reduces the stability of Zc3h12a mRNA without impacting other mRNAs, and additional proteins like IKKε and TNFR-associated factors are also necessary for this mRNA stabilization process triggered by IL-17.
Article Abstract
IL-17 is a proinflammatory cytokine that promotes the expression of different cytokines and chemokines via the induction of gene transcription and the posttranscriptional stabilization of mRNAs. In this study, we show that IL-17 increases the half-life of the Zc3h12a mRNA via interaction of the adaptor protein CIKS with the DEAD box protein DDX3X. IL-17 stimulation promotes the formation of a complex between CIKS and DDX3X, and this interaction requires the helicase domain of DDX3X but not its ATPase activity. DDX3X knockdown decreases the IL-17-induced stability of Zc3h12a without affecting the stability of other mRNAs. IKKε, TNFR-associated factor 2, and TNFR-associated factor 5 were also required to mediate the IL-17-induced Zc3h12a stabilization. DDX3X directly binds the Zc3h12a mRNA after IL-17 stimulation. Collectively, our findings define a novel, IL-17-dependent mechanism regulating the stabilization of a selected mRNA.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369453 | PMC |
| http://dx.doi.org/10.4049/jimmunol.1401589 | DOI Listing |
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