Abstract
Alternative splicing of the gene for Stat3, a transcription factor activated by the IL-6 family of cytokines, produces two isoforms: Stat3α and a dominant-negative variant, Stat3β. Stat3β-deficient mice were generated by gene targeting. Despite intact expression and phosphorylation of Stat3α, overall Stat3 activity was impaired in Stat3β −/− cells. Global comparison of transcription in Stat3β +/+ and Stat3β −/− cells revealed stable differences. Stat3β-deficient mice exhibit diminished recovery from endotoxic shock and hyperresponsiveness of a subset of endotoxin-inducible genes in liver. The hepatic response to endotoxin in wild-type mice is accompanied by a transient increase in the ratio of Stat3β to Stat3α. These findings indicate a critical role for Stat3β in the control of systemic inflammation.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
