Specific ablation of Stat3β distorts the pattern of stat3-responsive gene expression and impairs recovery from endotoxic shock

Joo Yeon Yoo, David L. Huso, Daniel Nathans, Stephen Desiderio

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
Pages (from-to)331-344
Number of pages14
JournalCell
Volume108
Issue number3
DOIs
StatePublished - Jan 1 2002

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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