KAP1 regulates type I interferon/STAT1-mediated IRF-1 gene expression

Shinya Kamitani, Norihiko Ohbayashi, Osamu Ikeda, Sumihito Togi, Ryuta Muromoto, Yuichi Sekine, Kazuhide Ohta, Hironobu Ishiyama, Tadashi Matsuda

研究成果: Article査読

32 被引用数 (Scopus)

抄録

Signal transducers and activators of transcription (STATs) mediate cell proliferation, differentiation, and survival in immune responses, hematopoiesis, neurogenesis, and other biological processes. Recently, we showed that KAP1 is a novel STAT-binding partner that regulates STAT3-mediated transactivation. KAP1 is a universal co-repressor protein for the KRAB zinc finger protein superfamily of transcriptional repressors. In this study, we found KAP1-dependent repression of interferon (IFN)/STAT1-mediated signaling. We also demonstrated that endogenous KAP1 associates with endogenous STAT1 in vivo. Importantly, a small-interfering RNA-mediated reduction in KAP1 expression enhanced IFN-induced STAT1-dependent IRF-1 gene expression. These results indicate that KAP1 may act as an endogenous regulator of the IFN/STAT1 signaling pathway.

本文言語English
ページ(範囲)366-370
ページ数5
ジャーナルBiochemical and biophysical research communications
370
2
DOI
出版ステータスPublished - 2008 5月 30
外部発表はい

ASJC Scopus subject areas

  • 生物理学
  • 生化学
  • 分子生物学
  • 細胞生物学

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