Thyroid hormone induces activation of mitogen-activated protein kinase in cultured cells

Hung Yun Lin, Faith B. Davis, Jennifer K. Gordinier, Leon J. Martino, Paul J. Davis

研究成果: 雜誌貢獻文章同行評審

185 引文 斯高帕斯(Scopus)

摘要

Thyroid hormone [L-thyroxine (T4)] rapidly induced phosphorylation and nuclear translocation (activation) of mitogen-activated protein kinase (MAPK) in HeLa and CV-1 cells in the absence of cytokine or growth factor. A pertussis toxin-sensitive and guanosine 5'-O-(3-thiotriphosphate)-sensitive cell surface mechanism responsive to T4 and agarose-T4, suggesting a G protein-coupled receptor, was implicated. Cells depleted of MAPK or treated with MAPK pathway inhibitors showed reduced activation of MAPK and of the signal transducer and activator of transcription STAT1α by T4; they also showed reduced T4 potentiation of the antiviral action of interferon-γ (IFN-γ). T4 treatment caused tyrosine-phosphorylated MAPK-STAT1α nuclear complex formation and enhanced Ser-727 phosphorylation of STAT1α, in the presence or absence of IFN-γ. STAT1α-deficient cells transfected with STAT1α containing an alanine-for-serine substitution at residue 727 (STAT1α(A727)) showed minimal T4-stimulated STAT1α activation. IFN-γ induced the antiviral state in cells containing wild-type STAT1. (STAT1α(wt)) or STAT1α(A727); T4 potentiated IFN-γ action in STAT1α(wt) cells but not in STAT1α(A727) cells. T4-directed STAT1α Ser-727 phosphorylation is MAPK mediated and results in potentiated STAT1α activation and enhanced IFN-γ activity.
原文英語
期刊American Journal of Physiology - Cell Physiology
276
發行號5 45-5
出版狀態已發佈 - 1999
對外發佈

ASJC Scopus subject areas

  • 臨床生物化學
  • 細胞生物學
  • 生理學
  • 生理學(醫學)

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