MEK is a negative regulator of Stat5b in PDGF‐stimulated cells

FEBS Letters

Heldin, Carl-Henrik¹  Valgeirsdóttir, Sigrı́dur¹  Ruusala, Aino¹ 

[1] Ludwig Institute for Cancer Research, Biomedical Center, Box 595, S-751 24 Uppsala, Sweden

关键词: Stat5b;    Platelet-derived growth factor β-receptor;    MEK;    Signal transduction;    EGF;    epidermal growth factor;    Jak;    Janus kinase;    MBP;    myelin basic protein;    PAE;    porcine aortic endothelial;    PDGF;    platelet-derived growth factor;    PMSF;    phenylmethylsulfonyl fluoride;    SDS-PAGE;    sodium dodecyl sulfate-polyacrylamide gel electrophoresis;    Stat;    signal transducer and activator of transcription;   

DOI  :  10.1016/S0014-5793(99)00459-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

In this study we show that platelet-derived growth factor (PDGF)-induced DNA binding as well as transcriptional activation of Stat5b are markedly increased by inhibition of the MAP (mitogen-activated protein) kinase kinase MEK. In addition to the previously demonstrated tyrosine phosphorylation, we show that serine and threonine phosphorylation of Stat5b is increased in response to PDGF stimulation. However, inhibition of MEK had no effect on the phosphorylation level of Stat5b or on the nuclear translocation of Stat5b. These observations indicate that MEK is a negative modulator of PDGF-induced Stat5b activation through a mechanism not involving direct phosphorylation of Stat5b.

【 授权许可】

Unknown