TGFβ1 suppresses EGF‐induced increase in nuclear type 1 protein phosphatase activity at the G1/S transition of hepatocyte proliferation

FEBS Letters

Kakinoki, Yasutaka²  Miyazaki, Tamotsu¹  Kikuchi, Kunimi²  Mizuno, Yusuke²  Imai, Yoko²  Takizawa, Norio² 

[1] Third Department of Internal Medicine, Hokkaido University School of Medicine, Kita-15, Nishi-7, Kita-ku, Sapporo 060, Japan;Section of Biochemistry, Institute of Immunological Science, Hokkaido University, Kita-15, Nishi-7, Kita-ku, Sapporo 060, Japan

关键词: Type 1 protein phosphatase;    Epidermal growth factor;    Transforming growth factor β1;    DNA synthesis;    Hepatocyte;    EGF(-R);    epidermal growth fctor (-receptor);    PDGF-(-R);    platelet-derived growth factor (-receptor);    CSF-1;    colony-stimulating factor-1;    SH2;    Src homology 2;    PTK;    protein tyrosine kinase;    PVDF;    polyvinylidene diflouride;   

DOI  :  10.1016/0014-5793(94)00993-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Nuclear type 1 protein phosphatase (PP1) activity in primary culture of EGF-stimulated hepatocytes was significantly and transiently increased at the G₁/S transition, being about 2.5-fold, while that in non-stimulated hepatocytes showed almost no change. On the other hand, non-nuclear PP1 activity was gradually increased until the G₁/S transition, but the activity showed no difference between EGF-stimulated and non-stimulated hepatocytes. Under growth-inhibited conditions in the presence of TGFβ1, the increase in nuclear PP1 activity was completely suppressed, whereas non-nuclear PP1 activity was little affected. Such close correlation between nuclear PP1 activity and growth factor-induced positive or negative growth signaling strongly suggests an involvement of PP1 in progression from G₁ to S phase of hepatocytes. On Western immunoblotting using antisera for PP1α, PP1γ1, and PP1δ, no isoform showed any change in amount under these conditions. Mechanism(s) of growth-associated alterations in nuclear PP1 activity is discussed.

【 授权许可】

Unknown