Release from G1 growth arrest by transforming growth factor beta 1 requires cellular ras activity.
作者： P.H. Howe , S.F. Dobrowolski , K.B. Reddy , D.W. Stacey
DOI: 10.1016/S0021-9258(19)36945-5
关键词: TGF alpha 、 TGF beta receptor 2 、 Transforming growth factor, beta 3 、 R-SMAD 、 Endoglin 、 TGF beta signaling pathway 、 Cancer research 、 TGF beta 1 、 Transforming growth factor beta 、 Biology
摘要: Transforming growth factor beta 1 (TGF 1) is a potent inhibitor of epithelial cell growth, although the mechanism inhibition remains unknown. We report here critical relationship between cellular p21ras activity and TGF action. Microinjection oncogenic Ha-ras protein into 1-arrested mink lung cells overcomes allows progression S phase. Cells released from following microinjection with anti-p21ras antibody, on other hand, remain do not enter phase, indicating requirement for activity. These biological data are substantiated biochemically in that shown to decrease activation state endogenous p21ras, as measured by level GTP-bound p21ras. In addition, phosphorylation kinase mitogen-activated kinase, which depends upon ras activity, elevated have been arrest 1. Together these demonstrate involvement 1-induced suggest controls proliferation modulating
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