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Oncogenic c-H-ras deregulates survivin expression: an improvement for survival
Authors:Sommer Klaus W  Rodgarkia-Dara Chantal J  Schreiner Claudia  Holzmann Klaus  Krupitza Georg  Cerni Christa
Affiliation:Clinics of Internal Medicine I, Division Institute of Cancer Research, Medical University of Vienna, Borschkegasse 8a, 1090 Vienna, Austria.
Abstract:Survivin protein accomplishes two basic functions: cell cycle regulation and control of apoptosis. It is only expressed in G2/M phase and it influences rescue pathways in apoptosis-induced cells. Overexpression of constitutive active c-H-ras in HeLa, or induction of c-H-ras in a stable HeLaDiR cell line, led to sustained survivin expression in all cell cycle phases and even protected cells from drug induced apoptosis. siRNA-mediated silencing of survivin reversed this protection. Here we link the anti-apoptotic property of survivin to its cell cycle (in)dependent regulation via the activity of oncogenic c-H-ras.
Keywords:IAP, inhibitor of apoptosis protein   DiR, dexamethasone inducible ras   Dex, dexamethasone
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