作者: Beata Pyrzynska , Manuel Serrano , Carlos Martı́nez-A. , Bozena Kaminska
关键词: Knockout mouse 、 Cyclosporin a 、 Suppressor 、 Apoptosis 、 Cell biology 、 Cancer research 、 Biology 、 Programmed cell death 、 Transfection 、 Mitochondrion 、 Glioma
摘要: The tumor suppressor p53 can induce growth arrest and cell death via apoptosis in response to a number of cellular stresses. We have shown previously that the immunosuppressant cyclosporin A (CsA) induces programmed with typical features rat glioma cells. report CsA treatment results increased level suppressor, its nuclear accumulation, transcriptional activation p53-dependent genes. increase correlates elevation p21Waf1 Bax protein expression. was accompanied changes subcellular localization association mitochondria. Importantly, we demonstrate cells stably transfected mutant (p53Val135) fail p21 levels are less sensitive CsA-induced apoptosis. Furthermore, primary fibroblasts from p53−/− knockout mice significantly more resistant compared their corresponding counterparts containing functional p53. Together, our suggest apoptotic program activated by be mediated potentiation ability initiate