Ioana Ferecatu

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p53 protein plays a central role in suppressing tumorigenesis by inducing cell cycle arrest or apoptosis through transcription-dependent and -independent mechanisms. Emerging publications suggest that following stress, a fraction of p53 translocates to mitochondria to induce cytochrome c release and apoptosis. However, the localization of p53 under(More)
A broad range of stressors - intrinsic and extrinsic to the cell - stabilize and activate p53, affecting it by a series of post-translational modifications such as phosphorylation, acetylation, ubiquitination, methylation and sumoylation. p53 is able to integrate each kind of post-translational modification and to adequately respond by inducing cell cycle(More)
Several caspase-cleaved forms of the retinoblastoma protein have been described. Here, we compared the effect of full-length Rb versus the truncated p76(Rb) and p100(Rb) proteins on cell death regulation in five human cell lines. Interestingly, we observed that p76(Rb) triggers cell death in all tested cell lines and that p100(Rb) protects two cell lines(More)
The retinoblastoma protein (Rb) plays a central role in the regulation of cell cycle, differentiation and apoptosis. In cancer cells, ablation of Rb function or its pathway is a consequence of genetic inactivation, viral oncoprotein binding or deregulated hyperphosphorylation. Some recent data suggest that Rb relocation could also account for the regulation(More)
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