R. M. Ardito Marretta∗,†, G. Barbaraci‡
Molecular & Cellular Biomechanics, Vol.7, No.3, pp. 135-164, 2010, DOI:10.3970/mcb.2010.007.135
Abstract Upon severe DNA damage, p21 acts in a dual mode; on the one hand, it inhibits the cyclin-CDK complex for arresting the G2/M transition and on the other hand, it indirectly becomes an apoptotic factor by activating - in sequence - the retinoblastoma protein, E2F1 and APAF1 expressions. But, in a cancer cells proliferation, the mechanisms of, and participants in, the apoptosis failure remain unclear. Since the p21/p53/Mdm2 proteins network normally involves a digital response in a cancer cell, through an original design of a cell signalling-protein simulator, we demonstrate,in silico, that apoptosis phase instability More >
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