Comput Math Methods Med - Dynamics of posttranslational modifications of p53.

Tópicos

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Resumo

The latest experimental evidence indicates that acetylation of p53 at K164 (lysine 164) and K120 may induce directly cell apoptosis under severe DNA damage. However, previous cell apoptosis models only studied the effects of active and/or inactive p53, that is, phosphorylation/dephosphorylation of p53. In the present paper, based partly on Geva-Zatorsky et al. (2006) and Batchelor et al. (2008), we propose a new cell apoptosis network, in which p53 has three statuses, that is, unphosphorylated p53, phosphorylated p53, and acetylated p53. The time delay differential equations (DDEs) are formulated based on our network to investigate the dynamical insights of p53-induced cell apoptosis. In agreement with experiments (Loewer et al. (2010)), our simulations indicate that acetylated p53 accumulates gradually and then induces the proapoptotic protein Bax under enough DNA damage. Moreover, phosphorylated p53 oscillates and initiates cell repair during DNA damage.

Resumo Limpo

latest experiment evid indic acetyl p k lysin k may induc direct cell apoptosi sever dna damag howev previous cell apoptosi model studi effect activ andor inact p phosphorylationdephosphoryl p present paper base part gevazatorski et al batchelor et al propos new cell apoptosi network p three status unphosphoryl p phosphoryl p acetyl p time delay differenti equat ddes formul base network investig dynam insight pinduc cell apoptosi agreement experi loewer et al simul indic acetyl p accumul gradual induc proapoptot protein bax enough dna damag moreov phosphoryl p oscil initi cell repair dna damag

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