Here, cell cycle in higher eukaryotes and their molecular networks signals both in G1/S and G2/M transitionsare in silico replicated. Systems control theory is employed to design multi-nestled digital layers to simulate protein-toproteinactivation and inhibition in the cancer cell cycle dynamics in presence of damaged genome. Sequencing andcontrolling the digital process of four micro-scale species networks (p53/Mdm2/DNA damage; p21mRNA/cyclin-CDKcomplex; CDK/CDC25/wee1/SKP2/APC/CKI and apoptosis target genes system) paved the way for unravelling theparticipants and their by-products having the task to execute (or not) cell death. The results of the proposed cell digitalmulti-layers give reason to believe in the existence of an universal apoptotic mechanism. We identified and selected cellcheckpoints, sizers, timers and specific target genes dynamics both for influencing mitotic process and avoiding cancerproliferation as much as for leading the cancer cell(s) to collapse into a steady stable apoptosis phase.
|Titolo della pubblicazione ospite||On Cancer Cell Cycle and Universal Apoptosis Parameters Signaling Unravelled In Silico|
|Numero di pagine||14|
|Stato di pubblicazione||Published - 2010|
Serie di pubblicazioni
Marretta, R. (2010). On Cancer Cell Cycle and Universal Apoptosis Parameters Signaling Unravelled In Silico. In On Cancer Cell Cycle and Universal Apoptosis Parameters Signaling Unravelled In Silico (pagg. 7-20). (TOCP Journal).