Membrane systems with peripheral proteins are essentially standard membrane systems with the possibility of having multisets of objects (proteins) embedded in the membranes and with the presence of rules that control the transport and the change of configurations of these proteins. The model intends to abstract the activities of the receptors embedded in the cellular membranes. In this paper we use an extension of this paradigm to model and simulate some of the mechanisms underlying cell cycle and breast tumor growth. In particular we have defined a membrane system that abstracts the G2/M cell cycle phase transition and extends the corresponding Reactome model. The model has been then simulated by using the software Cyto-Sim and we have monitored the interplay between activators and inhibitors of the cell cycle. This is the preliminary version of a paper that was published in Electronic Notes in Theoretical Computer Science 227(4) January 2009, pages 127-141. The original publication is available at http://dx.doi.org/10.1016/j.entcs.2008.12.108
Cell Cycle and Tumor Growth in Membrane Systems with Peripheral Proteins / Mazza, Tommaso; Cavaliere, Matteo. - ELETTRONICO. - (2008), pp. 1-7.
Cell Cycle and Tumor Growth in Membrane Systems with Peripheral Proteins
Mazza, Tommaso;
2008-01-01
Abstract
Membrane systems with peripheral proteins are essentially standard membrane systems with the possibility of having multisets of objects (proteins) embedded in the membranes and with the presence of rules that control the transport and the change of configurations of these proteins. The model intends to abstract the activities of the receptors embedded in the cellular membranes. In this paper we use an extension of this paradigm to model and simulate some of the mechanisms underlying cell cycle and breast tumor growth. In particular we have defined a membrane system that abstracts the G2/M cell cycle phase transition and extends the corresponding Reactome model. The model has been then simulated by using the software Cyto-Sim and we have monitored the interplay between activators and inhibitors of the cell cycle. This is the preliminary version of a paper that was published in Electronic Notes in Theoretical Computer Science 227(4) January 2009, pages 127-141. The original publication is available at http://dx.doi.org/10.1016/j.entcs.2008.12.108File | Dimensione | Formato | |
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