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Stochastic Simulation-based Prediction of the Behavior of the p16-mediated Signaling Pathway

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Języki publikacji
EN
Abstrakty
EN
In this work we use hybrid Petri nets to create a model of the p16-mediated signaling pathway in higher eukaryotes and conduct its stochastic simulation-based validation by wet lab observations available from literature. The validation is conducted in terms of stochastic simulations with respect to the wild-type p16 protein and its mutated form. Our model catches the behavior of the major molecular regulators of the p16-mediated signaling pathway in wild-type cells as well as when DNA damage is detected or replicative senescence occurs. We observe that the stochastic model predicts some characteristics of the underlying pathway more clearly, evidently and perspicuously compared to the deterministic model, enriching the breadth and the quality of the outcome.
Wydawca
Rocznik
Strony
167--179
Opis fizyczny
Bibliogr. 35 poz., rys., tab., wykr.
Twórcy
autor
  • Department of Applied Mathematics and Computer Science, Faculty of Arts and Sciences, Eastern Mediterranean University, Famagusta, North Cyprus, Mersin-10, Turkey
autor
  • Faculty of Medicine, Eastern Mediterranean University, Famagusta, North Cyprus, Mersin-10, Turkey
Bibliografia
  • [1] Akçay Nİ, Bashirov R, Tüzmen S¸ . Validation of signalling pathways: case study of the p16-mediated pathway. J Bioinform Comput Biol. 2015; 13(2):1550007. doi:10.1142/S0219720015500079.
  • [2] Arkin A, Ross J, McAdams HH. Stochastic kinetic analysis of developmental pathway bifurcation in phage lambda-infected Escherichia coli cells. Genetics. 1998; 149:1633-1648.
  • [3] Bird RC. Role of Cyclins and Cyclin-dependent kinases in G1 phase progression. In: G1 Phase Progression, Boonstra J (ed.), Kluwer Academic, New York; 2003. p. 40-57.
  • [4] Boonstra J. Restriction points to the G1 phase to the mammalian cell cycle. In: G1 Phase Progression, Boonstra J (ed.), Kluwer Academic, New York; 2003. p. 1-7.
  • [5] Csikasz-Nagy A. Computational systems biology of the cell cycle. Brief Bioinform. 2009; 10:424-434.
  • [6] Gibson MA, Bruck J. Efficient exact stochastic simulation of chemical systems with many species and many channels. J Phys Chem A. 2000; 104:1876-1889.
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  • [9] Heiner M, Gilbert D, Donaldson R. Petri Nets for Systems and Synthetic Biology. In: 8th international conference on formal methods for computational systems biology, Conference Proceedings. LNCS 5016, Springer; 2008. p. 215-264.
  • [10] Heiner M, Herajy M, Liu F, et al. Snoopy a unifying Petri net tool. LNCS. 2012; 7347:398-407.
  • [11] Herajy M, Schwarick M, Heiner M. Hybrid Petri nets for modelling the eukaryotic cell cycle. ToPNoC VIII, LNCS. 2013; 8100:121-141.
  • [12] Liu F, Heiner M. Fuzzy stochastic Petri sets for modeling biological systems with uncertain kinetic parameters. PLoS ONE. 2016; 11(2):e0149674. doi:10.1371/journal.pone.0149674.
  • [13] Ko MS, Nakauchi H, Takahashi N. The dose dependence of glucocorticoid-inducible gene expression results from changes in the number of transcriptionally active templates. EMBO J. 1990; 9:2835-2842.
  • [14] Kurtz TG. The relationship between stochastic and deterministic models for chemical reactions. The Journal of Chemical Physics. 1971; 57:2976-2978.
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  • [16] Li S, et al. A quantitative study of the cell division cycle of Cauloubacter crescentus stalked cells. PLoS Comput Biol. 2008; 4:e64.
  • [17] Liu Y, et al. Expression of p16(INK4a) in peripheral blood T-cells is a biomarker of human aging. Aging Cell. 2009; 8:439-448.
  • [18] Lygeros J, et al. Stochastic hybrid modeling of DNA replication across a complete genome. Proc Natl Acad Sci USA. 2008; 105:12295-12300.
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  • [20] Meng TC, Somani S, Dhar P. Modeling and simulation of biological systems with stochasticity. In Silico Biol. 2004; 4:293-309.
  • [21] Moeller SJ, Shearff RJ. G1 phase: components, conundrums, context, in cell cycle regulation. Kaldis P (ed.), Springer-Verlag, Berlin, Heidelberg, 2005.
  • [22] Mura I, Csikasz-Nagy A. Stochastic Petri net extensions of a yeast cell cycle model. J Theor Biol. 2008; 254:850-860.
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  • [24] Post SM, Lee E. Detection of kinase and phosphatase activities. Methods Mol Biol. 2004; 241:285-297.
  • [25] Qu Z, Weiss JN, et al. Regulation of the mammalian cell cycle: a model of the G1-to-S transition. Am J Physiol Cell Physiol. 2013; 254:344-364.
  • [26] Rayess H, Wang MB, Srivatsan ES. Cellular senescence and tumor suppressor gene p16. Int J Cancer. 2012; 139:1715-1725.
  • [27] Reddy V, Mavrovouniotis M, Liebman M, et al. Petri net representations in metabolic pathways. In: International Conf Intell Syst Mol Biol. Conference Proceedings; Vol. 1, 1993. 96038982. p. 328-336.
  • [28] Rocco JW, Sidransky D. p16(MTS-1/CDKN2/INK4a) in cancer progression. Exp Cell Res. 2001; 264:42-55.
  • [29] Sandmann W, Maier C. On the statistical accuracy of stochastic simulation algorithms implemented in dizzy. In: 5th International Workshop Comp Syst Biol, Leipzig, Germany, 11-13 June, TICSP, 2008, Wrokshop Proceedings; 2008. p. 153-157.
  • [30] Sheldon RM. Chapman Kolmogorov Equations. In: Introduction to Probability Models (11th ed.); 2014. p. 187.
  • [31] Sriram K, et al. A minimal mathematical model combining several regulatory cycles from the budding yeast cell cycle. IETSyst Biol. 2007; 1:326-341.
  • [32] Stacey DW. Three observations that have changed our understanding of Cyclin D1 and p27 in cell cycle control. Genes and Cancer. 2010; 12:1189-1199.
  • [33] Szallasi Z, et al. System Modeling in Cellular Biology: From Concepts to Nuts and Bolts. MIT Press, Cambridge, MA, 2006.
  • [34] Yang X, Han R, Guo Y, Bradley J, Cox B, Dickinson R, et al. Modelling and performance analysis of clinical pathways using the stochastic process algebra PEPA. BMC Bioinformatics. 2011;13(1-17).
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Uwagi
Opracowanie rekordu w ramach umowy 509/P-DUN/2018 ze środków MNiSW przeznaczonych na działalność upowszechniającą naukę (2018).
Typ dokumentu
Bibliografia
Identyfikator YADDA
bwmeta1.element.baztech-5acee49f-f5fc-45b5-a128-7d5696efcbc5
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