American Institute of Mathematical Sciences

Advanced
2004, 1(2): 325-338. doi: 10.3934/mbe.2004.1.325

A Mathematical Model of Receptor-Mediated Apoptosis: Dying to Know Why FasL is a Trimer

Ronald Lai 1, and  Trachette L. Jackson 1,

1. 

Department of Mathematics, University of Michigan, 525 E. University, Ann Arbor, Mi 48109-1109, United States, United States

Received  April 2004 Revised  May 2004 Published  July 2004

The scientific importance of understanding programmed cell death is undeniable; however, the complexity of death signal propagation and the formerly incomplete knowledge of apoptotic pathways has left this topic virtually untouched by mathematical modeling. In this paper, we use a mechanistic approach to frame the current understanding of receptor-mediated apoptosis with an immediate goal of isolating the role receptor trimerization plays in this process. Analysis and simulation suggest that if the death signal is to be successful at low-receptor, high-ligand concentration, Fas trimerization is unlikely to be the driving force in the signal propagation. However at high-receptor and low-ligand concentrations, the mathematical model illustrates how the ability of FasL to cluster three Fas receptors can be crucially important for downstream events that propagate the apoptotic signal.
Keywords: caspase activation., Fas/FasL, apoptosis.
Mathematics Subject Classification: 92C3.
Citation: Ronald Lai, Trachette L. Jackson. A Mathematical Model of Receptor-Mediated Apoptosis: Dying to Know Why FasL is a Trimer. Mathematical Biosciences & Engineering, 2004, 1 (2) : 325-338. doi: 10.3934/mbe.2004.1.325
[1]

Georgy Th. Guria, Miguel A. Herrero, Ksenia E. Zlobina. A mathematical model of blood coagulation induced by activation sources. Discrete & Continuous Dynamical Systems - A, 2009, 25 (1) : 175-194. doi: 10.3934/dcds.2009.25.175
[2]

Gheorghe Craciun, Baltazar Aguda, Avner Friedman. Mathematical Analysis Of A Modular Network Coordinating The Cell Cycle And Apoptosis. Mathematical Biosciences & Engineering, 2005, 2 (3) : 473-485. doi: 10.3934/mbe.2005.2.473
[3]

Songbai Guo, Wanbiao Ma. Global behavior of delay differential equations model of HIV infection with apoptosis. Discrete & Continuous Dynamical Systems - B, 2016, 21 (1) : 103-119. doi: 10.3934/dcdsb.2016.21.103
[4]

D. Criaco, M. Dolfin, L. Restuccia. Approximate smooth solutions of a mathematical model for the activation and clonal expansion of T cells. Mathematical Biosciences & Engineering, 2013, 10 (1) : 59-73. doi: 10.3934/mbe.2013.10.59
[5]

Angela Gallegos, Ami Radunskaya. Do longer delays matter? The effect of prolonging delay in CTL activation. Conference Publications, 2011, 2011 (Special) : 467-474. doi: 10.3934/proc.2011.2011.467
[6]

Toyohiko Aiki, Martijn Anthonissen, Adrian Muntean. On a one-dimensional shape-memory alloy model in its fast-temperature-activation limit. Discrete & Continuous Dynamical Systems - S, 2012, 5 (1) : 15-28. doi: 10.3934/dcdss.2012.5.15
[7]

Yu-Hong Dai, Zhouhong Wang, Fengmin Xu. A Primal-dual algorithm for unfolding neutron energy spectrum from multiple activation foils. Journal of Industrial & Management Optimization, 2020  doi: 10.3934/jimo.2020073

2018 Impact Factor: 1.313

Tools

Metrics

  • PDF downloads (15)
  • HTML views (0)
  • Cited by (0)

Other articles
by authors

[Back to Top]

Copyright © 2020 American Institute of Mathematical Sciences