By Stefan Kallenberger, Stefan Legewie (auth.), Inna N. Lavrik (eds.)
Systems Biology of Apoptosis summarizes all present achievements during this rising box. Apoptosis is a approach universal to all multicellular organisms. Apoptosis ends up in the removing of cells through a fancy yet hugely outlined mobile programme. Defects within the law of apoptosis bring about critical illnesses similar to melanoma, autoimmunity, AIDS and neurodegeneration. lately, a considerable breakthrough in knowing the complicated apoptotic pathways has been made via employing structures biology techniques. structures biology combines rigorous mathematical modelling with experimental techniques in a closed loop cycle for advancing our wisdom approximately advanced organic techniques. during this publication, the editor describes the modern platforms biology stories dedicated to apoptotic signaling and makes a speciality of the query how platforms biology is helping to appreciate life/death judgements made within the telephone and to enhance new methods to rational therapy strategies.
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Currently represents the most comprehensive and realistic large-scale model of apoptosis. In a combined experimental and theoretical study, Rehm et al. (2006) analyzed the kinetics of temporally switch-like effector caspase activation downstream of mitochondria. In particular, they focused on the control of effector caspase activation by XIAP. Their model described apoptosis signaling following MOMP induced by the drug staurosporine. The agent tetramethylrhodamine methylester (TMRM) was used to experimentally measure changes of the mitochondria membrane potential to monitor the occurrence of MOMP.
The critical roles of c-FLIPL and c-FLIPS, which potentially act as stoichiometric inhibitors in the DISC, were investigated in a model of Bentele et al. (2004). The dependence of the ligand concentration threshold on the concentrations of both splicing variants of c-FLIP was characterized, and it was concluded that c-FLIPs establish a stoichiometric switch. A large-scale model comprising DISC assembly, caspase activation, MOMP, interference from caspase inhibitors, and degradation processes was derived.
In their study the signal response behavior is characterized by the dependency of active Bax and Bcl-2 steady state levels as dependent on the production rate of activators. In a model containing both feedback mechanisms the interval of activator production rates that lead to bistability of active Bax and Bcl-2 concentrations is significantly enlarged compared to a variant with only one feedback mechanism. Therefore, the combination of both feedback mechanisms would provide a higher robustness for the bistable behavior of Bax activation and mitochondria pore formation.