The Experts below are selected from a list of 56838 Experts worldwide ranked by ideXlab platform
Irmgard Merfort - One of the best experts on this subject based on the ideXlab platform.
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on off and beyond a boolean model of apoptosis
PLOS Computational Biology, 2009Co-Authors: Rebekka Schlatter, Kathrin Schmich, Ima Avalos Vizcarra, Peter Scheurich, Thomas Sauter, Christoph Borner, Michael Ederer, Irmgard MerfortAbstract:Apoptosis is regulated by several signaling pathways which are extensively linked by crosstalks. Boolean or logical modeling has become a promising approach to capture the qualitative behavior of such complex networks. Here we built a largescale literature-based Boolean model of the central intrinsic and extrinsic apoptosis pathways as well as pathways connected with them. The model responds to several external stimuli such as Fas ligand, TNF-a, UV-B irradiation, interleukin1b and insulin. Timescales and multi-Value Node logic were used and turned out to be indispensable to reproduce the behavior of the apoptotic network. The coherence of the model was experimentally validated. Thereby an UV-B dose-effect is shown for the first time in mouse hepatocytes. Analysis of the model revealed a tight regulation emerging from high connectivity and spanning crosstalks and a particular importance of feedback loops. An unexpected feedback from Smac release to RIP could further increase complex II formation. The introduced Boolean model provides a comprehensive and coherent description of the apoptosis network behavior. It gives new insights into the complex interplay of pro- and antiapoptotic factors and can be easily expanded to other signaling pathways.
Ima Avalos Vizcarra - One of the best experts on this subject based on the ideXlab platform.
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on off and beyond a boolean model of apoptosis
PLOS Computational Biology, 2009Co-Authors: Rebekka Schlatter, Kathrin Schmich, Ima Avalos Vizcarra, Peter Scheurich, Thomas Sauter, Christoph Borner, Michael Ederer, Irmgard MerfortAbstract:Apoptosis is regulated by several signaling pathways which are extensively linked by crosstalks. Boolean or logical modeling has become a promising approach to capture the qualitative behavior of such complex networks. Here we built a largescale literature-based Boolean model of the central intrinsic and extrinsic apoptosis pathways as well as pathways connected with them. The model responds to several external stimuli such as Fas ligand, TNF-a, UV-B irradiation, interleukin1b and insulin. Timescales and multi-Value Node logic were used and turned out to be indispensable to reproduce the behavior of the apoptotic network. The coherence of the model was experimentally validated. Thereby an UV-B dose-effect is shown for the first time in mouse hepatocytes. Analysis of the model revealed a tight regulation emerging from high connectivity and spanning crosstalks and a particular importance of feedback loops. An unexpected feedback from Smac release to RIP could further increase complex II formation. The introduced Boolean model provides a comprehensive and coherent description of the apoptosis network behavior. It gives new insights into the complex interplay of pro- and antiapoptotic factors and can be easily expanded to other signaling pathways.
Michael Ederer - One of the best experts on this subject based on the ideXlab platform.
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on off and beyond a boolean model of apoptosis
PLOS Computational Biology, 2009Co-Authors: Rebekka Schlatter, Kathrin Schmich, Ima Avalos Vizcarra, Peter Scheurich, Thomas Sauter, Christoph Borner, Michael Ederer, Irmgard MerfortAbstract:Apoptosis is regulated by several signaling pathways which are extensively linked by crosstalks. Boolean or logical modeling has become a promising approach to capture the qualitative behavior of such complex networks. Here we built a largescale literature-based Boolean model of the central intrinsic and extrinsic apoptosis pathways as well as pathways connected with them. The model responds to several external stimuli such as Fas ligand, TNF-a, UV-B irradiation, interleukin1b and insulin. Timescales and multi-Value Node logic were used and turned out to be indispensable to reproduce the behavior of the apoptotic network. The coherence of the model was experimentally validated. Thereby an UV-B dose-effect is shown for the first time in mouse hepatocytes. Analysis of the model revealed a tight regulation emerging from high connectivity and spanning crosstalks and a particular importance of feedback loops. An unexpected feedback from Smac release to RIP could further increase complex II formation. The introduced Boolean model provides a comprehensive and coherent description of the apoptosis network behavior. It gives new insights into the complex interplay of pro- and antiapoptotic factors and can be easily expanded to other signaling pathways.
Rebekka Schlatter - One of the best experts on this subject based on the ideXlab platform.
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on off and beyond a boolean model of apoptosis
PLOS Computational Biology, 2009Co-Authors: Rebekka Schlatter, Kathrin Schmich, Ima Avalos Vizcarra, Peter Scheurich, Thomas Sauter, Christoph Borner, Michael Ederer, Irmgard MerfortAbstract:Apoptosis is regulated by several signaling pathways which are extensively linked by crosstalks. Boolean or logical modeling has become a promising approach to capture the qualitative behavior of such complex networks. Here we built a largescale literature-based Boolean model of the central intrinsic and extrinsic apoptosis pathways as well as pathways connected with them. The model responds to several external stimuli such as Fas ligand, TNF-a, UV-B irradiation, interleukin1b and insulin. Timescales and multi-Value Node logic were used and turned out to be indispensable to reproduce the behavior of the apoptotic network. The coherence of the model was experimentally validated. Thereby an UV-B dose-effect is shown for the first time in mouse hepatocytes. Analysis of the model revealed a tight regulation emerging from high connectivity and spanning crosstalks and a particular importance of feedback loops. An unexpected feedback from Smac release to RIP could further increase complex II formation. The introduced Boolean model provides a comprehensive and coherent description of the apoptosis network behavior. It gives new insights into the complex interplay of pro- and antiapoptotic factors and can be easily expanded to other signaling pathways.
Kathrin Schmich - One of the best experts on this subject based on the ideXlab platform.
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on off and beyond a boolean model of apoptosis
PLOS Computational Biology, 2009Co-Authors: Rebekka Schlatter, Kathrin Schmich, Ima Avalos Vizcarra, Peter Scheurich, Thomas Sauter, Christoph Borner, Michael Ederer, Irmgard MerfortAbstract:Apoptosis is regulated by several signaling pathways which are extensively linked by crosstalks. Boolean or logical modeling has become a promising approach to capture the qualitative behavior of such complex networks. Here we built a largescale literature-based Boolean model of the central intrinsic and extrinsic apoptosis pathways as well as pathways connected with them. The model responds to several external stimuli such as Fas ligand, TNF-a, UV-B irradiation, interleukin1b and insulin. Timescales and multi-Value Node logic were used and turned out to be indispensable to reproduce the behavior of the apoptotic network. The coherence of the model was experimentally validated. Thereby an UV-B dose-effect is shown for the first time in mouse hepatocytes. Analysis of the model revealed a tight regulation emerging from high connectivity and spanning crosstalks and a particular importance of feedback loops. An unexpected feedback from Smac release to RIP could further increase complex II formation. The introduced Boolean model provides a comprehensive and coherent description of the apoptosis network behavior. It gives new insights into the complex interplay of pro- and antiapoptotic factors and can be easily expanded to other signaling pathways.
