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DNA Damage, Autophagy, Cell Death, and Senescence Model

Posted Fri, Mar, 08,2013

Published today in Bioinformatics and Biology Insights is a new original research article by Stephan Gebel, Rosemarie B. Lichtner, Brian Frushour, Walter K. Schlage, Vy Hoang, Marja Talikka, Arnd Hengstermann, Carole Mathis, Emilija Veljkovic, Michael Peck, Manuel C. Peitsch, Renee Deehan, Julia Hoeng and Jurjen W. Westra.  Read more about this paper below:

Title

Construction of a Computable Network Model for DNA Damage, Autophagy, Cell Death, and Senescence

Abstract

Towards the development of a systems biology-based risk assessment approach for environmental toxicants, including tobacco products in a systems toxicology setting such as the “21st Century Toxicology”, we are building a series of computable biological network models specific to non-diseased pulmonary and cardiovascular cells/tissues which capture the molecular events that can be activated following exposure to environmental toxicants. Here we extend on previous work and report on the construction and evaluation of a mechanistic network model focused on DNA damage response and the four main cellular fates induced by stress: autophagy, apoptosis, necroptosis, and senescence. In total, the network consists of 34 sub-models containing 1052 unique nodes and 1538 unique edges which are supported by 1231 PubMed-referenced literature citations. Causal node-edge relationships are described using the Biological Expression Language (BEL), which allows for the semantic representation of life science relationships in a computable format. The Network is provided in .XGMML format and can be viewed using freely available network visualization software, such as Cytoscape.

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