Peer-Reviewed Publications

      Construction of a computable network model for DNA damage, autophagy, cell death, and senescence

      Gebel, S.; Lichtner, R. B.; Frushour, B. P.; Schlage, W. K.; Hoang, V.; Talikka, M.; Hengstermann, A.; Mathis, C.; Veljkovic, E.; Peck, M.; Peitsch, M. C.; Deehan, R.; Hoeng, J.; Westra, J. W.
      Published
      Mar 7, 2013
      DOI
      10.4137/bbi.s11154
      PMID
      23515068
      Link to publication
      Topic
      Summary

      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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