The failure to undergo apoptosis in response to genotoxic stress contributes to both tumor development and response to chemotherapy. Because apoptosis provoked by a large class of genotoxic factors is ultimately dependent on DNA damage, we aim to understand how the extent and type of DNA damage regulate programmed cell death.

The c-Jun N-terminal kinase (JNK) and p38 MAP kinase pathways are important, insufficiently understood networks involved in preapoptotic signaling. Sustained JNK activation causes cell death through c-Jun and ATF-2 activation, FAS ligand (FasL) upregulation, and caspase-8 activation. We aim to identify the pathways involved in JNK and p38 activation following DNA damage as well as the molecular interactions that determine the onset and duration of this activation.

Our approach consists of integrating mathematical/computational modeling with experimentation to generate and test new hypotheses. This is based on the interaction between laboratory members with different scientific backgrounds with the aim of creating a truly interdisciplinary environment.

Selected Publications:
Blake WJ, Balázsi G, Kohanski MA, Isaacs FJ, Murphy KF, Kuang Y, Cantor CR, Walt DR, Collins JJ. Phenotypic consequences of promoter-mediated transcriptional noise. Mol Cell, in press

Balázsi G, Oltvai ZN. Sensing your surroundings: How transcription-regulatory networks of the cell discern environmental signals. Sci STKE 282:pe20, 2005

Balázsi G, Barabási AL, Oltvai ZN. Topological units of environmental signal processing in the transcriptional regulatory network of Escherichia coli. Proc Natl Acad Sci U S A 102:7841-7846, 2005

Balázsi G, Kay KA, Barabási AL, Oltvai ZN. Spurious spatial periodicity of co-expression in microarray data due to printing design. Nucleic Acids Res 31:4425-4433, 2003


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