I continued to study the impact of genetic variations on gene expression and diseases. We have made progress towards extending our recent method of eQTL analysis to epistatic interaction (manuscript in preparation). We also developed a new method that allows to idnetyfy pathways dys-regulated in diseases and genotypic variation that are putative causes of such dys-regulation. In this method we model interaction network as an electric circuit and the flow of information from genotype to gene expression as current flow. A manuscript describing preliminary results of this work has been invited for an oral presentation on the recent Conference on Research in Molecular Computational Biology (RECOMB 2010). My group also continued to work on computational methods for simulation of signal propagation in signaling network. We developed a fuzzy logic based approach and used it to study the combined Epidermal Growth Factor Receptor (EGFR), Insulin-like Growth Factor-1 Receptor (IGF-1R), and Insulin Receptor (IR) signaling network and to elucidate the crosstalk between the component pathways (7). We made the simulation software is freely available (6). Continuing our work on codon usage, we have been able to demonstrate that codon usage is optimized towards avoiding frameshifting errors in translation (1). We used the frame shifting model developed in this paper to further study the robustness to frameshifting errors(5).
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