Comparison of modules of wild type and mutant Huntingtin and TP53 protein interaction networks: implications in biological processes and functions.

ABSTRACT: Disease-causing mutations usually change the interacting partners of mutant proteins. In this article, we propose that the biological consequences of mutation are directly related to the alteration of corresponding protein protein interaction networks (PPIN). Mutation of Huntingtin (HTT) which causes Huntington's disease (HD) and mutations to TP53 which is associated with different cancers are studied as two example cases. We construct the PPIN of wild type and mutant proteins separately and identify the structural modules of each of the networks. The functional role of these modules are then assessed by Gene Ontology (GO) enrichment analysis for biological processes (BPs). We find that a large number of significantly enriched ([Formula: see text]) GO terms in mutant PPIN were absent in th

SUBMITTER: Basu M 

PROVIDER: S-EPMC3669416 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature