Polyglutamine repeats are associated to specific sequence biases that are conserved among eukaryotes.

ABSTRACT: Nine human neurodegenerative diseases, including Huntington's disease and several spinocerebellar ataxia, are associated to the aggregation of proteins comprising an extended tract of consecutive glutamine residues (polyQs) once it exceeds a certain length threshold. This event is believed to be the consequence of the expansion of polyCAG codons during the replication process. This is in apparent contradiction with the fact that many polyQs-containing proteins remain soluble and are encoded by invariant genes in a number of eukaryotes. The latter suggests that polyQs expansion and/or aggregation might be counter-selected through a genetic and/or protein context. To identify this context, we designed a software that scrutinize entire proteomes in search for imperfect polyQs. The nature of r

SUBMITTER: Ramazzotti M 

PROVIDER: S-EPMC3270027 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature