Nrf2-related oxidative stress response and impaired dopamine biosynthesis in a PC12 cell model of Huntington’s disease

ABSTRACT: Huntington’s disease (HD) is a devastating disease for which currently no therapy is available. It is a progressive autosomal dominant neurodegenerative disorder that is caused by a CAG repeat expansion in the HD gene, resulting in an expansion of polyglutamines at the N-terminal end of the encoded protein, designated huntingtin, and the accumulation of cytoplasmic and nuclear aggregates. Not only is there a loss of normal huntingtin function, upon expansion of the CAG repeat there is also a gain of toxic function of the huntingtin protein and this affects a wide range of cellular processes. To identify groups of genes that could play a role in the pathology of Huntington’s disease, we studied mRNA changes in an inducible PC12 model of Huntington’s disease before and after aggregates

ORGANISM(S): Rattus norvegicus

SUBMITTER: Peter 't Hoen 

PROVIDER: E-GEOD-10581 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress