Absence of ataxin-3 leads to enhanced stress response in C. elegans.

Abstract excerpt

Ataxin-3, the protein involved in Machado-Joseph disease, is able to bind ubiquitylated substrates and act as a deubiquitylating enzyme in vitro, and it has been involved in the modulation of protein degradation by the ubiquitin-proteasome pathway. C. elegans and mouse ataxin-3 knockout models are viable and without any obvious phenotype in a basal condition however their phenotype in stress situations has never...

Topics

Share this publication in a Topic to start or enrich a Post.

• Share to Ataxin-3
• Share to Cold Temperature
• Share to Forkhead Transcription Factors