title: Insulin htts on autophagy.
abstract: Macroautophagy has been shown to participate in the degradation and clearance of polyglutamine (polyQ) tract-containing proteins generated by trinucleotide repeat expansion mutations. Large expansions are the genetic cause of diseases such as Huntington's Disease that lead to neuronal dysfunction due to polyQ protein aggregates. Recently, a functional screen performed by Yamamoto et al to investigate proteins that regulate such autophagic processes revealed a novel role for insulin signaling in the promotion of autophagy of mutant protein aggregates. This suggests that insulin/insulin-like growth factor signaling pathways not only prevent the induction of autophagy, but paradoxically may promote autophagy of deleterious proteins in certain circumstances.
authors.affiliation: Life Sciences Institute, Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, Michigan 48109, USA. dumeng@umich.edu
authors.forename: Carey N
authors.initials: CN
authors.lastname: Lumeng
authors.forename: Alan R
authors.initials: AR
authors.lastname: Saltiel
mesh_terms: D000818:Animals; D001343:Autophagy / Q000502:physiology*; D006801:Humans; D006816:Huntington Disease / Q000378:metabolism; D007328:Insulin / Q000502:physiology*; D008954:Models, Biological; D015398:Signal Transduction
chemical_list: D007328:Insulin