Sign up for Table of Contents Alerts!
Email this page
Print this page
Views and Commentaries
Insulin Signaling Gives Autophagy a Push
Carey N. Lumeng and Alan R. Saltiel
volume 2 | issue 3
July/August/September 2006Pages: 250 - 253
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.
Macroautophagocytosis 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.
Commentary to:
Autophagy-Mediated Clearance of Huntingtin Aggregates Triggered by the Insulin-Signaling Pathway
A. Yamamoto, M.L. Cremona and J.E. Rothman
J Cell Biol 2006; 172:719-31
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.