Showing papers by "Shouqing Luo published in 2009"
TL;DR: Autophagy refers to a set of non-specific bulk degradation processes in which cells deliver cytoplasmic substrates for lysosomal degradation.
Abstract: Autophagy refers to a set of non-specific bulk degradation processes in which cells deliver cytoplasmic substrates for lysosomal degradation. Types of autophagy include macroautophagy, chaperone-mediated autophagy and microautophagy. Chaperone-mediated autophagy is selective for specific cytosolic
181 citations
TL;DR: Huntington's disease is caused by a polyglutamine expansion in the huntingtin protein, and huntingtin exerts anti-apoptotic effects by binding to Pak2, which reduces the abilities of caspase-3 and caspases to cleave Pak2 and convert it into a mediator of cell death.
Abstract: Huntington9s disease is caused by a polyglutamine expansion in the huntingtin protein. Wild-type huntingtin, by contrast, appears to protect cells from pro-apoptotic insults. Here we describe a novel anti-apoptotic function for huntingtin. When cells are exposed to Fas-related signals, the ubiquitously expressed p21-activated kinase 2 (Pak2) can be activated via cleavage by caspases to release a constitutively active C-terminal fragment, which mediates cell death. Our data show that huntingtin interacts with Pak2. Overexpression of huntingtin significantly inhibits caspase-3-mediated and caspase-8-mediated cleavage of Pak2 in cells. Moreover, huntingtin prevents Pak2 cleavage by caspase-3 and caspase-8 in vitro. Although huntingtin is cytoprotective in wild-type cells that are exposed to TNFα, it has no significant benefit in TNFα-treated cells with Pak2 knockdown. Thus, huntingtin exerts anti-apoptotic effects by binding to Pak2, which reduces the abilities of caspase-3 and caspase-8 to cleave Pak2 and convert it into a mediator of cell death.
43 citations