Regulation of nicotinic receptor expression by the ubiquitin–proteasome system
AUTOR(ES)
Christianson, John C
FONTE
Nature Publishing Group
RESUMO
Control of ligand-gated ion channel (LGIC) expression is essential for the formation, maintenance and plasticity of synapses. Treatment of mouse myotubes with proteasome inhibitors increased the number of surface nicotinic acetylcholine receptors (AChRs), indicating LGIC expression is regulated by the ubiquitin–proteasome system (UPS). Elevated surface expression resulted from increased AChR delivery to the plasma membrane and not from decreased turnover from the surface. The rise in AChR trafficking was the direct result of increased assembly of subunits in the endoplasmic reticulum (ER). Because proteasome inhibitors also blocked ER-associated degradation (ERAD) of unassembled AChR subunits, the data indicate that the additional AChRs were assembled from subunits normally targeted for ERAD. Our data show that AChR surface expression is regulated by the UPS through ERAD, whose activity determines oligomeric receptor assembly efficiency.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=524400Documentos Relacionados
- Inhibition of the ubiquitin-proteasome system in Alzheimer's disease
- Degradation of the Met tyrosine kinase receptor by the ubiquitin-proteasome pathway.
- Equine Infectious Anemia Virus and the Ubiquitin-Proteasome System
- Regulation of Bovine Papillomavirus Replicative Helicase E1 by the Ubiquitin-Proteasome Pathway
- Rhabdoviruses and the Cellular Ubiquitin-Proteasome System: a Budding Interaction