Document Detail


Uncovering the role of Snapin in regulating autophagy-lysosomal function.
MedLine Citation:
PMID:  21233602     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The autophagy-lysosomal system is the major degradation pathway essential for the maintenance and survival of neurons. This process requires efficient late endocytic transport from distal processes to the soma, in which lysosomes are predominantly localized. However, it is not clear how late endocytic transport has an impact upon neuronal autophagy-lysosomal function. We recently revealed that Snapin acts as a dynein motor adaptor and coordinates retrograde transport and late endosomal-lysosomal trafficking, thus maintaining efficient autophagy-lysosomal function in neurons. Snapin(-/-) neurons display impaired retrograde transport and clustering of late endosomes along neuronal processes, aberrant accumulation of immature lysosomes, and impaired clearance of autolysosomes. Snapin deficiency leads to reduced neuron viability, neurodegeneration, and developmental defects in the central nervous system. Reintroducing the snapin transgene rescues these phenotypes by enhancing the delivery of endosomal cargos to lysosomes and by facilitating autophagy-lysosomal function. Our study suggests that Snapin is a candidate molecular target for autophagy-lysosomal regulation.
Authors:
Qian Cai; Zu-Hang Sheng
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural     Date:  2011-04-01
Journal Detail:
Title:  Autophagy     Volume:  7     ISSN:  1554-8635     ISO Abbreviation:  Autophagy     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-06-30     Completed Date:  2011-09-19     Revised Date:  2013-07-02    
Medline Journal Info:
Nlm Unique ID:  101265188     Medline TA:  Autophagy     Country:  United States    
Other Details:
Languages:  eng     Pagination:  445-7     Citation Subset:  IM    
Affiliation:
Synaptic Function Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Autophagy*
Endocytosis
Endosomes / metabolism
Gene Expression Regulation
Lysosomes / metabolism,  physiology*
Mice
Mice, Transgenic
Models, Biological
Neurodegenerative Diseases / metabolism
Neurons / metabolism
Vesicular Transport Proteins / metabolism*
Chemical
Reg. No./Substance:
0/SNAPIN protein, human; 0/Vesicular Transport Proteins
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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