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PMID: 20670274 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Review

Selective autophagy regulates various cellular functions.

Genes to cells : devoted to molecular & cellular mechanisms ·Vol. 15 ·No. 9 ·2010-09-01 ·Pages 923-33

Komatsu M, Ichimura Y

Abstract

Autophagy is a self-eating system conserved among eukaryotes, in which cellular components including organelles are entrapped into a double membrane structure called the autophagosome and then degraded by lysosomal hydrolases. In addition to its role in supplying amino acids in response to nutrient starvation, autophagy is involved in quality control to maintain cell health. Thus, inactivation of autophagy causes the formation of cytoplasmic protein inclusions, which comprise misfolded proteins and the accumulation of many degenerated organelles, resulting in liver injury, diabetes, myopathy and neurodegeneration. Furthermore, although autophagy has been considered nonselective, increasing evidence points to the selectivity of autophagy in sorting vacuolar enzymes and removal of aggregate-prone proteins and unwanted organelles. Such selectivity allows diverse cellular regulation, similar to the ubiquitin proteasome pathway. In this review, we discuss the physiological roles of selective autophagy and their molecular mechanisms.

MeSH Terms
Animals Autophagy/physiology Cell Physiological Phenomena/physiology Cytoplasm/metabolism Humans Lysosomes/metabolism Microtubule-Associated Proteins/metabolism Models, Biological Phagosomes/metabolism Vacuoles/metabolism
Chemicals
MAP1LC3A protein, human Microtubule-Associated Proteins
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Komatsu Masaaki
Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Japan. [email protected]
Ichimura Yoshinobu
Article Info
Journal
Genes to cells : devoted to molecular & cellular mechanisms
Abbr.
Genes Cells
ISSN
1365-2443
Published
2010-09-01
Epub
2010-00-28
Pages
923-33
Language
English
Region
England
NLM ID
9607379
Subset
IM
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