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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2008-12-26
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pubmed:abstractText |
Autophagy is a catabolic process involved in cell death and in cell protective mechanism. Autophagic cell death is differentiated from apoptosis by the presence of double or multiple-membrane enclosed vesicles, and the ATG proteins are essential for the formation of these autophagic vesicles. Here, we show that ATG6/Beclin-1 is a novel caspase substrate. ATG6 is directly cleaved by caspases in a process inhibited by the pan caspase inhibitor, zVAD. Ectopic expression of ATG6 suppresses cell death while reduction of ATG6 levels by siRNA sensitizes cells to TRAIL-induced cell death. Also, the inhibition of caspases leads to an increase in autophagy. These results suggest that caspase-mediated cleavage of ATG6 links the apoptotic and autophagic signaling pathways.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1872-7980
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
8
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pubmed:volume |
274
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
95-100
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pubmed:meshHeading |
pubmed-meshheading:18842334-Apoptosis,
pubmed-meshheading:18842334-Apoptosis Regulatory Proteins,
pubmed-meshheading:18842334-Autophagy,
pubmed-meshheading:18842334-Blotting, Western,
pubmed-meshheading:18842334-Caspase 3,
pubmed-meshheading:18842334-Enzyme Inhibitors,
pubmed-meshheading:18842334-HeLa Cells,
pubmed-meshheading:18842334-Humans,
pubmed-meshheading:18842334-Membrane Proteins,
pubmed-meshheading:18842334-RNA, Small Interfering,
pubmed-meshheading:18842334-TNF-Related Apoptosis-Inducing Ligand,
pubmed-meshheading:18842334-Transfection
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pubmed:year |
2009
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pubmed:articleTitle |
Caspase-mediated cleavage of ATG6/Beclin-1 links apoptosis to autophagy in HeLa cells.
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pubmed:affiliation |
Institute for Innovative Cancer Research, University of Ulsan College of Medicine and Asan Medical Center, Seoul 138-736, Republic of Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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