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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
10
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pubmed:dateCreated |
2008-10-14
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pubmed:abstractText |
The genetic risk factors predisposing individuals to the development of inflammatory bowel disease are beginning to be deciphered by genome-wide association studies. Surprisingly, these new data point towards a critical role of autophagy in the pathogenesis of Crohn's disease. A single common coding variant in the autophagy protein ATG16L1 predisposes individuals to the development of Crohn's disease: while ATG16L1 encoding threonine at amino acid position 300 (ATG16L1*300T) confers protection, ATG16L1 encoding for alanine instead of threonine (ATG16L1*300A, also known as T300A) mediates risk towards the development of Crohn's disease. Here we report that, in human epithelial cells, the Crohn's disease-associated ATG16L1 coding variant shows impairment in the capture of internalized Salmonella within autophagosomes. Thus, we propose that the association of ATG16L1*300A with increased risk of Crohn's disease is due to impaired bacterial handling and lowered rates of bacterial capture by autophagy.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-10406794,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-11060023,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-11897782,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-12665549,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-15620219,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-15680321,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-16495224,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-16888103,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-17085449,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-17182262,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-17200669,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-17350577,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-17435756,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-17486044,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-17653185,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-18006683,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-18242222,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-18305538,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-18321988,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18852889-18587394
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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:issn |
1932-6203
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
3
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
e3391
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pubmed:dateRevised |
2011-10-31
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pubmed:meshHeading |
pubmed-meshheading:18852889-Autophagy,
pubmed-meshheading:18852889-Carrier Proteins,
pubmed-meshheading:18852889-Cells, Cultured,
pubmed-meshheading:18852889-Crohn Disease,
pubmed-meshheading:18852889-Epithelial Cells,
pubmed-meshheading:18852889-Genetic Predisposition to Disease,
pubmed-meshheading:18852889-Genome-Wide Association Study,
pubmed-meshheading:18852889-Humans,
pubmed-meshheading:18852889-Mutation, Missense,
pubmed-meshheading:18852889-Salmonella
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pubmed:year |
2008
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pubmed:articleTitle |
Impaired autophagy of an intracellular pathogen induced by a Crohn's disease associated ATG16L1 variant.
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pubmed:affiliation |
Gastrointestinal Unit and Center for Computational and Integrative Biology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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