rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5771
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pubmed:dateCreated |
2006-4-14
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pubmed:abstractText |
Liver mass depends on one or more unidentified humoral signals that drive regeneration when liver functional capacity is diminished. Bile acids are important liver products, and their levels are tightly regulated. Here, we identify a role for nuclear receptor-dependent bile acid signaling in normal liver regeneration. Elevated bile acid levels accelerate regeneration, and decreased levels inhibit liver regrowth, as does the absence of the primary nuclear bile acid receptor FXR. We propose that FXR activation by increased bile acid flux is a signal of decreased functional capacity of the liver. FXR, and possibly other nuclear receptors, may promote homeostasis not only by regulating expression of appropriate metabolic target genes but also by driving homeotrophic liver growth.
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Bile Acids and Salts,
http://linkedlifedata.com/resource/pubmed/chemical/Cholesterol 7-alpha-Hydroxylase,
http://linkedlifedata.com/resource/pubmed/chemical/Cholestyramine Resin,
http://linkedlifedata.com/resource/pubmed/chemical/Cholic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Forkhead Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Foxm1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Substances,
http://linkedlifedata.com/resource/pubmed/chemical/Myc protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-myc,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytoplasmic and Nuclear,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/cytochrome P450 7A1, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/farnesoid X-activated receptor,
http://linkedlifedata.com/resource/pubmed/chemical/nuclear receptor subfamily 0...
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1095-9203
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
14
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pubmed:volume |
312
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
233-6
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:16614213-Animals,
pubmed-meshheading:16614213-Bile Acids and Salts,
pubmed-meshheading:16614213-Cell Count,
pubmed-meshheading:16614213-Cholesterol 7-alpha-Hydroxylase,
pubmed-meshheading:16614213-Cholestyramine Resin,
pubmed-meshheading:16614213-Cholic Acid,
pubmed-meshheading:16614213-Cytokines,
pubmed-meshheading:16614213-DNA Replication,
pubmed-meshheading:16614213-DNA-Binding Proteins,
pubmed-meshheading:16614213-Diet,
pubmed-meshheading:16614213-Forkhead Transcription Factors,
pubmed-meshheading:16614213-Gene Expression Regulation,
pubmed-meshheading:16614213-Genes, myc,
pubmed-meshheading:16614213-Growth Substances,
pubmed-meshheading:16614213-Hepatectomy,
pubmed-meshheading:16614213-Hepatocytes,
pubmed-meshheading:16614213-Homeostasis,
pubmed-meshheading:16614213-Liver,
pubmed-meshheading:16614213-Liver Regeneration,
pubmed-meshheading:16614213-Mice,
pubmed-meshheading:16614213-Mice, Knockout,
pubmed-meshheading:16614213-Proto-Oncogene Proteins c-myc,
pubmed-meshheading:16614213-RNA, Messenger,
pubmed-meshheading:16614213-Receptors, Cytoplasmic and Nuclear,
pubmed-meshheading:16614213-Signal Transduction,
pubmed-meshheading:16614213-Transcription Factors
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pubmed:year |
2006
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pubmed:articleTitle |
Nuclear receptor-dependent bile acid signaling is required for normal liver regeneration.
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pubmed:affiliation |
Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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