Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5771
pubmed:dateCreated
2006-4-14
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.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
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...
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1095-9203
pubmed:author
pubmed:issnType
Electronic
pubmed:day
14
pubmed:volume
312
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
233-6
pubmed:dateRevised
2009-11-19
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
pubmed:year
2006
pubmed:articleTitle
Nuclear receptor-dependent bile acid signaling is required for normal liver regeneration.
pubmed:affiliation
Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural