pubmed-article:16611688 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16611688 | lifeskim:mentions | umls-concept:C0105770 | lld:lifeskim |
pubmed-article:16611688 | lifeskim:mentions | umls-concept:C0030274 | lld:lifeskim |
pubmed-article:16611688 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
pubmed-article:16611688 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:16611688 | pubmed:dateCreated | 2006-5-2 | lld:pubmed |
pubmed-article:16611688 | pubmed:abstractText | A recent study has shown that deletion of beta-catenin within the pancreatic epithelium results in a loss of pancreas mass. Here, we show that ectopic stabilization of beta-catenin within mouse pancreatic epithelium can have divergent effects on both organ formation and growth. Robust stabilization of beta-catenin during early organogenesis drives changes in hedgehog and Fgf10 signaling and induces a loss of Pdx1 expression in early pancreatic progenitor cells. Together, these perturbations in early pancreatic specification culminate in a severe reduction of pancreas mass and postnatal lethality. By contrast, inducing the stabilized form of beta-catenin at a later time point in pancreas development causes enhanced proliferation that results in a dramatic increase in pancreas organ size. Taken together, these data suggest a previously unappreciated temporal/spatial role for beta-catenin signaling in the regulation of pancreas organ growth. | lld:pubmed |
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pubmed-article:16611688 | pubmed:language | eng | lld:pubmed |
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pubmed-article:16611688 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:16611688 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16611688 | pubmed:month | May | lld:pubmed |
pubmed-article:16611688 | pubmed:issn | 0950-1991 | lld:pubmed |
pubmed-article:16611688 | pubmed:author | pubmed-author:TaketoMakoto... | lld:pubmed |
pubmed-article:16611688 | pubmed:author | pubmed-author:HerreraPedro... | lld:pubmed |
pubmed-article:16611688 | pubmed:author | pubmed-author:HebrokMatthia... | lld:pubmed |
pubmed-article:16611688 | pubmed:author | pubmed-author:HeiserPatrick... | lld:pubmed |
pubmed-article:16611688 | pubmed:author | pubmed-author:LauJanetJ | lld:pubmed |
pubmed-article:16611688 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16611688 | pubmed:volume | 133 | lld:pubmed |
pubmed-article:16611688 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16611688 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16611688 | pubmed:pagination | 2023-32 | lld:pubmed |
pubmed-article:16611688 | pubmed:dateRevised | 2011-6-1 | lld:pubmed |
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pubmed-article:16611688 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:16611688 | pubmed:articleTitle | Stabilization of beta-catenin impacts pancreas growth. | lld:pubmed |
pubmed-article:16611688 | pubmed:affiliation | Diabetes Center, Department of Medicine, University of California, San Francisco, CA 94143, USA. | lld:pubmed |
pubmed-article:16611688 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16611688 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:16611688 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:16611688 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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