| pubmed-article:20657013 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20657013 | lifeskim:mentions | umls-concept:C0597032 | lld:lifeskim |
| pubmed-article:20657013 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:20657013 | lifeskim:mentions | umls-concept:C0117719 | lld:lifeskim |
| pubmed-article:20657013 | lifeskim:mentions | umls-concept:C0431085 | lld:lifeskim |
| pubmed-article:20657013 | lifeskim:mentions | umls-concept:C0596290 | lld:lifeskim |
| pubmed-article:20657013 | lifeskim:mentions | umls-concept:C0311400 | lld:lifeskim |
| pubmed-article:20657013 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:20657013 | lifeskim:mentions | umls-concept:C1704735 | lld:lifeskim |
| pubmed-article:20657013 | pubmed:issue | 39 | lld:pubmed |
| pubmed-article:20657013 | pubmed:dateCreated | 2010-9-20 | lld:pubmed |
| pubmed-article:20657013 | pubmed:abstractText | In organs involved in metabolic homeostasis, transmembrane ? and ?klothos direct FGFR signaling to control of metabolic pathways. Coordinate expression of ?klotho and FGFR4 is a property of mature hepatocytes. Genetic deletion of FGFR4 or ?klotho in mice disrupts hepatic cholesterol/bile acid and lipid metabolism. The deletion of FGFR4 has no effect on the proliferative response of hepatocytes after liver injury. However, its absence results in accelerated progression of dimethynitrosamine-initiated hepatocellular carcinomas, indicating that FGFR4 suppresses hepatoma proliferation. The mechanism underlying the FGFR4-mediated hepatoma suppression has not been addressed. Here we show that ?klotho expression is more consistently down-regulated in human and mouse hepatomas than FGFR4. Co-expression and activation by either endocrine FGF19 or cellular FGF1 of the FGFR4 kinase in a complex with ?klotho restricts cell population growth through induction of apoptotic cell death in both hepatic and nonhepatic cells. The ?klotho-FGFR4 partnership caused a depression of activated AKT and mammalian target of rapamycin while activating ERK1/2 that may underlie the pro-apoptotic effect. Our results show that ?klotho not only interacts with heparan sulfate-FGFR4 to form a complex with high affinity for endocrine FGF19 but also impacts the quality of downstream signaling and biological end points activated by either FGF19 or canonical FGF1. Thus the same ?klotho-heparan sulfate-FGFR4 partnership that mediates endocrine control of hepatic metabolism plays a role in cellular homeostasis and hepatoma suppression through negative control of cell population growth mediated by pro-apoptotic signaling. | lld:pubmed |
| pubmed-article:20657013 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20657013 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20657013 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20657013 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20657013 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20657013 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20657013 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20657013 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20657013 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20657013 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20657013 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20657013 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:20657013 | pubmed:issn | 1083-351X | lld:pubmed |
| pubmed-article:20657013 | pubmed:author | pubmed-author:HuangPengP | lld:pubmed |
| pubmed-article:20657013 | pubmed:author | pubmed-author:McKeehanWalla... | lld:pubmed |
| pubmed-article:20657013 | pubmed:author | pubmed-author:WangFenF | lld:pubmed |
| pubmed-article:20657013 | pubmed:author | pubmed-author:QinKunK | lld:pubmed |
| pubmed-article:20657013 | pubmed:author | pubmed-author:JinChengliuC | lld:pubmed |
| pubmed-article:20657013 | pubmed:author | pubmed-author:LuoYongdeY | lld:pubmed |
| pubmed-article:20657013 | pubmed:author | pubmed-author:LuWeiqinW | lld:pubmed |
| pubmed-article:20657013 | pubmed:author | pubmed-author:YangChaofengC | lld:pubmed |
| pubmed-article:20657013 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20657013 | pubmed:day | 24 | lld:pubmed |
| pubmed-article:20657013 | pubmed:volume | 285 | lld:pubmed |
| pubmed-article:20657013 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20657013 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20657013 | pubmed:pagination | 30069-78 | lld:pubmed |
| pubmed-article:20657013 | pubmed:dateRevised | 2011-9-30 | lld:pubmed |
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| pubmed-article:20657013 | pubmed:meshHeading | pubmed-meshheading:20657013... | lld:pubmed |
| pubmed-article:20657013 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20657013 | pubmed:articleTitle | Metabolic regulator betaKlotho interacts with fibroblast growth factor receptor 4 (FGFR4) to induce apoptosis and inhibit tumor cell proliferation. | lld:pubmed |
| pubmed-article:20657013 | pubmed:affiliation | IBT Proteomics and Nanotechnology Laboratory, Institute of Biosciences and Technology, Texas A & MHealth Science Center, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA. | lld:pubmed |
| pubmed-article:20657013 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20657013 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:20657013 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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