| pubmed-article:12601366 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12601366 | lifeskim:mentions | umls-concept:C0044602 | lld:lifeskim |
| pubmed-article:12601366 | lifeskim:mentions | umls-concept:C0007590 | lld:lifeskim |
| pubmed-article:12601366 | lifeskim:mentions | umls-concept:C0062534 | lld:lifeskim |
| pubmed-article:12601366 | lifeskim:mentions | umls-concept:C0108685 | lld:lifeskim |
| pubmed-article:12601366 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:12601366 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:12601366 | lifeskim:mentions | umls-concept:C1515877 | lld:lifeskim |
| pubmed-article:12601366 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:12601366 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:12601366 | pubmed:dateCreated | 2003-2-25 | lld:pubmed |
| pubmed-article:12601366 | pubmed:abstractText | Hepatocyte growth factor (HGF), a ligand of c-Met receptor, stimulates activation of cellular kinases via phosphatidylinositol 3-kinase (PI3-kinase). CCAAT/enhancer binding protein (C/EBP) controls cell cycle progression. The present study was designed to determine whether HGF activates C/EBP in association with the S-phase entrance for cell replication and whether PI3-kinase contributes to the activation of C/EBP. Treatment of H4IIE cells, a hepatocyte-derived cell line, with HGF increased protein binding to the C/EBP binding site at an early time. Immunodepletion, subcellular fractionation, and confocal microscopic analyses showed that the HGF-induced C/EBP DNA binding activity depended on nuclear translocation of C/EBP beta. Whereas stable transfection of the p110 catalytic subunit of PI3-kinase enhanced HGF-mediated nuclear translocation of C/EBP beta and DNA binding, stable transfection of p85 subunit or chemical inhibition of PI3-kinase completely blocked C/EBP activation. HGF increased luciferase reporter activity in cells transfected with a mammalian cell expression vector containing -1.65 kilobase rGSTA2 promoter comprising C/EBP response element (pGL-1651). Whereas transfection with pCMV500, a control vector, allowed pGL-1651 to respond to HGF, expression of dominant negative mutant C/EBP completely inhibited the ability of HGF to stimulate the reporter gene expression. Flow cytometric analysis showed that HGF caused an increase in the area of S phase with a reciprocal decrease in that of G(1) phase, suggesting that HGF promoted cell cycle progression to S phase. In conclusion, HGF induces nuclear translocation of C/EBP beta via the PI3-kinase pathway and stimulates C/EBP DNA binding and gene transcription and that the PI3-kinase-mediated C/EBP activation by HGF may contribute to cell replication. | lld:pubmed |
| pubmed-article:12601366 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12601366 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12601366 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12601366 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12601366 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12601366 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12601366 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12601366 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12601366 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12601366 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:12601366 | pubmed:issn | 0270-9139 | lld:pubmed |
| pubmed-article:12601366 | pubmed:author | pubmed-author:ChoMin... | lld:pubmed |
| pubmed-article:12601366 | pubmed:author | pubmed-author:KimSang... | lld:pubmed |
| pubmed-article:12601366 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12601366 | pubmed:volume | 37 | lld:pubmed |
| pubmed-article:12601366 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12601366 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12601366 | pubmed:pagination | 686-95 | lld:pubmed |
| pubmed-article:12601366 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
| pubmed-article:12601366 | pubmed:meshHeading | pubmed-meshheading:12601366... | lld:pubmed |
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| pubmed-article:12601366 | pubmed:meshHeading | pubmed-meshheading:12601366... | lld:pubmed |
| pubmed-article:12601366 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12601366 | pubmed:articleTitle | Hepatocyte growth factor activates CCAAT enhancer binding protein and cell replication via PI3-kinase pathway. | lld:pubmed |
| pubmed-article:12601366 | pubmed:affiliation | National Research Laboratory (MDT), College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, Korea. | lld:pubmed |
| pubmed-article:12601366 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12601366 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:12601366 | lld:pubmed |
