| pubmed-article:15809749 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15809749 | lifeskim:mentions | umls-concept:C2239176 | lld:lifeskim |
| pubmed-article:15809749 | lifeskim:mentions | umls-concept:C0078058 | lld:lifeskim |
| pubmed-article:15809749 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:15809749 | lifeskim:mentions | umls-concept:C1171892 | lld:lifeskim |
| pubmed-article:15809749 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:15809749 | lifeskim:mentions | umls-concept:C0086982 | lld:lifeskim |
| pubmed-article:15809749 | lifeskim:mentions | umls-concept:C1707310 | lld:lifeskim |
| pubmed-article:15809749 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
| pubmed-article:15809749 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:15809749 | pubmed:dateCreated | 2005-4-5 | lld:pubmed |
| pubmed-article:15809749 | pubmed:abstractText | It has been shown that the interaction between the potent angiogenic factor; the vascular endothelial growth factor (VEGF) and its receptors (VEGFR-1 and VEGFR-2), plays a pivotal role in tumor development, including hepatocellular carcinoma (HCC). However, the properties of the respective VEGF receptor in the signaling transduction pathway of VEGF-mediated effects in HCC have not been elucidated yet. The aim of this study was to examine the respective signaling pathway of two VEGFRs in the VEGF-mediated murine HCC development and angiogenesis. We examined the signaling cascades of VEGFR-1 and VEGFR-2 in the VEGF-mediated HCC development in combination with a retroviral tetracycline (tet)-regulated (Retro-Tet) gene expression system, which can manipulate the gene expression in vivo by providing tet in the drinking water, as well as VEGFR-1 and VEGFR-2 specific neutralizing monoclonal antibodies (R-1mAb and R-2mAb, respectively). Both R-1mAb and R-2mAb significantly suppressed the VEGF-mediated tumor growth associated with reduction of the tumoral neovascularization, and the combination treatment with both mAbs almost completely attenuated the tumor development and angiogenesis. The protein kinase-C (PKC) and MEK1/2 activities in the tumor were markedly attenuated by treatment with R-2mAb, whereas R-1mAb did not alter these activities. These results suggested that both VEGFR-1 and VEGFR-2 play important roles, and lie in the different signaling cascades by which VEGF augments HCC development and angiogenesis. | lld:pubmed |
| pubmed-article:15809749 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15809749 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15809749 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15809749 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15809749 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15809749 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15809749 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15809749 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15809749 | pubmed:month | May | lld:pubmed |
| pubmed-article:15809749 | pubmed:issn | 1021-335X | lld:pubmed |
| pubmed-article:15809749 | pubmed:author | pubmed-author:KuriyamaShige... | lld:pubmed |
| pubmed-article:15809749 | pubmed:author | pubmed-author:IkenakaYasuhi... | lld:pubmed |
| pubmed-article:15809749 | pubmed:author | pubmed-author:FukuiHiroshiH | lld:pubmed |
| pubmed-article:15809749 | pubmed:author | pubmed-author:YoshijiHitosh... | lld:pubmed |
| pubmed-article:15809749 | pubmed:author | pubmed-author:YoshiiJunichi... | lld:pubmed |
| pubmed-article:15809749 | pubmed:author | pubmed-author:NoguchiRyuich... | lld:pubmed |
| pubmed-article:15809749 | pubmed:author | pubmed-author:YanaseKojiK | lld:pubmed |
| pubmed-article:15809749 | pubmed:author | pubmed-author:YamazakiMasah... | lld:pubmed |
| pubmed-article:15809749 | pubmed:author | pubmed-author:UemuraMasahit... | lld:pubmed |
| pubmed-article:15809749 | pubmed:author | pubmed-author:NamisakiTadas... | lld:pubmed |
| pubmed-article:15809749 | pubmed:author | pubmed-author:KitadeMitsute... | lld:pubmed |
| pubmed-article:15809749 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15809749 | pubmed:volume | 13 | lld:pubmed |
| pubmed-article:15809749 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15809749 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15809749 | pubmed:pagination | 853-7 | lld:pubmed |
| pubmed-article:15809749 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:15809749 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15809749 | pubmed:articleTitle | Different cascades in the signaling pathway of two vascular endothelial growth factor (VEGF) receptors for the VEGF-mediated murine hepatocellular carcinoma development. | lld:pubmed |
| pubmed-article:15809749 | pubmed:affiliation | The Third Department of Internal Medicine, Nara Medical University, Shijo-cho 840, Kashihara, Nara 634-8522, Japan. yoshijih@naramed-u.ac.jp | lld:pubmed |
| pubmed-article:15809749 | pubmed:publicationType | Journal Article | lld:pubmed |
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