pubmed-article:10688652 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10688652 | lifeskim:mentions | umls-concept:C0027627 | lld:lifeskim |
pubmed-article:10688652 | lifeskim:mentions | umls-concept:C0062534 | lld:lifeskim |
pubmed-article:10688652 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:10688652 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:10688652 | lifeskim:mentions | umls-concept:C0205419 | lld:lifeskim |
pubmed-article:10688652 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
pubmed-article:10688652 | lifeskim:mentions | umls-concept:C1420563 | lld:lifeskim |
pubmed-article:10688652 | lifeskim:mentions | umls-concept:C1705924 | lld:lifeskim |
pubmed-article:10688652 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:10688652 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:10688652 | lifeskim:mentions | umls-concept:C0205296 | lld:lifeskim |
pubmed-article:10688652 | lifeskim:mentions | umls-concept:C0205460 | lld:lifeskim |
pubmed-article:10688652 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
pubmed-article:10688652 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:10688652 | pubmed:dateCreated | 2000-3-23 | lld:pubmed |
pubmed-article:10688652 | pubmed:abstractText | Hepatocyte growth factor/scatter factor (HGF/SF) stimulates numerous cellular activities capable of contributing to the metastatic phenotype, including growth, motility, invasiveness, and morphogenetic transformation. When inappropriately expressed in vivo, an HGF/SF transgene induces numerous hyperplastic and neoplastic lesions. NK1 and NK2 are natural splice variants of HGF/SF; all interact with a common receptor, Met. Although both agonistic and antagonistic properties have been ascribed to each isoform in vitro, NK1 retains the full spectrum of HGF/SF-like activities when expressed as a transgene in vivo. Here we report that transgenic mice broadly expressing NK2 exhibit none of the phenotypes characteristic of HGF/SF or NK1 transgenic mice. Instead, when coexpressed in NK2-HGF/SF bitransgenic mice, NK2 antagonizes the pathological consequences of HGF/SF and discourages the subcutaneous growth of transplanted Met-containing melanoma cells. Remarkably, the metastatic efficiency of these same melanoma cells is dramatically enhanced in NK2 transgenic host mice relative to wild-type recipients, rivaling levels achieved in HGF/SF and NK1 transgenic hosts. Considered in conjunction with reports that in vitro NK2 induces scatter, but not other activities, these data strongly suggest that cellular motility is a critical determinant of metastasis. Moreover, our results demonstrate how alternatively structured ligands can be exploited in vivo to functionally dissociate Met-mediated activities and their downstream pathways. | lld:pubmed |
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pubmed-article:10688652 | pubmed:language | eng | lld:pubmed |
pubmed-article:10688652 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10688652 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10688652 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10688652 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10688652 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10688652 | pubmed:month | Mar | lld:pubmed |
pubmed-article:10688652 | pubmed:issn | 0270-7306 | lld:pubmed |
pubmed-article:10688652 | pubmed:author | pubmed-author:OtsukaTT | lld:pubmed |
pubmed-article:10688652 | pubmed:author | pubmed-author:MerliniMM | lld:pubmed |