| pubmed-article:12650607 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12650607 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
| pubmed-article:12650607 | lifeskim:mentions | umls-concept:C0040682 | lld:lifeskim |
| pubmed-article:12650607 | lifeskim:mentions | umls-concept:C1514559 | lld:lifeskim |
| pubmed-article:12650607 | lifeskim:mentions | umls-concept:C1332083 | lld:lifeskim |
| pubmed-article:12650607 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:12650607 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:12650607 | pubmed:dateCreated | 2003-3-24 | lld:pubmed |
| pubmed-article:12650607 | pubmed:abstractText | Autocrine motility factor receptor (AMFR) is a cell surface glycoprotein of 78000 molecular weight (gp78), regulating cell motility signaling in vitro and metastasis in vivo. To test whether AMFR could be a common mediator of transformation and oncogenic itself, we transfected NIH3T3 fibroblast cells with expression vectors carrying the full-length cDNA for mouse AMFR and evaluated the effects of increased AMFR on transforming potential. The cells stably expressing high levels of AMFR as a result of transfection displayed a complete morphological change and acquired the ability to grow even in low serum. Furthermore, they were anchorage-independent for growth in soft agar and more motile in phagokinetic track assay. Interestingly, the enhanced expression of AMFR produced tumors in nude mice. Our findings provide a direct evidence that overexpression of the AMFR is associated with the acquisition of a transformation phenotype. | lld:pubmed |
| pubmed-article:12650607 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12650607 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12650607 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12650607 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12650607 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12650607 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12650607 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12650607 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12650607 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12650607 | pubmed:issn | 0262-0898 | lld:pubmed |
| pubmed-article:12650607 | pubmed:author | pubmed-author:RazAvrahamA | lld:pubmed |
| pubmed-article:12650607 | pubmed:author | pubmed-author:TsukadaKazuhi... | lld:pubmed |
| pubmed-article:12650607 | pubmed:author | pubmed-author:YokotaJunJ | lld:pubmed |
| pubmed-article:12650607 | pubmed:author | pubmed-author:OnishiYasuhar... | lld:pubmed |
| pubmed-article:12650607 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12650607 | pubmed:volume | 20 | lld:pubmed |
| pubmed-article:12650607 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12650607 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12650607 | pubmed:pagination | 51-8 | lld:pubmed |
| pubmed-article:12650607 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
| pubmed-article:12650607 | pubmed:meshHeading | pubmed-meshheading:12650607... | lld:pubmed |
| pubmed-article:12650607 | pubmed:meshHeading | pubmed-meshheading:12650607... | lld:pubmed |
| pubmed-article:12650607 | pubmed:meshHeading | pubmed-meshheading:12650607... | lld:pubmed |
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| pubmed-article:12650607 | pubmed:meshHeading | pubmed-meshheading:12650607... | lld:pubmed |
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| pubmed-article:12650607 | pubmed:meshHeading | pubmed-meshheading:12650607... | lld:pubmed |
| pubmed-article:12650607 | pubmed:meshHeading | pubmed-meshheading:12650607... | lld:pubmed |
| pubmed-article:12650607 | pubmed:meshHeading | pubmed-meshheading:12650607... | lld:pubmed |
| pubmed-article:12650607 | pubmed:meshHeading | pubmed-meshheading:12650607... | lld:pubmed |
| pubmed-article:12650607 | pubmed:meshHeading | pubmed-meshheading:12650607... | lld:pubmed |
| pubmed-article:12650607 | pubmed:meshHeading | pubmed-meshheading:12650607... | lld:pubmed |
| pubmed-article:12650607 | pubmed:meshHeading | pubmed-meshheading:12650607... | lld:pubmed |
| pubmed-article:12650607 | pubmed:meshHeading | pubmed-meshheading:12650607... | lld:pubmed |
| pubmed-article:12650607 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12650607 | pubmed:articleTitle | Overexpression of autocrine motility factor receptor (AMFR) in NIH3T3 fibroblasts induces cell transformation. | lld:pubmed |
| pubmed-article:12650607 | pubmed:affiliation | Tumor Progression and Metastasis Program, Karmanos Cancer Institute, Detroit, Michigan 48201, USA | lld:pubmed |
| pubmed-article:12650607 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12650607 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| entrez-gene:23802 | entrezgene:pubmed | pubmed-article:12650607 | lld:entrezgene |
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