| pubmed-article:3027579 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3027579 | lifeskim:mentions | umls-concept:C0035647 | lld:lifeskim |
| pubmed-article:3027579 | lifeskim:mentions | umls-concept:C0080092 | lld:lifeskim |
| pubmed-article:3027579 | lifeskim:mentions | umls-concept:C1510411 | lld:lifeskim |
| pubmed-article:3027579 | lifeskim:mentions | umls-concept:C0079053 | lld:lifeskim |
| pubmed-article:3027579 | pubmed:issue | 6104 | lld:pubmed |
| pubmed-article:3027579 | pubmed:dateCreated | 1987-3-24 | lld:pubmed |
| pubmed-article:3027579 | pubmed:abstractText | The c-fms proto-oncogene encodes a transmembrane glycoprotein that is probably identical to the receptor for the macrophage colony stimulating factor, CSF-1. Forty C-terminal amino acids of the normal receptor are replaced by 11 unrelated residues in the feline v-fms oncogene product, deleting a C-terminal tyrosine residue (Tyr969) whose phosphorylation might negatively regulate the receptor kinase activity. We show that the human c-fms gene stimulates growth of mouse NIH 3T3 cells in agar in response to human recombinant CSF-1, indicating that receptor transduction is sufficient to induce a CSF-1 responsive phenotype. Although cells transfected with c-fms genes containing either Tyr969 or Phe969 were not transformed, cotransfection of these genes with CSF-1 complementary DNA induced transformation, with c-fms(Phe969) showing significantly more activity than c-fms(Tyr969). In the absence of CSF-1, chimaeric v-fms/c-fms genes encoding the wild-type c-fms C terminus were poorly transforming, whereas chimaeras bearing Phe969 were as transforming as v-fms. Thus, the Phe969 mutation, although not in itself sufficient to induce transformation, activates the oncogenic potential of c-fms in association with an endogenous ligand or in conjunction with mutations elsewhere in the c-fms gene that confer ligand-independent signals for growth. | lld:pubmed |
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| pubmed-article:3027579 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:3027579 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:3027579 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3027579 | pubmed:issn | 0028-0836 | lld:pubmed |
| pubmed-article:3027579 | pubmed:author | pubmed-author:RalphPP | lld:pubmed |
| pubmed-article:3027579 | pubmed:author | pubmed-author:SherrC JCJ | lld:pubmed |
| pubmed-article:3027579 | pubmed:author | pubmed-author:RettenmierC... | lld:pubmed |
| pubmed-article:3027579 | pubmed:author | pubmed-author:UllrichAA | lld:pubmed |
| pubmed-article:3027579 | pubmed:author | pubmed-author:FitzA EAE | lld:pubmed |
| pubmed-article:3027579 | pubmed:author | pubmed-author:RousselM FMF | lld:pubmed |
| pubmed-article:3027579 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3027579 | pubmed:volume | 325 | lld:pubmed |
| pubmed-article:3027579 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3027579 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3027579 | pubmed:pagination | 549-52 | lld:pubmed |
| pubmed-article:3027579 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:3027579 | pubmed:articleTitle | Transforming potential of the c-fms proto-oncogene (CSF-1 receptor). | lld:pubmed |
| pubmed-article:3027579 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3027579 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:3027579 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:3027579 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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