| pubmed-article:15867340 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15867340 | lifeskim:mentions | umls-concept:C0029016 | lld:lifeskim |
| pubmed-article:15867340 | lifeskim:mentions | umls-concept:C0079427 | lld:lifeskim |
| pubmed-article:15867340 | lifeskim:mentions | umls-concept:C0020793 | lld:lifeskim |
| pubmed-article:15867340 | lifeskim:mentions | umls-concept:C1325410 | lld:lifeskim |
| pubmed-article:15867340 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:15867340 | pubmed:dateCreated | 2005-5-3 | lld:pubmed |
| pubmed-article:15867340 | pubmed:abstractText | Fps/Fes proteins were among the first members of the protein tyrosine kinase family to be characterized as dominant-acting oncoproteins. Addition of retroviral GAG sequences or other experimentally induced mutations activated the latent transforming potential of Fps/Fes. However, activating mutations in fps/fes had not been found in human tumors until recently, when mutational analysis of a panel of colorectal cancers identified four somatic mutations in sequences encoding the Fps/Fes kinase domain. Here, we report biochemical and theoretical structural analysis demonstrating that three of these mutations result in inactivation, not activation, of Fps/Fes, whereas the fourth mutation compromised in vivo activity. These results did not concur with a classic dominant-acting oncogenic role for fps/fes involving activating somatic mutations but instead raised the possibility that inactivating fps/fes mutations might promote tumor progression in vivo. Consistent with this, we observed that tumor onset in a mouse model of breast epithelial cancer occurred earlier in mice targeted with either null or kinase-inactivating fps/fes mutations. Furthermore, a fps/fes transgene restored normal tumor onset kinetics in targeted fps/fes null mice. These data suggest a novel and unexpected tumor suppressor role for Fps/Fes in epithelial cells. | lld:pubmed |
| pubmed-article:15867340 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15867340 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15867340 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15867340 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15867340 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15867340 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15867340 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15867340 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15867340 | pubmed:month | May | lld:pubmed |
| pubmed-article:15867340 | pubmed:issn | 0008-5472 | lld:pubmed |
| pubmed-article:15867340 | pubmed:author | pubmed-author:YenI HIH | lld:pubmed |
| pubmed-article:15867340 | pubmed:author | pubmed-author:JiaZongchaoZ | lld:pubmed |
| pubmed-article:15867340 | pubmed:author | pubmed-author:MullerWilliam... | lld:pubmed |
| pubmed-article:15867340 | pubmed:author | pubmed-author:GreerPeter... | lld:pubmed |
| pubmed-article:15867340 | pubmed:author | pubmed-author:SangrarWaheed... | lld:pubmed |
| pubmed-article:15867340 | pubmed:author | pubmed-author:ZirgniblRalph... | lld:pubmed |
| pubmed-article:15867340 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15867340 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:15867340 | pubmed:volume | 65 | lld:pubmed |
| pubmed-article:15867340 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15867340 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15867340 | pubmed:pagination | 3518-22 | lld:pubmed |
| pubmed-article:15867340 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:15867340 | pubmed:meshHeading | pubmed-meshheading:15867340... | lld:pubmed |
| pubmed-article:15867340 | pubmed:meshHeading | pubmed-meshheading:15867340... | lld:pubmed |
| pubmed-article:15867340 | pubmed:meshHeading | pubmed-meshheading:15867340... | lld:pubmed |
| pubmed-article:15867340 | pubmed:meshHeading | pubmed-meshheading:15867340... | lld:pubmed |
| pubmed-article:15867340 | pubmed:meshHeading | pubmed-meshheading:15867340... | lld:pubmed |
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| pubmed-article:15867340 | pubmed:meshHeading | pubmed-meshheading:15867340... | lld:pubmed |
| pubmed-article:15867340 | pubmed:meshHeading | pubmed-meshheading:15867340... | lld:pubmed |
| pubmed-article:15867340 | pubmed:meshHeading | pubmed-meshheading:15867340... | lld:pubmed |
| pubmed-article:15867340 | pubmed:meshHeading | pubmed-meshheading:15867340... | lld:pubmed |
| pubmed-article:15867340 | pubmed:meshHeading | pubmed-meshheading:15867340... | lld:pubmed |
| pubmed-article:15867340 | pubmed:meshHeading | pubmed-meshheading:15867340... | lld:pubmed |
| pubmed-article:15867340 | pubmed:meshHeading | pubmed-meshheading:15867340... | lld:pubmed |
| pubmed-article:15867340 | pubmed:meshHeading | pubmed-meshheading:15867340... | lld:pubmed |
| pubmed-article:15867340 | pubmed:meshHeading | pubmed-meshheading:15867340... | lld:pubmed |
| pubmed-article:15867340 | pubmed:meshHeading | pubmed-meshheading:15867340... | lld:pubmed |
| pubmed-article:15867340 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15867340 | pubmed:articleTitle | An identity crisis for fps/fes: oncogene or tumor suppressor? | lld:pubmed |
| pubmed-article:15867340 | pubmed:affiliation | Division of Cancer Biology and Genetics, Queen's University Cancer Research Institute, Queen's University, Kingston, Ontario, Canada. | lld:pubmed |
| pubmed-article:15867340 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15867340 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:15867340 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:14159 | entrezgene:pubmed | pubmed-article:15867340 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:15867340 | lld:entrezgene |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:15867340 | lld:pubmed |
