Linked Life Data

7970719

Source:http://linkedlifedata.com/resource/pubmed/id/7970719

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1994-12-20
pubmed:databankReference
pubmed:abstractText
Fos oncoproteins transform cells by functioning as transcription factors. Over-expression of c-fos results in minimal morphological transformation while the two viral isolates, FBJ and FBR v-fos, result in full morphological transformation. Fos-transformed cells are serum dependent for proliferation but not for morphological transformation. To identify Fos target genes which might be involved in morphological transformation we screened a cDNA library constructed from RNA isolated from serum starved FBR-transformed cells with cDNA probes prepared from both FBR-transformed cells and untransformed parental fibroblasts, 208F. We identified 10 genes which are differentially expressed between FBR and 208F cells. One is a novel gene. Nine are upregulated in c-fos- and FBJ-transformed cells and also in mutant c-Ha-Ras-transformed 208Fs. All nine of the upregulated genes have been associated previously with invasion or metastasis. We demonstrate that the FBR-transformed cells are invasive in an in vitro assay and that their ability to invade is enhanced by platelet derived growth factor. We conclude that the fos oncogenes target genes involved in morphological transformation, and invasion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:geneSymbol
c-fos, v-fos
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3591-600
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Fos-transformation activates genes associated with invasion.
pubmed:affiliation
Department of Microbiology, University of Texas Southwestern Medical Center, Dallas 75235.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't