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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2001-2-2
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pubmed:abstractText |
Transforming growth factor (TGF)-beta1 plays an important role during hematopoiesis. Previously, we had shown that the growth of a v-Src-transformed myeloid cell line was markedly more inhibited by TGF-beta treatment when compared with the wild-type myeloid cell line. To investigate the increased growth sensitivity of the v-Src-transformed myeloid cell line, 32D-src, to TGF-beta, we examined expression of the TGF-beta type II receptor (TGF-beta RII) gene in myeloid cell lines. Northem blot analysis showed that expression of approximately 8- and 6-kb species of TGF-beta RII transcripts was markedly increased in the 32D-src cell line. The expression of the TGF-beta RII promoter linked to a reporter gene was increased 23-fold by v-Src. DNA transfection and electrophoretic mobility shift assay revealed that v-Src induces TGF-beta RII promoter activity through an AP1/ATF2-like sequence (-219 to -172), ETS binding sites (+1 to +36), and the inverted CCAAT box (-81 to -77). Novel DNA-protein complexes with ETS binding sites are significantly increased in v-src-transformed cell lines compared with the control cell line. These results suggest that v-Src induces activity of the TGF-beta RII promoter through multiple elements by inducing expression of nuclear proteins interacting with these elements.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1044-9523
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
9-18
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11205746-Animals,
pubmed-meshheading:11205746-Base Sequence,
pubmed-meshheading:11205746-Binding, Competitive,
pubmed-meshheading:11205746-Binding Sites,
pubmed-meshheading:11205746-Blotting, Northern,
pubmed-meshheading:11205746-Blotting, Western,
pubmed-meshheading:11205746-Cell Line,
pubmed-meshheading:11205746-Cell Nucleus,
pubmed-meshheading:11205746-Cross-Linking Reagents,
pubmed-meshheading:11205746-Electrophoresis, Polyacrylamide Gel,
pubmed-meshheading:11205746-Gene Expression Regulation,
pubmed-meshheading:11205746-Genes, Reporter,
pubmed-meshheading:11205746-Luciferases,
pubmed-meshheading:11205746-Mice,
pubmed-meshheading:11205746-Models, Genetic,
pubmed-meshheading:11205746-Molecular Sequence Data,
pubmed-meshheading:11205746-Mutagenesis, Site-Directed,
pubmed-meshheading:11205746-Myeloid Cells,
pubmed-meshheading:11205746-Oncogene Protein pp60(v-src),
pubmed-meshheading:11205746-Plasmids,
pubmed-meshheading:11205746-Promoter Regions, Genetic,
pubmed-meshheading:11205746-Protein Binding,
pubmed-meshheading:11205746-Protein-Serine-Threonine Kinases,
pubmed-meshheading:11205746-RNA, Messenger,
pubmed-meshheading:11205746-Receptors, Transforming Growth Factor beta,
pubmed-meshheading:11205746-Response Elements,
pubmed-meshheading:11205746-Transcriptional Activation,
pubmed-meshheading:11205746-Transfection
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pubmed:year |
2001
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pubmed:articleTitle |
Mechanism of induction of transforming growth factor-beta type II receptor gene expression by v-Src in murine myeloid cells.
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pubmed:affiliation |
Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892-5055, USA.
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pubmed:publicationType |
Journal Article
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