Source:http://linkedlifedata.com/resource/pubmed/id/11564732
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
49
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pubmed:dateCreated |
2001-12-3
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pubmed:abstractText |
Mouse As4.1 cells, obtained after transgene-targeted oncogenesis to induce neoplasia in renal renin expressing cells, express high levels of renin mRNA from their endogenous Ren-1(c) gene. We have previously identified a 242-base pair enhancer (coordinates -2866 to -2625 relative to the CAP site) upstream of the mouse Ren-1(c) gene. This enhancer, in combination with the proximal promoter (-117 to +6), activates transcription nearly 2 orders of magnitude in an orientation independent fashion. To further delimit sequences necessary for transcriptional activation, renin promoter-luciferase reporter gene constructs containing selected regions of the Ren-1(c) enhancer were analyzed after transfection into As4.1 cells. These results demonstrate that several regions are required for full enhancer activity. Sequences from -2699 to -2672, which are critical for the enhancer activity, contain a cyclic AMP responsive element (CRE) and an E-box. Electrophoretic mobility shift assays demonstrated that transcription factors CREB/CREM and USF1/USF2 in As4.1 cell nuclear extracts bind to oligonucleotides containing the Ren-1(c) CRE and E-box, respectively. These two elements are capable of synergistically activating transcription from the Ren-1(c) promoter. Moreover, mutation of either the CRE or E-box results in almost complete loss of enhancer activity, suggesting the critical roles these two elements play in regulating mouse Ren-1(c) gene expression. Although the Ren-1(c) gene contains a CRE, its expression is not induced by cAMP in As4.1 cells. This appears to reflect constitutive activation of protein kinase A in As4.1 cells since treatment with the protein kinase A inhibitor, H-89, caused a significant reduction in Ren-1(c) gene expression and this reduction is mediated through the CRE at -2699 to -2688.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP-Dependent Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Renin,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Upstream Stimulatory Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Usf1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Usf2 protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0021-9258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
7
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pubmed:volume |
276
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
45530-8
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:11564732-Animals,
pubmed-meshheading:11564732-Base Sequence,
pubmed-meshheading:11564732-Cell Line,
pubmed-meshheading:11564732-Cyclic AMP,
pubmed-meshheading:11564732-Cyclic AMP-Dependent Protein Kinases,
pubmed-meshheading:11564732-DNA,
pubmed-meshheading:11564732-DNA-Binding Proteins,
pubmed-meshheading:11564732-Enhancer Elements, Genetic,
pubmed-meshheading:11564732-Gene Expression Regulation,
pubmed-meshheading:11564732-Mice,
pubmed-meshheading:11564732-Molecular Sequence Data,
pubmed-meshheading:11564732-Renin,
pubmed-meshheading:11564732-Sequence Homology, Nucleic Acid,
pubmed-meshheading:11564732-Transcription, Genetic,
pubmed-meshheading:11564732-Transcription Factors,
pubmed-meshheading:11564732-Upstream Stimulatory Factors
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pubmed:year |
2001
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pubmed:articleTitle |
Critical roles of a cyclic AMP responsive element and an E-box in regulation of mouse renin gene expression.
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pubmed:affiliation |
Department of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, New York 14263, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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