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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
20
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pubmed:dateCreated |
1999-10-21
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pubmed:abstractText |
Estrogens induce cell proliferation in target tissues by stimulating progression through the G(1) phase of the cell cycle. Induction of cyclin D1 expression is a critical feature of the mitogenic action of estrogen. We have determined a region between -96 and -29 in the cyclin D1 promoter that confers regulation by estrogens in the human mammary carcinoma cells MCF-7. This region encompasses a unique known transcription factor binding site with a sequence of a potential cAMP response element (CRE-D1). The induction is strictly hormone dependent and requires the DNA binding domain as well as both AF-1 and AF-2 domains of the estrogen receptor (ER) alpha. Destruction of the CRE-D1 motif caused complete loss of estrogen responsiveness. Both c-Jun and ATF-2 transactivated the cyclin D1 promoter in transient transfection experiments, and a clear additional increase was detected when ER was cotransfected with either c-Jun or with c-Jun and ATF-2 but not with ATF-2 alone. Furthermore, the expression of a dominant negative variant of c-Jun, TAM67, completely abolished the induction of the cyclin D1 promoter both in the absence and presence of ER. We show that ATF-2 homodimers and ATF-2/c-Jun heterodimers, but not c-Jun homodimers, were able to bind the CRE of the cyclin D1 promoter. To interpret these results, we propose a mechanism in which ATF-2/c-Jun heterodimers bind to the CRE-D1 element and mediate the activation of cyclin D1 promoter by the ER. This mechanism represents a pathway by which estrogens control the proliferation of target cells.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-10219237,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-1540336,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-1655749,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-1667464,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-1855205,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-2041787,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-2143810,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-2169352,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-2573431,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-2848037,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-3135940,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-3690665,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-6871841,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-6996577,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-7659088,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-7664341,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-8078914,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-8134134,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-8202514,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-8270002,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-8336939,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-8382609,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-8384217,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-8521509,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-8649771,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-8660284,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-8853897,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-9039267,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-9099745,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-9235905,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-9242925,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10500157-9841876
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/ATF2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Activating Transcription Factor 2,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP Response...,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin D1,
http://linkedlifedata.com/resource/pubmed/chemical/Estrogens,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-jun,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Estrogen,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
28
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pubmed:volume |
96
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
11217-22
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:10500157-Activating Transcription Factor 2,
pubmed-meshheading:10500157-Cyclic AMP,
pubmed-meshheading:10500157-Cyclic AMP Response Element-Binding Protein,
pubmed-meshheading:10500157-Cyclin D1,
pubmed-meshheading:10500157-Estrogens,
pubmed-meshheading:10500157-HeLa Cells,
pubmed-meshheading:10500157-Humans,
pubmed-meshheading:10500157-Promoter Regions, Genetic,
pubmed-meshheading:10500157-Proto-Oncogene Proteins c-jun,
pubmed-meshheading:10500157-Receptors, Estrogen,
pubmed-meshheading:10500157-Response Elements,
pubmed-meshheading:10500157-Transcription Factors
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pubmed:year |
1999
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pubmed:articleTitle |
Estrogen induction of the cyclin D1 promoter: involvement of a cAMP response-like element.
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pubmed:affiliation |
Institut National de la Santé et de la Recherche Médicale U482, Hôpital Saint-Antoine, 184 Rue du Faubourg Saint-Antoine, 75571 Paris Cedex 12, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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