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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
Pt 2
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pubmed:dateCreated |
2005-11-18
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pubmed:abstractText |
TfR1 (transferrin receptor 1) mediates the uptake of transferrin-bound iron and thereby plays a critical role in cellular iron metabolism. Its expression is coupled to cell proliferation/differentiation and controlled in response to iron levels and other signals by transcriptional and post-transcriptional mechanisms. It is well established that TfR1 levels decline when cultured cells reach a high density and in the present study we have investigated the underlying mechanisms. Consistent with previous findings, we demonstrate that TfR1 expression is attenuated in a cell-density-dependent manner in human lung cancer H1299 cells and in murine B6 fibroblasts as the result of a marked decrease in mRNA content. This response is not associated with alterations in the RNA-binding activity of iron regulatory proteins that are indicative of a transcriptional mechanism. Reporter assays reveal that the human TfR1 promoters contains sequences mediating cell-density-dependent transcriptional inhibition. Mapping of the human and mouse TfR1 promoters identified a conserved hexa-nucleotide 5'-GAGGGC-3' motif with notable sequence similarity to a previously described element within the IGF-2 (insulin-like growth factor-2) promoter. We show that this motif is necessary for the formation of specific complexes with nuclear extracts and for cell-density-dependent regulation in reporter gene assays. Thus the TfR1 promoter contains a functional 'cell density response element' (CDRE).
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-10192390,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-10446187,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-10446188,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-10518614,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-10582342,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-10777218,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-10811637,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-11112775,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-11885287,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-11986201,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-12052872,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-12057761,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-12439744,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-12957296,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-15105251,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-15109490,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-15313461,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-15629195,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-2041787,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-3162307,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-3389645,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-3476165,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-3491079,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-3608980,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-6313760,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-8382776,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-8514748,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-8612513,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-8637898,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16092918-9892202
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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/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/CD71 antigen,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/Iron-Regulatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Transferrin,
http://linkedlifedata.com/resource/pubmed/chemical/Tfrc protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1470-8728
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
392
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
383-8
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:16092918-Animals,
pubmed-meshheading:16092918-Antigens, CD,
pubmed-meshheading:16092918-Base Sequence,
pubmed-meshheading:16092918-Cell Count,
pubmed-meshheading:16092918-Cell Line,
pubmed-meshheading:16092918-DNA,
pubmed-meshheading:16092918-Fibroblasts,
pubmed-meshheading:16092918-Gene Expression Regulation,
pubmed-meshheading:16092918-Humans,
pubmed-meshheading:16092918-Iron-Regulatory Proteins,
pubmed-meshheading:16092918-Lung Neoplasms,
pubmed-meshheading:16092918-Promoter Regions, Genetic,
pubmed-meshheading:16092918-RNA, Messenger,
pubmed-meshheading:16092918-Receptors, Transferrin,
pubmed-meshheading:16092918-Response Elements,
pubmed-meshheading:16092918-Transcription, Genetic
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pubmed:year |
2005
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pubmed:articleTitle |
Inhibition of transferrin receptor 1 transcription by a cell density response element.
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pubmed:affiliation |
Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital, 3755 Cote-Ste-Catherine Road, Montreal, Quebec, Canada H3T 1E2.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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