Source:http://linkedlifedata.com/resource/pubmed/id/12296377
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3-4
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pubmed:dateCreated |
2002-9-25
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pubmed:abstractText |
The human RNA methyltransferase like 1 gene (RNMTL1) is one of thirteen newly discovered genes within a 116 Kb segment of the chromosome 17p13.3 that suffers from a high frequent loss of heterozygosity in human hepatocellular carcinoma in China[1-5]. To understand the molecular mechanisms underlying transcription control of the RNMTL1 gene in human cancers, we decline using of the conventional approach where the cis-elements bound by the known transcription factors are primary targets, and carried out the systematic analyses to dissect the promoter structure and identify/characterize the key cis-elements that are responsible for its strong expression in cell. The molecular approaches applied included 1, the primer extension for mapping of the transcription starts; 2, the transient transfection/reporter assays on a large number of deletion and site-specific mutants of the promoter segment for defining the minimal promoter and the crucial elements within; and 3, the electrophoresis mobility shift assay with specific antibodies for reconfirming the nature of the transcription factors and their cognate cis-elements. We have shown that the interaction of an ATF/CREB element (-38 to -31) and its cognate transcription factors play a predominant role in the promoter activity of the RNMTL1 gene. The secondary DNA structures of the ATF/CREB element play a more vital role in the protein-DNA interaction. Finally, we reported a novel mechanism underlying the YY1 mediated transcription repression, namely, the ATF/CREB dependent transcription-repression by YY1 is executed in absence of its own sequence-specific binding.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Activating Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Blood Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP Response...,
http://linkedlifedata.com/resource/pubmed/chemical/Methyltransferases,
http://linkedlifedata.com/resource/pubmed/chemical/RNA,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins,
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 |
1001-0602
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pubmed:author | |
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 |
177-97
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pubmed:dateRevised |
2010-2-4
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pubmed:meshHeading |
pubmed-meshheading:12296377-Activating Transcription Factors,
pubmed-meshheading:12296377-Base Sequence,
pubmed-meshheading:12296377-Binding Sites,
pubmed-meshheading:12296377-Blood Proteins,
pubmed-meshheading:12296377-Cell Line,
pubmed-meshheading:12296377-Chromosomes, Human, Pair 17,
pubmed-meshheading:12296377-Cyclic AMP Response Element-Binding Protein,
pubmed-meshheading:12296377-Gene Deletion,
pubmed-meshheading:12296377-Gene Expression,
pubmed-meshheading:12296377-Genes, Reporter,
pubmed-meshheading:12296377-Humans,
pubmed-meshheading:12296377-Methyltransferases,
pubmed-meshheading:12296377-Models, Genetic,
pubmed-meshheading:12296377-Mutagenesis, Site-Directed,
pubmed-meshheading:12296377-Promoter Regions, Genetic,
pubmed-meshheading:12296377-RNA,
pubmed-meshheading:12296377-Recombinant Proteins,
pubmed-meshheading:12296377-Repressor Proteins,
pubmed-meshheading:12296377-Transcription, Genetic,
pubmed-meshheading:12296377-Transcription Factors,
pubmed-meshheading:12296377-Tumor Cells, Cultured
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pubmed:year |
2002
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pubmed:articleTitle |
The ATF/CREB site is the key element for transcription of the human RNA methyltransferase like 1(RNMTL1) gene, a newly discovered 17p13.3 gene.
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pubmed:affiliation |
The State-key Laboratory for Oncogenes and Related Genes, Shanghai Cancer Institute, Xie-tu China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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