Abstract：
:Telomerase activity, not detectable in somatic cells but frequently activated during carcinogenesis, confers immortality to tumors. Mechanisms governing expression of the catalytic subunit hTERT, the limiting factor for telomerase activity, still remain unclear. We previously proposed a model in which the binding of the transcription factor CTCF to the two first exons of hTERT results in transcriptional inhibition in normal cells. This inhibition is abrogated, however, by methylation of CTCF binding sites in 85% of tumors. Here, we showed that hTERT was unmethylated in testicular and ovarian tumors and in derivative cell lines. We demonstrated that CTCF and its paralogue, BORIS/CTCFL, were both present in the nucleus of the same cancer cells and bound to the first exon of hTERT in vivo. Moreover, exogenous BORIS expression in normal BORIS-negative cells was sufficient to activate hTERT transcription with an increasing number of cell passages. Thus, expression of BORIS was sufficient to allow hTERT transcription in normal cells and to counteract the inhibitory effect of CTCF in testicular and ovarian tumor cells. These results define an important contribution of BORIS to immortalization during tumorigenesis.
journal_name
Nucleic Acids Resjournal_title
Nucleic acids researchauthors
Renaud S,Loukinov D,Alberti L,Vostrov A,Kwon YW,Bosman FT,Lobanenkov V,Benhattar Jdoi
10.1093/nar/gkq827subject
Has Abstractpub_date
2011-02-01 00:00:00pages
862-73issue
3eissn
0305-1048issn
1362-4962pii
gkq827journal_volume
39pub_type
杂志文章abstract：:We have used in vitro transcription in isolated pea nuclei to determine whether the expression of genes for the seed storage proteins legumin and vicilin is regulated transcriptionally or post-transcriptionally in response to changing sulfur status in the developing seed. During the first 48 h of recovery from S defic...
journal_title：Nucleic acids research
pub_type： 杂志文章
doi：10.1093/nar/13.3.999
更新日期：1985-02-11 00:00:00
abstract：:The (cytosine-5) DNA methyltransferase M.HhaI causes its target cytosine base to be flipped completely out of the DNA helix upon binding. We have investigated the effects of replacing the target cytosine by other, mismatched bases, including adenine, guanine, thymine and uracil. We find that M.HhaI binds more tightly ...
journal_title：Nucleic acids research
pub_type： 杂志文章
doi：10.1093/nar/23.8.1388
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journal_title：Nucleic acids research
pub_type： 杂志文章
doi：10.1093/nar/gkr325
更新日期：2011-09-01 00:00:00
abstract：:Cryptic splice sites are used only when use of a natural splice site is disrupted by mutation. To determine the features that distinguish authentic from cryptic 5' splice sites (5'ss), we systematically analyzed a set of 76 cryptic 5'ss derived from 46 human genes. These cryptic 5'ss have a similar frequency distribut...
journal_title：Nucleic acids research
pub_type： 杂志文章
doi：10.1093/nar/gkg830
更新日期：2003-11-01 00:00:00
abstract：:We have studied the regulation of DNA ligase I gene expression in UV-C irradiated human primary fibroblasts. An increase of approximately 6-fold both in DNA ligase I messenger and activity levels was observed 24 h after UV treatment, when nucleotide excision repair (NER) is no longer operating. DNA ligase I induction ...
journal_title：Nucleic acids research
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journal_title：Nucleic acids research
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journal_title：Nucleic acids research
pub_type： 杂志文章
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journal_title：Nucleic acids research
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journal_title：Nucleic acids research
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journal_title：Nucleic acids research
pub_type： 杂志文章
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journal_title：Nucleic acids research
pub_type： 杂志文章
doi：10.1093/nar/gkq1070
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journal_title：Nucleic acids research
pub_type： 杂志文章
doi：10.1093/nar/gku242
更新日期：2014-06-01 00:00:00
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journal_title：Nucleic acids research
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journal_title：Nucleic acids research
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journal_title：Nucleic acids research
pub_type： 杂志文章
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journal_title：Nucleic acids research
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journal_title：Nucleic acids research
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journal_title：Nucleic acids research
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journal_title：Nucleic acids research
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journal_title：Nucleic acids research
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journal_title：Nucleic acids research
pub_type： 杂志文章
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journal_title：Nucleic acids research
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更新日期：2019-01-08 00:00:00
