DNA methylation, nuclear structure, gene expression and cancer
Identifieur interne : 000B16 ( Main/Exploration ); précédent : 000B15; suivant : 000B17DNA methylation, nuclear structure, gene expression and cancer
Auteurs : Heinrich Leonhardt [Allemagne] ; M. Cristina Cardoso [Allemagne]Source :
- Journal of Cellular Biochemistry [ 0730-2312 ] ; 2000.
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Abstract
DNA methylation, chromatin structure, transcription, and cancer have traditionally been studied as separate phenomena. Recent data provide now direct physical and functional links between these processes revealing a complex network of interactions and mutual dependences. Methylated DNA is bound by methyl‐CpG binding protein (MeCP) complexes that include histone deacetylases (HDACs). This recruitment of HDACs is suggested to promote local chromatin condensation and thereby repress gene expression. Most recently, also complexes of DNA methyltransferase (Dnmt1) with transcriptional repressors, DMAP1 and pRB, have been described providing a direct link to transcriptional regulation and tumor suppression. Inactivation of the DNA methyltransferase genes (Dnmt1, 3a, and 3b) was found to be lethal in mice and several human diseases (ICF and Rett syndrome) turned out to be linked to DNA methylation. In particular, global hypomethylation has been found in tumor samples together with cancer‐type‐specific, local hypermethylation. Taken together, these lines of evidence clearly underscore the central role of DNA methylation in the regulation of gene expression and chromatin structure during normal development and diseases like cancer. J. Cell. Biochem. Suppl. 35:78–83, 2000. © 2001 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/1097-4644(2000)79:35+<78::AID-JCB1129>3.0.CO;2-J
Affiliations:
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Cristina" last="Cardoso">M. Cristina Cardoso</name><affiliation wicri:level="3"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Max Delbrück Center for Molecular Medicine, 13125 Berlin</wicri:regionArea><placeName><region type="land" nuts="3">Berlin</region><settlement type="city">Berlin</settlement></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Cellular Biochemistry</title><title level="j" type="abbrev">J. Cell. Biochem.</title><idno type="ISSN">0730-2312</idno><idno type="eISSN">1097-4644</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2000">2000</date><biblScope unit="volume">79</biblScope><biblScope unit="issue">S35</biblScope><biblScope unit="page" from="78">78</biblScope><biblScope unit="page" to="83">83</biblScope></imprint><idno type="ISSN">0730-2312</idno></series><idno type="istex">18E347FAD4D5F20640062161EFADC71604D9126C</idno><idno type="DOI">10.1002/1097-4644(2000)79:35+<78::AID-JCB1129>3.0.CO;2-J</idno><idno type="ArticleID">JCB1129</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0730-2312</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>CpG island</term><term>DNA methyltransferase (Dnmt)</term><term>DNA replication</term><term>MeCP2</term><term>Transcription</term><term>chromatin structure</term><term>histone deacetylase (HDAC)</term><term>histone deacetylation</term><term>proliferating cell nuclear antigen (PCNA)</term><term>transcriptional silencing</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">DNA methylation, chromatin structure, transcription, and cancer have traditionally been studied as separate phenomena. Recent data provide now direct physical and functional links between these processes revealing a complex network of interactions and mutual dependences. Methylated DNA is bound by methyl‐CpG binding protein (MeCP) complexes that include histone deacetylases (HDACs). This recruitment of HDACs is suggested to promote local chromatin condensation and thereby repress gene expression. Most recently, also complexes of DNA methyltransferase (Dnmt1) with transcriptional repressors, DMAP1 and pRB, have been described providing a direct link to transcriptional regulation and tumor suppression. Inactivation of the DNA methyltransferase genes (Dnmt1, 3a, and 3b) was found to be lethal in mice and several human diseases (ICF and Rett syndrome) turned out to be linked to DNA methylation. In particular, global hypomethylation has been found in tumor samples together with cancer‐type‐specific, local hypermethylation. Taken together, these lines of evidence clearly underscore the central role of DNA methylation in the regulation of gene expression and chromatin structure during normal development and diseases like cancer. J. Cell. Biochem. Suppl. 35:78–83, 2000. © 2001 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country><region><li>Berlin</li></region><settlement><li>Berlin</li></settlement></list><tree><country name="Allemagne"><region name="Berlin"><name sortKey="Leonhardt, Heinrich" sort="Leonhardt, Heinrich" uniqKey="Leonhardt H" first="Heinrich" last="Leonhardt">Heinrich Leonhardt</name></region><name sortKey="Cardoso, M Cristina" sort="Cardoso, M Cristina" uniqKey="Cardoso M" first="M. Cristina" last="Cardoso">M. Cristina Cardoso</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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