Linked Life Data

12183402

Source:http://linkedlifedata.com/resource/pubmed/id/12183402

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
16
pubmed:dateCreated
2002-8-16
pubmed:abstractText
Epigenetic lesions are common in neoplasia and range from hypermethylation of subsets of CpG islands to loss of imprinting. By exploiting an episomal model system and the strong de novo methylation capacity of a human cancer cell line, we show that an H19 minigene rapidly becomes methylated and silenced, mimicking the inactivation of the maternal H19 allele in a range of cancers. Although the H19 imprinting control region (ICR) initially displayed methylation protection, it eventually succumbed to the pressure mounted by the de novo methylation machinery of the JEG-3 cells. Importantly, we were able to visualize the kinetics of the loss of the H19 ICR chromatin insulator function in association with chromatin compaction. Our results document that a strong de novo methylation machinery leads to loss of methylation privilege states of H19 ICR to functionally manifest loss of insulator function in a matter of only a few days in human cancer cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
62
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4545-8
pubmed:dateRevised
2011-10-7
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
The kinetics of deregulation of expression by de novo methylation of the h19 imprinting control region in cancer cells.
pubmed:affiliation
Department of Development and Genetics, Evolution Biology Centre, Uppsala University, S-752 36 Uppsala, Sweden. Kanduri.Chandrasekhar@ebc.uu.se
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't