| pubmed-article:10775525 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10775525 | lifeskim:mentions | umls-concept:C1708726 | lld:lifeskim |
| pubmed-article:10775525 | lifeskim:mentions | umls-concept:C0032897 | lld:lifeskim |
| pubmed-article:10775525 | lifeskim:mentions | umls-concept:C1156200 | lld:lifeskim |
| pubmed-article:10775525 | lifeskim:mentions | umls-concept:C0205369 | lld:lifeskim |
| pubmed-article:10775525 | lifeskim:mentions | umls-concept:C1554080 | lld:lifeskim |
| pubmed-article:10775525 | lifeskim:mentions | umls-concept:C1706198 | lld:lifeskim |
| pubmed-article:10775525 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:10775525 | pubmed:dateCreated | 2001-1-26 | lld:pubmed |
| pubmed-article:10775525 | pubmed:abstractText | To examine the chromatin basis of imprinting in chromosome 15q11-q13, we have investigated the status of histone acetylation of the SNURF-SNRPN locus, which is a key imprinted gene locus in Prader-Willi syndrome (PWS). Chromatin immunoprecipitation (ChIP) studies revealed that the unmethylated CpG island of the active, paternally derived allele of SNURF-SNRPN was associated with acetylated histones, whereas the methylated maternally derived, inactive allele was specifically hypoacetylated. The body of the SNURF-SNRPN gene was associated with acetylated histones on both alleles. Furthermore, treatment of PWS cells with the DNA methyltransferase inhibitor 5-azadeoxycytidine (5-aza-dC) induced demethylation of the SNURF-SNRPN CpG island and restoration of gene expression on the maternal allele. The reactivation was associated with increased H4 acetylation but not with H3 acetylation at the SNURF-SNRPN CpG island. These findings indicate that (1) a significant role for histone deacetylation in gene silencing is associated with imprinting in 15q11-q13 and (2) silenced genes in PWS can be reactivated by drug treatment. | lld:pubmed |
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| pubmed-article:10775525 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10775525 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10775525 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10775525 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10775525 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:10775525 | pubmed:issn | 0002-9297 | lld:pubmed |
| pubmed-article:10775525 | pubmed:author | pubmed-author:WadaTT | lld:pubmed |
| pubmed-article:10775525 | pubmed:author | pubmed-author:SaitohSS | lld:pubmed |
| pubmed-article:10775525 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10775525 | pubmed:volume | 66 | lld:pubmed |
| pubmed-article:10775525 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10775525 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10775525 | pubmed:pagination | 1958-62 | lld:pubmed |
| pubmed-article:10775525 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:10775525 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10775525 | pubmed:articleTitle | Parent-of-origin specific histone acetylation and reactivation of a key imprinted gene locus in Prader-Willi syndrome. | lld:pubmed |
| pubmed-article:10775525 | pubmed:affiliation | Department of Pediatrics, Hokkaido University School of Medicine, Sapporo 060-8638, Japan. ss11@med.hokudai.ac.jp | lld:pubmed |
| pubmed-article:10775525 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10775525 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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