pubmed-article:11331588 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11331588 | lifeskim:mentions | umls-concept:C1708726 | lld:lifeskim |
pubmed-article:11331588 | lifeskim:mentions | umls-concept:C1705165 | lld:lifeskim |
pubmed-article:11331588 | lifeskim:mentions | umls-concept:C1156200 | lld:lifeskim |
pubmed-article:11331588 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:11331588 | lifeskim:mentions | umls-concept:C2700061 | lld:lifeskim |
pubmed-article:11331588 | pubmed:issue | 9 | lld:pubmed |
pubmed-article:11331588 | pubmed:dateCreated | 2001-5-2 | lld:pubmed |
pubmed-article:11331588 | pubmed:abstractText | We have studied developmentally regulated patterns of histone acetylation at high resolution across approximately 54 kb of DNA containing three independently regulated but neighboring genetic loci. These include a folate receptor gene, a 16 kb condensed chromatin region, the chicken beta-globin domain and an adjacent olfactory receptor gene. Within these regions the relative levels of acetylation appear to fall into three classes. The condensed chromatin region maintains the lowest acetylation at every developmental stage. Genes that are inactive show similarly low levels, but activation results in a dramatic increase in acetylation. The highest levels of acetylation are seen at regulatory sites upstream of the genes. These patterns imply the action of more than one class of acetylation. Notably, there is a very strong constitutive focus of hyperacetylation at the 5' insulator element separating the globin locus from the folate receptor region, which suggests that this insulator element may harbor a high concentration of histone acetylases. | lld:pubmed |
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pubmed-article:11331588 | pubmed:language | eng | lld:pubmed |
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pubmed-article:11331588 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:11331588 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11331588 | pubmed:month | May | lld:pubmed |
pubmed-article:11331588 | pubmed:issn | 0261-4189 | lld:pubmed |
pubmed-article:11331588 | pubmed:author | pubmed-author:FelsenfeldGG | lld:pubmed |
pubmed-article:11331588 | pubmed:author | pubmed-author:SimpsonMM | lld:pubmed |
pubmed-article:11331588 | pubmed:author | pubmed-author:LittM DMD | lld:pubmed |
pubmed-article:11331588 | pubmed:author | pubmed-author:PrioleauM NMN | lld:pubmed |
pubmed-article:11331588 | pubmed:author | pubmed-author:Recillas-Targ... | lld:pubmed |
pubmed-article:11331588 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11331588 | pubmed:day | 1 | lld:pubmed |
pubmed-article:11331588 | pubmed:volume | 20 | lld:pubmed |
pubmed-article:11331588 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11331588 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11331588 | pubmed:pagination | 2224-35 | lld:pubmed |
pubmed-article:11331588 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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pubmed-article:11331588 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11331588 | pubmed:articleTitle | Transitions in histone acetylation reveal boundaries of three separately regulated neighboring loci. | lld:pubmed |
pubmed-article:11331588 | pubmed:affiliation | Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0540, USA . | lld:pubmed |
pubmed-article:11331588 | pubmed:publicationType | Journal Article | lld:pubmed |
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