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| pubmed-article:19956589 | lifeskim:mentions | umls-concept:C0016719 | lld:lifeskim |
| pubmed-article:19956589 | lifeskim:mentions | umls-concept:C1422163 | lld:lifeskim |
| pubmed-article:19956589 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
| pubmed-article:19956589 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:19956589 | lifeskim:mentions | umls-concept:C0669443 | lld:lifeskim |
| pubmed-article:19956589 | lifeskim:mentions | umls-concept:C1707931 | lld:lifeskim |
| pubmed-article:19956589 | lifeskim:mentions | umls-concept:C0333668 | lld:lifeskim |
| pubmed-article:19956589 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:19956589 | pubmed:dateCreated | 2009-12-3 | lld:pubmed |
| pubmed-article:19956589 | pubmed:abstractText | Over 15 inherited diseases are caused by expansion of triplet-repeats. Friedreich ataxia (FRDA) patients are homozygous for an expanded GAA triplet-repeat sequence in intron 1 of the FXN gene. The expanded GAA triplet-repeat results in deficiency of FXN gene transcription, which is reversed via administration of histone deacetylase inhibitors indicating that transcriptional silencing is at least partially due to an epigenetic abnormality. | lld:pubmed |
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| pubmed-article:19956589 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:19956589 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19956589 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19956589 | pubmed:issn | 1932-6203 | lld:pubmed |
| pubmed-article:19956589 | pubmed:author | pubmed-author:De... | lld:pubmed |
| pubmed-article:19956589 | pubmed:author | pubmed-author:BidichandaniS... | lld:pubmed |
| pubmed-article:19956589 | pubmed:author | pubmed-author:ChutakeYogesh... | lld:pubmed |
| pubmed-article:19956589 | pubmed:author | pubmed-author:RindlerPaul... | lld:pubmed |
| pubmed-article:19956589 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19956589 | pubmed:volume | 4 | lld:pubmed |
| pubmed-article:19956589 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19956589 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19956589 | pubmed:pagination | e7914 | lld:pubmed |
| pubmed-article:19956589 | pubmed:dateRevised | 2010-9-27 | lld:pubmed |
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| pubmed-article:19956589 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19956589 | pubmed:articleTitle | Epigenetic silencing in Friedreich ataxia is associated with depletion of CTCF (CCCTC-binding factor) and antisense transcription. | lld:pubmed |
| pubmed-article:19956589 | pubmed:affiliation | Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America. | lld:pubmed |
| pubmed-article:19956589 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19956589 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:19956589 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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