19956589

Source:http://linkedlifedata.com/resource/pubmed/id/19956589

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Predicate	Object
rdf:type	pubmed:Citation
lifeskim:mentions	umls-concept:C0016719, umls-concept:C0040649, umls-concept:C0332281, umls-concept:C0333668, umls-concept:C0669443, umls-concept:C1422163, umls-concept:C1707931
pubmed:issue	11
pubmed:dateCreated	2009-12-3
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.
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pubmed:language	eng
pubmed:journal	http://linkedlifedata.com/resource/pubmed/journal/101285081
pubmed:citationSubset	IM
pubmed:chemical	http://linkedlifedata.com/resource/pubmed/chemical/5' Untranslated Regions, http://linkedlifedata.com/resource/pubmed/chemical/CCCTC-binding factor, http://linkedlifedata.com/resource/pubmed/chemical/FOXH1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Forkhead Transcription Factors, http://linkedlifedata.com/resource/pubmed/chemical/Heterochromatin, http://linkedlifedata.com/resource/pubmed/chemical/Iron-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Oligonucleotides, Antisense, http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins, http://linkedlifedata.com/resource/pubmed/chemical/frataxin
pubmed:status	MEDLINE
pubmed:issn	1932-6203
pubmed:author	pubmed-author:BidichandaniSanjay ISI, pubmed-author:ChutakeYogesh KYK, pubmed-author:De BiaseIreneI, pubmed-author:RindlerPaul MPM
pubmed:issnType	Electronic
pubmed:volume	4
pubmed:owner	NLM
pubmed:authorsComplete	Y
pubmed:pagination	e7914
pubmed:dateRevised	2010-9-27
pubmed:meshHeading	pubmed-meshheading:19956589-5' Untranslated Regions, pubmed-meshheading:19956589-Alleles, pubmed-meshheading:19956589-Epigenesis, Genetic, pubmed-meshheading:19956589-Fibroblasts, pubmed-meshheading:19956589-Forkhead Transcription Factors, pubmed-meshheading:19956589-Friedreich Ataxia, pubmed-meshheading:19956589-Gene Expression Profiling, pubmed-meshheading:19956589-Gene Silencing, pubmed-meshheading:19956589-Heterochromatin, pubmed-meshheading:19956589-Humans, pubmed-meshheading:19956589-Iron-Binding Proteins, pubmed-meshheading:19956589-Oligonucleotides, Antisense, pubmed-meshheading:19956589-Repressor Proteins, pubmed-meshheading:19956589-Transcription, Genetic, pubmed-meshheading:19956589-Zinc Fingers
pubmed:year	2009
pubmed:articleTitle	Epigenetic silencing in Friedreich ataxia is associated with depletion of CTCF (CCCTC-binding factor) and antisense transcription.
pubmed:affiliation	Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
pubmed:publicationType	Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural