Please use this identifier to cite or link to this item: http://buratest.brunel.ac.uk/handle/2438/7745
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dc.contributor.authorAl-Mahdawi, S-
dc.contributor.authorSandi, C-
dc.contributor.authorMouro Pinto, R-
dc.contributor.authorPook, MA-
dc.date.accessioned2013-12-02T16:08:52Z-
dc.date.available2013-12-02T16:08:52Z-
dc.date.issued2013-
dc.identifier.citationPLoS One, 8(9), e74956 , 2013en_US
dc.identifier.issn1932-6203-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/pubmed/24023969en
dc.identifier.urihttp://bura.brunel.ac.uk/handle/2438/7745-
dc.description© 2013 Al-Mahdawi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use,distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.descriptionThis article has been made available through the Brunel Open Access Publishing Fund.-
dc.description.abstractFriedreich ataxia (FRDA) is caused by a homozygous GAA repeat expansion mutation within intron 1 of the FXN gene, which induces epigenetic changes and FXN gene silencing. Bisulfite sequencing studies have identified 5-methylcytosine (5 mC) DNA methylation as one of the epigenetic changes that may be involved in this process. However, analysis of samples by bisulfite sequencing is a time-consuming procedure. In addition, it has recently been shown that 5-hydroxymethylcytosine (5 hmC) is also present in mammalian DNA, and bisulfite sequencing cannot distinguish between 5 hmC and 5 mC.en_US
dc.description.sponsorshipThe research leading to these results has received funding from the European Union Seventh Framework Programme (FP7/2007-2013) under grant agreement number 242193/EFACTS (CS), the Wellcome Trust [089757] (SA) and Ataxia UK (RMP) to MAP.en_US
dc.languageeng-
dc.language.isoenen_US
dc.publisherPublic Library of Scienceen_US
dc.titleFriedreich ataxia patient tissues exhibit increased 5-hydroxymethylcytosine modification and decreased CTCF binding at the FXN locusen_US
dc.typeArticleen_US
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0074956-
pubs.organisational-data/Brunel-
pubs.organisational-data/Brunel/Brunel Active Staff-
pubs.organisational-data/Brunel/Brunel Active Staff/School of Health Sciences & Social Care-
pubs.organisational-data/Brunel/Brunel Active Staff/School of Health Sciences & Social Care/Biological Sciences-
pubs.organisational-data/Brunel/University Research Centres and Groups-
pubs.organisational-data/Brunel/University Research Centres and Groups/School of Health Sciences and Social Care - URCs and Groups-
pubs.organisational-data/Brunel/University Research Centres and Groups/School of Health Sciences and Social Care - URCs and Groups/Brunel Institute for Ageing Studies-
pubs.organisational-data/Brunel/University Research Centres and Groups/School of Health Sciences and Social Care - URCs and Groups/Brunel Institute of Cancer Genetics and Pharmacogenomics-
pubs.organisational-data/Brunel/University Research Centres and Groups/School of Health Sciences and Social Care - URCs and Groups/Centre for Systems and Synthetic Biology-
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Brunel OA Publishing Fund
Dept of Life Sciences Research Papers

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