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DC Field | Value | Language |
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dc.contributor.author | Al-Mahdawi, S | - |
dc.contributor.author | Sandi, C | - |
dc.contributor.author | Mouro Pinto, R | - |
dc.contributor.author | Pook, MA | - |
dc.date.accessioned | 2013-12-02T16:08:52Z | - |
dc.date.available | 2013-12-02T16:08:52Z | - |
dc.date.issued | 2013 | - |
dc.identifier.citation | PLoS One, 8(9), e74956 , 2013 | en_US |
dc.identifier.issn | 1932-6203 | - |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/pubmed/24023969 | en |
dc.identifier.uri | http://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.description | This article has been made available through the Brunel Open Access Publishing Fund. | - |
dc.description.abstract | Friedreich 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.sponsorship | The 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.language | eng | - |
dc.language.iso | en | en_US |
dc.publisher | Public Library of Science | en_US |
dc.title | Friedreich ataxia patient tissues exhibit increased 5-hydroxymethylcytosine modification and decreased CTCF binding at the FXN locus | en_US |
dc.type | Article | en_US |
dc.identifier.doi | http://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 | - |
Appears in Collections: | Publications Brunel OA Publishing Fund Dept of Life Sciences Research Papers |
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Fulltext.pdf | 416.12 kB | Adobe PDF | View/Open |
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