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dc.contributor.authorYang, Jing
dc.contributor.authorMcGovern, Amanda; orcid: 0000-0001-7727-3283
dc.contributor.authorMartin, Paul; orcid: 0000-0002-1016-6851
dc.contributor.authorDuffus, Kate
dc.contributor.authorGe, Xiangyu
dc.contributor.authorZarrineh, Peyman
dc.contributor.authorMorris, Andrew P.
dc.contributor.authorAdamson, Antony; orcid: 0000-0002-5408-0013
dc.contributor.authorFraser, Peter; orcid: 0000-0002-0041-1227
dc.contributor.authorRattray, Magnus; orcid: 0000-0001-8196-5565; email: magnus.rattray@manchester.ac.uk
dc.contributor.authorEyre, Stephen; orcid: 0000-0002-1251-6974; email: steve.eyre@manchester.ac.uk
dc.date.accessioned2021-09-02T15:32:04Z
dc.date.available2021-09-02T15:32:04Z
dc.date.issued2020-09-02
dc.date.submitted2019-10-22
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/625755/41467_2020_Article_18180.pdf?sequence=2
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/625755/additional-files.zip?sequence=3
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/625755/41467_2020_18180_MOESM5_ESM.pdf?sequence=4
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/625755/41467_2020_18180_MOESM2_ESM.pdf?sequence=5
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/625755/41467_2020_18180_MOESM1_ESM.pdf?sequence=6
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/625755/41467_2020_Article_18180_nlm.xml?sequence=7
dc.identifier.citationNature Communications, volume 11, issue 1, page 4402
dc.identifier.urihttp://hdl.handle.net/10034/625755
dc.descriptionFrom Springer Nature via Jisc Publications Router
dc.descriptionHistory: received 2019-10-22, accepted 2020-08-06, registration 2020-08-11, pub-electronic 2020-09-02, online 2020-09-02, collection 2020-12
dc.descriptionPublication status: Published
dc.descriptionFunder: RCUK | MRC | Medical Research Foundation; doi: https://doi.org/10.13039/501100009187; Grant(s): MR/N00017X/1
dc.descriptionFunder: Arthritis Research UK; doi: https://doi.org/10.13039/501100000341; Grant(s): 21754
dc.description.abstractAbstract: Genome-wide association studies have identified genetic variation contributing to complex disease risk. However, assigning causal genes and mechanisms has been more challenging because disease-associated variants are often found in distal regulatory regions with cell-type specific behaviours. Here, we collect ATAC-seq, Hi-C, Capture Hi-C and nuclear RNA-seq data in stimulated CD4+ T cells over 24 h, to identify functional enhancers regulating gene expression. We characterise changes in DNA interaction and activity dynamics that correlate with changes in gene expression, and find that the strongest correlations are observed within 200 kb of promoters. Using rheumatoid arthritis as an example of T cell mediated disease, we demonstrate interactions of expression quantitative trait loci with target genes, and confirm assigned genes or show complex interactions for 20% of disease associated loci, including FOXO1, which we confirm using CRISPR/Cas9.
dc.languageen
dc.publisherNature Publishing Group UK
dc.rightsLicence for this article: http://creativecommons.org/licenses/by/4.0/
dc.sourceeissn: 2041-1723
dc.subjectArticle
dc.subject/631/1647/1513/2216
dc.subject/631/208/4041/3196
dc.subject/631/208/191/2018
dc.subject/631/208/200
dc.subject/631/337/100/101
dc.subject/38/91
dc.subject/38/77
dc.subject/42/109
dc.subject/38/43
dc.subject/38/39
dc.subjectarticle
dc.titleAnalysis of chromatin organization and gene expression in T cells identifies functional genes for rheumatoid arthritis
dc.typearticle
dc.date.updated2021-09-02T15:32:03Z
dc.date.accepted2020-08-06


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