Journal
NATURE COMMUNICATIONS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms10069
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Funding
- Arthritis Research UK [20385, 20571]
- Wellcome Trust [AM 095684, 097820/Z/11/B, 089989, 091157, 100140]
- European Union [FP7-HEALTH-F2-2012-305549, 241447]
- Innovative Medicines Initiative (BeTheCure project) [115142]
- JDRF [9-2011-253]
- National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre
- National Institute for Health Research Manchester Musculoskeletal Biomedical Research Unit
- Biotechnology and Biological Sciences Research Council UK [BBS/E/B/000C0405]
- BBSRC [BBS/E/B/000C0405, BBS/E/B/000C0404] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BBS/E/B/000C0404, BBS/E/B/000C0405] Funding Source: researchfish
- Versus Arthritis [20571] Funding Source: researchfish
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Genome-wide association studies have been tremendously successful in identifying genetic variants associated with complex diseases. The majority of association signals are intergenic and evidence is accumulating that a high proportion of signals lie in enhancer regions. We use Capture Hi-C to investigate, for the first time, the interactions between associated variants for four autoimmune diseases and their functional targets in B- and T-cell lines. Here we report numerous looping interactions and provide evidence that only a minority of interactions are common to both B- and T-cell lines, suggesting interactions may be highly cell-type specific; some disease-associated SNPs do not interact with the nearest gene but with more compelling candidate genes (for example, FOXO1, AZI2) often situated several megabases away; and finally, regions associated with different autoimmune diseases interact with each other and the same promoter suggesting common autoimmune gene targets (for example, PTPRC, DEXI and ZFP36L1).
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