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dc.contributor.authorOnengut-Gumuscu, Sunaen_US
dc.contributor.authorChen, Wei-Minen_US
dc.contributor.authorBurren, Oliveren_US
dc.contributor.authorCooper, Nick J.en_US
dc.contributor.authorQuinlan, Aaron R.en_US
dc.contributor.authorMychaleckyj, Josyf C.en_US
dc.contributor.authorFarber, Emilyen_US
dc.contributor.authorBonnie, Jessica K.en_US
dc.contributor.authorSzpak, Michalen_US
dc.contributor.authorSchofield, Ellenen_US
dc.contributor.authorAchuthan, Premananden_US
dc.contributor.authorGuo, Huien_US
dc.contributor.authorFortune, Mary D.en_US
dc.contributor.authorStevens, Helenen_US
dc.contributor.authorWalker, Neil M.en_US
dc.contributor.authorWard, Luke D.en_US
dc.contributor.authorKundaje, Anshulen_US
dc.contributor.authorKellis, Manolisen_US
dc.contributor.authorDaly, Mark J.en_US
dc.contributor.authorBarrett, Jeffrey C.en_US
dc.contributor.authorCooper, Jason D.en_US
dc.contributor.authorDeloukas, Panosen_US
dc.contributor.authorTodd, John A.en_US
dc.contributor.authorWallace, Chrisen_US
dc.contributor.authorConcannon, Patricken_US
dc.contributor.authorRich, Stephen S.en_US
dc.date.accessioned2015-11-03T15:57:47Z
dc.date.issued2015en_US
dc.identifier.citationOnengut-Gumuscu, S., W. Chen, O. Burren, N. J. Cooper, A. R. Quinlan, J. C. Mychaleckyj, E. Farber, et al. 2015. “Fine mapping of type 1 diabetes susceptibility loci and evidence for colocalization of causal variants with lymphoid gene enhancers.” Nature genetics 47 (4): 381-386. doi:10.1038/ng.3245. http://dx.doi.org/10.1038/ng.3245.en
dc.identifier.issn1061-4036en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:23473926
dc.description.abstractGenetic studies of type 1 diabetes (T1D) have identified 50 susceptibility regions1,2 (www.T1DBase.org) revealing major pathways contributing to risk3, with some loci shared across immune disorders4–6. In order to make genetic comparisons across autoimmune disorders as informative as possible a dense genotyping array, the ImmunoChip, was developed, from which four novel T1D regions were identified (P < 5 × 10−8). A comparative analysis with 15 immune diseases (www.ImmunoBase.org) revealed that T1D is more similar genetically to other autoantibody-positive diseases, most significantly to juvenile idiopathic arthritis and least to ulcerative colitis, and provided support for three additional novel T1D loci. Using a Bayesian approach, we defined credible sets for the T1D SNPs. These T1D SNPs localized to enhancer sequences active in thymus, T and B cells, and CD34+ stem cells. Enhancer-promoter interactions can now be analyzed in these cell types to identify which particular genes and regulatory sequences are causal.en
dc.language.isoen_USen
dc.relation.isversionofdoi:10.1038/ng.3245en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4380767/pdf/en
dash.licenseLAAen_US
dc.titleFine mapping of type 1 diabetes susceptibility loci and evidence for colocalization of causal variants with lymphoid gene enhancersen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalNature geneticsen
dash.depositing.authorDaly, Mark J.en_US
dc.date.available2015-11-03T15:57:47Z
dc.identifier.doi10.1038/ng.3245*
dash.authorsorderedfalse
dash.contributor.affiliatedDaly, Mark


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