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Farh, Kyle Kai-How; Marson, Alexander; Zhu, Jiang; Kleinewietfeld, Markus; Housley, William J; Beik, Samantha; Shoresh, Noam; Whitton, Holly; Ryan, Russell J H; Shishkin, Alexander A; Hatan, Meital; Carrasco-Alfonso, Marlene J; Mayer, Dita; Luckey, C John; Patsopoulos, Nikolaos A; De Jager, Philip L; Kuchroo, Vijay K; Epstein, Charles B; Daly, Mark J; Hafler, David A; Bernstein, Bradley E
Nature (London), 02/2015, Letnik: 518, Številka: 7539Journal Article
Genome-wide association studies have identified loci underlying human diseases, but the causal nucleotide changes and mechanisms remain largely unknown. Here we developed a fine-mapping algorithm to identify candidate causal variants for 21 autoimmune diseases from genotyping data. We integrated these predictions with transcription and cis-regulatory element annotations, derived by mapping RNA and chromatin in primary immune cells, including resting and stimulated CD4(+) T-cell subsets, regulatory T cells, CD8(+) T cells, B cells, and monocytes. We find that ∼90% of causal variants are non-coding, with ∼60% mapping to immune-cell enhancers, many of which gain histone acetylation and transcribe enhancer-associated RNA upon immune stimulation. Causal variants tend to occur near binding sites for master regulators of immune differentiation and stimulus-dependent gene activation, but only 10-20% directly alter recognizable transcription factor binding motifs. Rather, most non-coding risk variants, including those that alter gene expression, affect non-canonical sequence determinants not well-explained by current gene regulatory models.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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