Nicholas A Sinnott-Armstrong

TL;DR: It is shown that disease- and trait-associated genetic variants are enriched in tissue-specific epigenomic marks, revealing biologically relevant cell types for diverse human traits, and providing a resource for interpreting the molecular basis of human disease.

TL;DR: In this article, the authors describe the integrative analysis of 111 reference human epigenomes generated as part of the NIH Roadmap Epigenomics Consortium, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression.

TL;DR: The Omni-ATAC protocol generates chromatin accessibility profiles from archival frozen tissue samples and 50-μm sections, revealing the activities of disease-associated DNA elements in distinct human brain structures.

TL;DR: A super-resolution chromatin tracing method that allows determination of both the structural features and their genomic coordinates with high resolution in single cells is reported, suggesting that cohesin is not required for the formation or maintenance of single-cell domain structures, but that their preferential boundary positions are influenced by cohes in-CTCF interaction.

TL;DR: The best candidate causal variants for ER− tumors lie in four separate enhancer elements, and the risk alleles of the strongest candidates for the remaining independent causal variant disrupt a silencer element and putatively increase ESR1 and RMND1 expression.