Stephen Eyre

This study performs ancestry-specific TWAS across six tissues to refine T2D GWAS loci, identifying 289-322 independent signals and highlighting tissue and ancestry-specific effects.

This study identifies causal genes and mechanisms for juvenile idiopathic arthritis by integrating GWAS, PCHi-C, ATAC-seq, and CRISPRa/i in CD4+ T cells from JIA patients.

The paper identifies ERRFI1 as a novel gene involved in psoriasis and psoriatic arthritis by showing its regulation by a non-coding risk variant at 1p36.23 through enhancer activity in keratinocytes.

The paper identifies a regulatory pathway involving rs7034653, FRA2, and TRAF1 that explains how a non-coding variant increases risk of inflammatory arthritis.

The paper identifies intergenic duplications at Xq26.1 as the genetic cause of Bazex-Dupre-Christol syndrome, linking them to ARHGAP36 dysregulation and BCC susceptibility.

This study conducts a trans-ancestry GWAS of rheumatoid arthritis, identifying 124 loci, 34 novel, and shows improved polygenic risk score performance across populations.

The paper identifies gene targets at risk loci for skin-related disorders by integrating HiChIP data from relevant cell lines and public datasets.

The paper investigates the overlap between RA susceptibility loci and lncRNA annotations, finding that immune-enriched lncRNA show a small but significant enrichment among RA variants.

This study uses Capture Hi-C and CRISPR activation to identify KLF4 as a target gene in the 9q31 psoriasis risk locus, linking GWAS variants to functional interactions.

This study fine-maps RA and T1D loci outside the MHC, identifying causal variants and confirming their functional impact through allele-specific binding and enhancer activity.