Jamie R. J. Inshaw

The paper identifies a genetic variant that affects transcription factor binding and reduces type 1 diabetes risk in infants by altering thymic gene expression.

This study identifies causal variants, cells, genes, and drug targets for type 1 diabetes using large-scale genetic and functional genomic analyses.

The paper identifies 302 new genetic signals for type 1 diabetes and autoimmune thyroid disease by combining effect size and significance, showing that only 28% of genome-wide significant signals have large effects.

This paper identifies four genetic regions associated with both type 1 and type 2 diabetes, with three showing opposite effect directions and one showing concordant effects.

The paper develops a platform combining ATAC-seq, DNaseI footprints, NG Capture-C, and machine learning to identify causal variants and genes for polygenic human traits.

This study shows that pro-inflammatory cytokines reveal plasticity in β-cell regulatory landscapes and identify T1D-associated variants disrupting cytokine-responsive enhancers.

The paper identifies genetic risk factors associated with early-onset type 1 diabetes, showing stronger effects in children diagnosed before age 7 compared to those diagnosed at 13 or older.