Diabetes and associated disorders

This study identifies the lncRNA ARGI as a mediator of virus-induced inflammation in pancreatic beta cells linked to type 1 diabetes through allele-specific transcriptional activation.

This study investigates the genotype-phenotype relationship in Wolfram syndrome, finding that specific WFS1 gene variants correlate with earlier onset and more severe disease manifestations.

The paper identifies T1D risk genes and regulatory elements that influence beta cell survival under proinflammatory cytokine exposure using functional genomics and genetics.

This study shows that TYK2 is critical for β-cell development by regulating KRAS and IFN responses, suggesting TYK2 inhibition as a therapeutic target for type 1 diabetes.

The paper describes the integration of a genetic risk prediction platform into the NHS newborn screening program for Type 1 Diabetes, demonstrating a model for population-based genetic research.

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 paper uses Mendelian randomization to find that low birth weight and high adult BMI are causally linked to latent autoimmune diabetes in adults, with BMI having a stronger effect than birth weight.

The paper identifies sequence and motif similarities between bacterial and human GAD65, suggesting a potential link between gut microbiome dysbiosis and T1D via immune cross-reactivity.

This study identifies 22 novel genetic loci associated with low polygenic risk score type 1 diabetes by analyzing rare variants in two independent cohorts.

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

This study combines large-scale GWAS and single-cell epigenomics to identify cell type-specific mechanisms of type 1 diabetes risk.

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.

The paper identifies gene expression patterns linked to Cesarean section and islet autoimmunity, showing shared transcriptional changes associated with immune cell activation.

This study identifies immune regulatory networks influenced by T1D-associated genetic variants using 3D genome organization and gene expression data.

The paper investigates whether DNA methylation mediates genetic risk for type 1 diabetes by analyzing SNP-methylation associations across different life stages.