Blagoje Soskic

The paper maps RNA-DNA interactions in 16 human cell types, showing cell-type-specific and dynamic networks that correlate with gene regulation and disease traits.

VIDRA models genetic dose-response relationships to predict drug mechanisms, therapeutic potential, and adverse events using phenotypically associated variants.

The paper identifies Tent5 poly(A) polymerases as stabilizers of insulin mRNA, showing their specific activity regulated by glucose and localization.

This study identifies distinct gene regulatory networks driving naive and memory B cell differentiation, showing IRF4's role in both GC and plasma cell development independently of PRDM1.

The paper uses division-resolved single-cell transcriptomics to study T cell activation and identifies gene programmes linked to immune disease by analyzing variant effects on cell division states.

This study uses genomic SEM on GWAS data to identify three distinct immune disease groups and their associated genetic loci, showing convergence on common pathways.

The paper maps eQTLs during T cell activation and identifies immune disease risk variants that regulate gene expression dynamics, showing colocalization with disease-associated genes.

The paper identifies T cell states associated with immune disease variants by analyzing chromatin activity across different activation states.

The paper identifies immune disease variants affecting Treg gene expression and highlights potential drug targets by linking GWAS signals with Treg QTLs.

Genomic profiling of CD4 T cell activation reveals a sensitivity switch from TCR in naive to CD28 in memory cells.