Danny Simpson

This paper identifies challenges in GWAS integration and fine-mapping for variant interpretation and suggests a multi-modal approach for prioritizing causal variants.

The paper integrates multi-omic QTLs and predictive models to identify regulatory variants in CD4+ T cells and their role in immune-related GWAS loci.

The paper benchmarks a high-efficiency prime editing platform for multiplexed dropout screening of genetic variants, identifying negative growth phenotypes for nonsense mutations and splice-disrupting synonymous mutations.

The paper maps the genetic interaction network of PARP inhibitor response by analyzing 147,153 pairwise interactions and reveals hierarchical pathway organization and context-specific buffering interactions.

The paper introduces Repair-seq to study DSB repair by profiling genetic perturbations and identifies dependencies and novel mechanisms in repair pathways.