James E. Peters

The paper constructs a multi-ancestry single-cell eQTL map for SLE, identifying colocalized eQTLs with GWAS loci and highlighting cell-type-specific regulatory mechanisms.

This study identifies genetic determinants of blood gene expression and splicing, linking them to molecular phenotypes and health outcomes through QTL analysis and colocalization.

The paper identifies genetic regulators of 184 neuro-related proteins in human plasma and links them to disease traits and drug targets.

This paper identifies a protective association between apolipoprotein L1 polygenic risk scores and reduced risk of giant cell arteritis, supported by Mendelian randomization and pathway analysis.

The paper identifies pQTLs for 91 plasma proteins, finds novel associations, and uses MR to uncover causal roles in immune-mediated diseases, suggesting new therapeutic targets.

The paper develops genetic scores for 17,227 molecular traits using multi-omic data from INTERVAL and validates them across ancestries, demonstrating their utility in pathway analysis and disease association discovery.

This study uses Mendelian randomization to identify plasma proteins associated with stroke risk and potential therapeutic targets.

This study identifies 592 genetic loci associated with 184 plasma proteins in 26,494 individuals and finds causal relationships between protein levels and disease.

This study uses Mendelian randomization to examine if ACE inhibitors or cardiometabolic risk factors affect lung ACE2 and TMPRSS2 expression or plasma ACE2 levels, finding no overall association.

The paper identifies pQTLs for cardiovascular proteins and uses them to evaluate drug targets and suggest new candidates for precision medicine.

The paper identifies a genetic variant in PROCR that influences protein C and factor VII levels, linking it to both reduced coronary artery disease risk and increased venous thromboembolism risk through opposing inflammatory and thrombotic mechanisms.

This study performs GWAS on blood cell flow-cytometry phenotypes, identifies variant-trait associations, and links them to cellular structures and disease mechanisms.

The paper investigates the effect of the IL6R-Asp358Ala variant on AAA growth and evaluates IL-6 pathway blockade in mouse models, finding no significant growth rate reduction but improved survival with trans-signalling inhibition.

This study identifies genetic subsets of EGPA associated with asthma and eosinophil levels, revealing two distinct clinical and genetic syndromes.

The paper identifies 1,927 genetic associations with 1,478 plasma proteins using 10.6 million DNA variants and 3,301 individuals, revealing new drug targets and safety concerns.