Kent D. Taylor

The paper introduces the Proteomic Sex Index (PSI), a continuous measure of plasma proteome alignment with chromosomal sex, showing its association with health and disease traits.

TorchGWAS2 improves genome-wide association testing in related samples by using a deterministic variance-correction algorithm, achieving faster and more powerful results across large-scale omics data.

This study identifies metabolic differences between MPS IH and MPS IA patients treated with different therapies, highlighting potential biomarkers and therapeutic pathways.

The paper examines short-term, long-term, and genetic factors influencing human plasma proteome variability using longitudinal cohort data.

The paper identifies genetic drivers of protein change over time using longitudinal proteomics data from MESA, UK Biobank, and CARDIA, finding that baseline adjustment improves replication but may introduce biases.

This study integrates CAD GWAS with transcriptomic data to identify genes and networks associated with CAD and subclinical atherosclerosis.

The paper analyzes expression and splicing quantitative trait loci (e/sQTL) across multiple tissues in the TOPMed dataset and finds that secondary e/sQTL signals are still discoverable, with many GWAS signals colocalizing with these e/sQTL.

This study improves proteome-wide association study results by using multi-ancestry data, finding more protein-phenotype associations and better prediction models.

This paper develops a machine learning framework to impute cross-platform proteomic data, improving replication of epidemiological findings and protein quality scoring.

The paper integrates genomics and transcriptomics data from human heart samples to identify regulatory mechanisms linking genetic variation to dilated cardiomyopathy.

cellSTAAR integrates single-cell ATAC-seq with whole-genome sequencing to enhance power and interpretation of rare variant association tests in non-coding regions.

This study identifies FNDC1 as a key regulator of vascular calcification through the FNDC1-NAMPT-NAD axis, showing its role in both microvascular and macrovascular diseases and its potential as a therapeutic target.

This study shows that deleterious mitochondrial DNA mutations increase over time and are associated with higher mortality risk, suggesting positive selection rather than genetic drift.

This paper develops a method to improve Mendelian randomization analysis by integrating GWAS results across ancestries, enhancing accuracy and power in discovering causal genes for autoimmune diseases.

The paper introduces MultiSTAAR, a statistical framework for multi-trait rare variant analysis in WGS studies, identifying new lipid trait associations in diverse populations.

This study performs genome-wide association analysis on composite sleep health scores, identifying 28 novel loci and confirming 341 previously reported loci, with insights into genetic mechanisms and pathways.

The paper refines a gene-physical activity interaction affecting HDL-cholesterol by analyzing lipoprotein subfractions and exploring sex differences across multiple cohorts.

The paper conducts proteome-wide and transcriptome-wide association studies for blood lipids, finding high-level consistency between proteome and transcriptome-lipid associations across tissues.

This study identifies 17 genetic loci associated with sleep duration and lipid levels, offering potential druggable targets for dyslipidemia in individuals with sleep disturbances.

The paper develops a method to quantify somatic mutation burden in whole-genome sequencing data without paired-tissue samples and identifies genetic and phenotypic correlates of clonal hematopoiesis without known driver mutations.

This paper conducts a multi-ancestry time-to-event GWAS to identify genetic variants associated with incident cardiovascular disease in people with type 2 diabetes, finding three novel loci and confirming known CAD variants.

This study identifies Lac-Phe as a mediator of metformin's anti-obesity effects through experiments in mice and human cohorts.

The paper maps interaction QTLs (iQTLs) for cell type, age, and other variables in blood multi-omic data to identify context-specific genetic regulatory effects.

The paper identifies impactful rare variants by integrating multi-omic data from MESA, showing that combining expression and protein data increases the detection of rare stop and frameshift variants.

The paper identifies IL1RAP and AIM2 as key modifiers of CHIP-associated cardiovascular risk using UK Biobank data and CRISPR experiments in mice.

The paper validates novel telomere length regulation genes POP5 and KBTBD6 identified through trans-ancestry GWAS using functional experiments in blood cells.

This paper introduces MCFA, an unsupervised integration method for multi-omic data, and applies it to five omics types across 614 samples to infer shared and private factors.

This study shows that MASHR improves transcriptome prediction across populations, leading to more replicable discoveries in multi-ethnic transcriptome-wide association studies.

The paper develops PACER to infer clonal expansion rates from single timepoint data and identifies TCL1A activation as a mediator of clonal hematopoiesis fitness.