Gabriel Kenneth Griffin

The paper identifies plasma proteins associated with clonal hematopoiesis and links them to cardiovascular disease through proteomic and genetic analyses.

The paper identifies recipient stem-cell persistence and T-cell dysregulation as predictors of relapse after HSCT in AML/MDS by analyzing single-cell RNA and TCR sequencing data.

This study creates a spatial and cellular atlas of the colon across age groups using spatial transcriptomics and single nucleus RNA-seq, identifying age-related molecular gradients and multicellular programs.

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

This study analyzes clonal hematopoiesis in over a million diverse individuals, identifying 72 genome-wide significant loci and linking CHIP to various phenotypes.

The paper uses bidirectional Mendelian randomization to show LTL lengthening increases CHIP risk, while CHIP accelerates LTL shortening, with modest mediation between CHIP and CAD via LTL.

The paper develops a method to detect mitochondrial mutations from single-cell RNA-seq to identify clonal expansions in human hematopoiesis.

This study shows that clonal hematopoiesis, especially with DDR gene mutations, increases the risk of peripheral artery disease and atherosclerosis.

This paper introduces HDST, a high-resolution spatial transcriptomics method, and demonstrates its application in mouse brain tissue to resolve spatial expression patterns and cell types.

The paper profiles the enteric nervous system of human and mouse colon at single-cell resolution, revealing diverse neuron subsets and shared transcriptional programs between species.