Publications by authors named "F M Dewey"
Article Synopsis
- The study identifies a new variant in the WTIP gene associated with hypertrophic cardiomyopathy (HCM), suggesting its role in cardiac hypertrophy mechanisms.
- Utilizing exome sequencing and other analyses, researchers found that knocking down WTIP in rat heart cells led to increased hypertrophy and altered calcium dynamics, which also appeared in patient-derived cells with the same genetic variant.
- These findings highlight WTIP's critical involvement in cardiac health, showing that disruptions in its function can lead to significant heart conditions, particularly regarding calcium balance in heart cells.
Heart failure is a leading cause of mortality, yet our understanding of the genetic interactions underlying this disease remains incomplete. Here, we harvest 1352 healthy and failing human hearts directly from transplant center operating rooms, and obtain genome-wide genotyping and gene expression measurements for a subset of 313. We build failing and non-failing cardiac regulatory gene networks, revealing important regulators and cardiac expression quantitative trait loci (eQTLs).
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- Truncating variants in the Titin gene (TTNtvs) are linked to idiopathic dilated cardiomyopathy (DCM) but their effects across different ancestries and clinical contexts have not been fully explored.
- The study analyzed genetic data from over 71,000 individuals, identifying those with TTNtvs, particularly in heart-expressed regions, and assessed their health records for DCM-related outcomes.
- The findings revealed that TTNtvs significantly increased the risk of DCM in individuals of European ancestry, but had a negligible association in those of African ancestry, pointing to the influence of genetic background on disease risk profiles.
Protein-coding genetic variants that strongly affect disease risk can yield relevant clues to disease pathogenesis. Here we report exome-sequencing analyses of 20,791 individuals with type 2 diabetes (T2D) and 24,440 non-diabetic control participants from 5 ancestries. We identify gene-level associations of rare variants (with minor allele frequencies of less than 0.
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