The <i>FES</i> Gene at the 15q26 Coronary-Artery-Disease Locus Inhibits Atherosclerosis.

ABSTRACT:

Background

Genome-wide association studies have discovered a link between genetic variants on human chromosome 15q26.1 and increased coronary artery disease (CAD) susceptibility; however, the underlying pathobiological mechanism is unclear. This genetic locus contains the FES (FES proto-oncogene, tyrosine kinase) gene encoding a cytoplasmic protein-tyrosine kinase involved in the regulation of cell behavior. We investigated the effect of the 15q26.1 variants on FES expression and whether FES plays a role in atherosclerosis.

Methods and results

Analyses of isogenic monocytic cell lines generated by CRISPR (clustered regularly interspaced short palindromic repeats)-mediated genome editing showed that monocytes with an engineered 15q26.1 CAD risk genotype had reduced FES

SUBMITTER: Karamanavi E 

PROVIDER: S-EPMC9770135 | biostudies-literature | 2022 Dec

REPOSITORIES: biostudies-literature