Genetic and molecular analyses show that FOXC1 and FOXC2 play a role in controlling lymphatic valve maintenance as key mediators of mechanotransduction to control cytoskeletal organization and RhoA/ROCK signaling.
As the first fully genetically encoded method, PARIS allows cell-specific, long-term, repeated measurements of gap junctional coupling with high spatiotemporal resolution, facilitating its study in both health and disease.
TBX5-loss associated cardiomyocyte ectopy and atrial fibrillation is prevented by augmentation of SERCA2 activity, establishing a mechanism underlying the genetic basis for a Ca2+-dependent pathway for AF risk.
β-adrenergic receptors at the Golgi apparatus activate a local signaling pathway, not accessed by cell surface receptors, to drive cardiac hypertrophy and could represent a target for heart failure therapy.
Promoter capture Hi-C in human iPSCs and iPSC-derived cardiomyocytes provides a platform to interrogate gene-regulatory dynamics of cardiomyocyte differentiation and directly links thousands of cardiovascular disease risk loci to hundreds of distal target genes.
Development of a robust Th1 response to infection against an intracellular parasite requires T-cell intrinsic MyD88 signaling, mostly through the upstream IL-18 receptor, for the induction of genes involved in proliferation, cytokine production and migration.
Mapping the locations of hypertrophic cardiomyopathy gene variants onto the three-dimensional structures of contractile proteins revealed that these disrupt protein interactions are critical for normal cardiac relaxation and efficient energy usage.