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.
A mutation that causes heart disease in humans increases the number of active myosin heads during contraction in the muscles of fruit flies, leading to the progressive dysfunction of the flight muscles and heart tube.
A simple and effective method facilitates the study of in vivo transcriptional dynamics using transcriptional enhancers and destabilized fluorescent protein, which is suitable for both live imaging and fixed studies.
The activation and membrane localization of the broadly-tuned noxious chemosensory cation channel TRPA1 are regulated by direct interactions with cholesterol via CRAC motifs in transmembane segments 2 and 4.
Vascular endothelial cells in the brain, heart and lung exhibit tissue-specific heterogeneity and plasticity, expressing genes that were traditionally thought to be only expressed by the surrounding parenchymal tissue cells.
Unique biosensor design and protein-engineering enables direct visualization of the active form of Fyn kinase with high specificity, minimal perturbation and shows cellular signaling to be compartmentalized and pulsatile.