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Cover Image
Cover Image
ON THE COVER
Human cardiac myosin molecular motors (magenta, cyan) power the heart by moving actin (grey filaments). Motors exist as either active (outstretched) or inhibited (folded). Genetic dilated cardiomyopathy patients may have too many inhibited motors, leading to compromised cardiac function. Shown are myosin, surface-attached by their green fluorescent protein tails, propelling actin. Image © Duno-Miranda et al., 2024. See https://doi.org/10.1085/jgp.202313522. - PDF Icon PDF LinkTable of Contents
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Research News
A mutation that prevents myosin from overcoming its inhibitions
JGP study shows that a mutation linked to dilated cardiomyopathy stabilizes β-cardiac myosin in its autoinhibited, super-relaxed state.
Viewpoint
Sensory transduction in auditory hair cells—PIEZOs can’t touch this
In this Viewpoint, Holt, Fettiplace, and Müller weigh the evidence supporting a role for PIEZO and TMC channels in mechanosensory transduction in inner ear hair cells.
Articles
Tail length and E525K dilated cardiomyopathy mutant alter human β-cardiac myosin super-relaxed state
Duno-Miranda et al. investigate the E525K mutation in human β-cardiac myosin, a protein crucial for heart contraction, and its role in causing dilated cardiomyopathy (DCM). They demonstrate that the length of the myosin tail influences its self-inhibition and that the E525K mutation strengthens this effect, potentially reducing heart contractility in DCM.
Cannabidiol potentiates hyperpolarization-activated cyclic nucleotide–gated (HCN4) channels
HCN4 channels play an important role in cardiac action potential initiation in the sinoatrial node. In this study, Page and Ruben find that cannabidiol potentiates HCN4 channels independently of other activators (cAMP) and agonists (PIP2) via binding to a lipid-binding pocket at the C-terminus of the voltage sensor.
