Previous crystallographic studies depicted a physical gate of the NaK channel localized at a bundle crossing of pore-lining helices, but solution NMR studies in the current issue of JGP suggest otherwise.
The dominant models explaining potassium channel gating often invoke widening and narrowing of the helix bundle crossing. This paper shows that a closely related channel, NaK, is not gated by this mechanism as the helix bundle crossing in the nonconducting channel is already open.
The funny current (If) is critical for cardiac pacemaking. Here, we show that If is also essential for the fight-or-flight increase in heart rate, accounting for ∼40% of the increase in AP firing rate in mouse sinoatrial node myocytes.
The assembly of Ca2+ entry units in soleus muscle fibers depends strongly on calsequestrin expression and correlates with both enhanced force production during repetitive high-frequency stimulation and Orai1 expression, consistent with junctions providing a source of Ca2+ influx.
The present study critically examined the hypothesis that the membrane protein TMEM150C contributes to the sensitivity of mouse skin mechanoreceptors. We conclude that TMEM150C does not form a transduction channel, nor does it modulate sensory neuron sensitivity in vivo.
Calcium induces a structural transition of myosin heads from ordered off states close to the thick filament to disordered on states near the thin filaments associated with a biochemical shift from the super-relaxed state(s) to the disordered-relaxed state(s) of myosin.
Claudins in tight junctions form ion channels that regulate paracellular permeability. We use molecular dynamics simulations of claudin-15 strands formed by up to 300 monomers to uncover the molecular mechanism of strand flexibility.
Methods and Approaches
A reconstituted depolarization-induced Ca2+ release platform for validation of skeletal muscle disease mutations and drug discovery
Mutations in essential components for depolarization-induced Ca2+ release (DICR) are implicated into various skeletal muscle diseases. Murayama et al. establish a reconstituted DICR platform in nonmuscle cells for validation of disease-causing mutations and drug discovery.