Newest Articles
A hypothetical molecular mechanism for TRPV1 activationTRPV1 channels comprise four subunits containing six transmembrane segments (S1–S6) that surround a central pore. Kasimova et al. hypothesize that channel opening involves rotation of an S6 asparagine residue toward the pore, as well as associated pore hydration and external cavity dehydration.
Linkage analysis of Kir2.1 channelsInwardly rectifying potassium (Kir) channels experience strong (blocking) and weak (intrinsic) rectification. Linkage analysis in the form of a conductance Hill plot is a sensitive method of resolving allosteric interactions between the pore and mediators of the Kir gating process.
Kv6.4 S6 gate influences K+ channel stoichiometryAtypical substitutions in the S6 activation gate sequence distinguish “regulatory” Kv subunits, which cannot homotetramerize due to T1 self-incompatibility. Pisupati et al. show that such substitutions in Kv6 work together with self-incompatibility to restrict Kv2:Kv6 heteromeric stoichiometry to 3:1.
Reduced thin filament stiffness in nebulin KO miceNebulin stabilizes the thin filament and regulates force generation in skeletal muscle, but its precise role is not understood. Using conditional knockout mice, Kawai et al. demonstrate that nebulin functions to increase the force per cross-bridge in skinned slow-twitch soleus muscle fibers.
INaP-dependent oscillatory burstingIntrinsically oscillatory neurons in the pre-Bötzinger complex contribute to the rhythmic pattern of breathing. Yamanishi et al. show that the slow inactivation and slow recovery from inactivation exhibited by the persistent sodium current are important for bursting activity in these neurons.
Action potentials in oocytesVoltage-gated Na+ and K+ channels are known to underlie the temporal characteristics of action potentials. Corbin-Leftwich et al. establish reliable action potential recordings from Xenopus oocytes coexpressing these channels and show how different K+ channel subtypes can modulate excitability.
ANO5, phospholipid scrambling, and myoblast fusionLimb-girdle muscular dystrophy type 2L arises from mutations in the anoctamin ANO5, whose role in muscle physiology is unknown. Whitlock et al. show that loss of ANO5 perturbs phosphatidylserine exposure and cell–cell fusion in muscle precursor cells, which is an essential step in muscle repair.
Current Issue
October 1, 2018
Volume 150, No. 10
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Reviews & Opinions
- Nebulin no longer nebulous
JGP study probes how nebulin affects muscle function.
- A clearer image of the structure and regulation of bestrophin
Stockbridge highlights new work revealing an allosteric inactivation mechanism for the bestrophin channel.
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Bezanilla recalls the profound influence that the Laboratory of Cell Physiology in Montemar, with its investigators and visitors, have had in shaping his scientific career.