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CFTR, unique among ABC transporters, evolved to function as an ion channel in part by optimizing the stability of the open state.

External potassium inhibits KCNQ1 channel through a mechanism involving increased occupancy of the filter S0 site by K+o.


Occupation of the uppermost ion-binding site of the selectivity filter of K+ channels by external K+ promotes channel activity. Such a phenomenon is not observed in KCNQ1 voltage-gated channels, allowing a deeper understanding of their conduction and permeability mechanism.

Membrane stretch activates mechanosensitive PIEZO1 channels, but how this stimulus modulates microscopic open and shut states to increase open probability is unknown. Here, Wijerathne et al. investigate this mechanism using single channel dwell time analysis and Markov-chain modeling.

We show here that a similar voltage-sensor movement in mutant hyperpolarization-activated cyclic nucleotide-gated (HCN) channels can lead to more closing or more opening depending on the cAMP concentration, suggesting that voltage sensor-to-gate coupling is easily altered in HCN channels.

Intracellular fibroblast growth factors (iFGF) regulate voltage-gated sodium (NaV) channel expression and gating. Using a mouse model and heterologous expression in Xenopus oocytes, we describe mechanisms of how iFGF alters NaV channel activation and inactivation.

TRPV5 and TRPV6 are unique among TRP channels due to their high Ca2+ selectivity, while most other members of this ion channel family do not select for a specific cation type. Ives et al. used biomolecular simulations and in silico electrophysiology to determine the mechanism underlying this unusual Ca2+ selectivity.

This manuscript reports discovery of voltage-dependent inhibition of TRPV channels by intracellular polyamines and develops a kinetic model of this process. Polyamines are inhibitors of each TRPV sub-type.

Spontaneous glutamatergic postsynaptic currents recorded in developing cerebellar interneurons are enhanced by presynaptic depolarization. In response to depolarization, they are organized in bursts. Le Guellec, Gomez et al. propose that bursts signal simultaneous pre- and postsynaptic calcium elevation in single synapses, and that they help synapse formation or stabilization.

Myofilament Function 2022

Phosphorylation of the N-terminal region of cardiac troponin I was found to regulate myofilament power output, and this posttranslational modification can be leveraged to increase power output in myofilaments from human failing hearts.

Myofilament Function 2022

Asencio et al. use a spatially explicit model to simulate muscle twitch forces representing cardiac disease states. Using this dataset, they apply dimension reduction techniques and machine learning methods to build a novel classifier of perturbation type from twitch timing.

A heterozygous BK channelopathy G375R/WT expresses five different types of channels differing in voltage activation and conductance. Four of the five are pathogenic.

Mechanotransduction by Membrane Proteins

The kinetics of hypotonic osmolyte release from E. coli is analyzed in conjunction with bacterial survival. It is shown that MscL, the high-threshold “emergency release valve,” rescues bacteria from down-shocks only in the presence of MscS, MscK, or other low-threshold channels that are necessary to pacify MscL at the end of the release phase.

Letters to the Editor

This letter proposes an alternative explanation to the work published by Cowgill and Chanda on the nature of hysteresis in the voltage-gated, potassium-selective channel Shaker.


Our response points out the deficiencies in the alternative explanation proposed by Villalba-Galea to account for our findings on hysteresis (or lack thereof) in steady state charge–voltage curves of Shaker potassium channel.

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