Newest Articles

Article | Ion Channels in Health and Disease
Augustus J. Lowry, Pengfei Liang, Maria A. Gonzalez Torres, Huanghe Yang
Lowry et al. show that the disease-associated TMEM63B I475del variant uniquely promotes both mechanosensitive ion channel gain of function and acquired lipid scramblase activity. Their findings reveal graded hydrophobic gate destabilization as a mechanism for variant-specific TMEM63B channelopathies and suggest new directions for targeted therapeutic strategies to treat TMEM63B channelopathy.
Communication | Ion Channels in Health and Disease
Kate M. Crowther, Thibault R.H. Jouen-Tachoire, Peter Proks, Peter Rory Hall, Emma L. Veale, Janina Sörmann, Karin E.J. Rödström, Thomas Müller, Saskia B. Wortmann, Nina Barisic, Natalie Hauser, Vincenzo Salpietro, RaeLynn Forsyth, Linford Williams, Nora Derrabi, Carlos A. Bacino, Jill A. Rosenfeld, Henry Houlden, Simon Newstead, Caroline F. Wright, James Fasham, Alistair A. Mathie, Reza Maroofian, Stephen J. Tucker
In this study, Crowther and colleagues report new disease-causing variants in the TASK-1 and TASK-3 potassium channels responsible for two different neurodevelopmental disorders. They also examine the structural and functional properties of these variants and examine their effects when incorporated into heteromeric TASK-1/TASK-3 channels.
Article | Ion Channels in Health and Disease
Arpan Bysack, H. Raghuraman
Bysack and Raghuraman show specific lipid–protein interactions mediate the cholesterol-induced reorganization of the slide helix in membranes during cholesterol-dependent regulation of KirBac1.1. Importantly, they hypothesize that the slide helix movement might function as a lipid-sensitive “conformational-switch” controlling KirBac1.1 gating.
Article | Voltage-Gated Na Channels 2026
Boris S. Zhorov
Sodium channel antagonist bulleyaconitine and agonist aconitine bind in the pore-domain fenestration I/II and stabilize the open activation gate. Aconitine transiently chelates passing sodium ions, while protonated bulleyaconitine blocks the permeation.
Article
Eduardo Rios, Gonzalo Pizarro
The contraction of skeletal muscles is turned on by Ca2+ released from the cellular store by RyR channels in a quasi-crystalline array, half of which only have contacts with neighbor RyRs. Rios and Pizarro’s model assumes these channels to be controlled allosterically by their neighbors and matches quantitatively observations of Ca2+ release gathered over decades.
Article
Madeleine R. Howell, Rosalind J. Xu, Adam E. Cohen
Bioelectrical signaling is important in many small structures, such as bacteria, viruses, and intracellular vesicles. The dynamics in small structures are strongly affected by stochastic gating of single ion channels. Howell et al. provide a framework for predicting and interpreting bioelectrical dynamics in small structures.
Article
Takashi Tominaga, Yoko Tominaga
We developed a kinetic framework for the major membrane-current components in Paramecium. The framework integrates late-component, leak, and inward Ca2+ currents, including Ca2+-dependent inactivation and slow recovery. It reproduces graded membrane responses under the present recording conditions.
Journal of General Physiology Cover Image for Volume 158, Issue 4
Current Issue
Volume 158,
Issue 4,
6 July 2026

Reviews & Opinions

Commentary
Elizabeth A. Jonas, Eleanora Margulis, Ava Yu, Nelli Mnatsakanyan
Akosah et al. highlight the multifaceted nature of mitochondrial swelling, and its relationship to membrane potential changes, to mitochondrial permeability, and to activation of the mitochondrial permeability transition pore. This study reinforces the need to use direct and comprehensive approaches to evaluate mitochondrial physiology.
Research News
Ben Short
JGP study identifies passive “leak” currents as a likely common mechanism underlying hypomagnesemia with treatment-resistant seizures in patients with certain mutations in the Na+, K+-ATPase α1 subunit.
Commentary
Werner Melzer
Couplons are large multi-protein clusters consisting of CaV1.1 and RyR1 channels that connect SR and transverse tubulus in skeletal muscle cells and permit voltage-controlled Ca2+ release. Rios and Pizarro (2026) simulate allosteric interactions within the couplon using Markov chain modelling to successfully describe many characteristics of whole-cell and microdomain Ca2+ signals.

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