Journal of General Physiology

Journal of General Physiology

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The Journal of General Physiology publishes research in physiological problems at cellular and molecular level. Published by Rockefeller University Press.

The Journal of General Physiology publishes peer-reviewed research in biological, chemical, or physical mechanisms of broad physiological significance, with an emphasis on physiological problems at the cellular and molecular level. Areas include, but are not limited to:

- Membrane protein physiology
- Protein structure and dynamics
- Lipid and membrane biophysics
- Cell mechanics
- Intracellular

06/25/2026

Jerome Clatot, Ethan M. Goldberg et al. reveal that, while the p.Thr399Met variant of Kᵥ3.1 shows complete LOF alone, co-expression with WT subunits reveals a “dominant-positive” GOF, highlighting complex subunit interactions. https://hubs.la/Q04mJWhK0

06/25/2026

"JUST-B was founded to create a more inclusive and equitable scientific community, and that work requires sustained support from partners who share that vision. JGP has been exactly that kind of partner. Their funding has been instrumental in allowing us to build and sustain the program, and their commitment signals to early-career scientists from underrepresented backgrounds that the broader biophysics and physiology community is invested in their success. JGP is also a journal I turn to for rigorous, impactful science, and it's wonderful when scientific excellence and a commitment to equity go hand in hand.” — Theanne Griffith, Assistant Professor, Department of Physiology & Membrane Biology, University of California, Davis School of Medicine

As a non-profit journal, Journal of General Physiology (JGP) is committed to fostering an inclusive, globally representative scientific community. Learn how scientists set the course at JGP. https://hubs.la/Q04ms3n00

Learn more about the JUST-B Poster Session at BPS.
https://hubs.la/Q04mr_dY0

06/23/2026

Samsudeen Ponissery Saidu, Alexander Kross, Johannes Reisertet al. address how the two olfactory transduction channels, the CNG channel and the Cl− channel TMEM16B, are modulated by cholesterol. https://hubs.la/Q04mkW1t0

06/18/2026

Sofia F. Nazarova, Vadim А. Alekhin, Nikolay S. Ilyinsky et al. (Moscow Institute of Physics and Technology) present an interactive model of lysosomal ion homeostasis that remains robust during different biologically relevant stresses. https://hubs.la/Q04lTg8M0

06/15/2026

New commentary: Richard D. Rainbow and Richard Barrett-Jolley discuss Scala et al. (https://hubs.la/Q04ln75l0) who demonstrated that Kir6.2/SUR2-containing KATP potassium are the functionally relevant isoform that modulate contractile behavior of fast-twitch muscle during fatigue. https://hubs.la/Q04ln8FL0

06/12/2026

Latest in our Research News: JGP study from Lukyanenko et al. (https://hubs.la/Q04lcBMP0) shows that, in the absence of full-length dysferlin, its C2A domain alone can support normal Ca2⁺ signaling and sarcolemma repair, suggesting that it could be used in gene replacement therapies. https://hubs.la/Q04lbM3M0

05/28/2026

Adam Feher (The University of Chicago), Zoltan Varga (University of Debrecen) and colleagues examine the molecular mechanism of NZ-58, a novel hHv1 inhibitor. Their findings suggest that it binds to the upper gating triad containing countercharges D112 & D185, leading to a “kinetic trapping” mechanism of inhibition. https://hubs.la/Q04jcvQn0

05/22/2026

Varun Verma, Alan S. Verkman and colleagues develop a computational model linking tear production, evaporation, & drainage with ocular surface epithelial transport to predict tear film thickness & osmolality, evaluate current therapies for disease, & propose novel cellular targets. https://hubs.la/Q04hFdny0

05/22/2026

Yenisleidy Lorenzo-Ceballos, Christopher J. Lingle et al. (WashU Medicine) show that long-term inactivation (LTI) of Naᵥ1.2 channels mediated by A-isoforms of different FGF homologues (FGF11–FGF14) differ both in intrinsic rates of onset and rates of recovery from LTI. https://hubs.la/Q04hFtsJ0

05/20/2026

Using specific gene subunit knockout mice, Rosa Scala, Yuezhou Chen et al. of the Colin Nichols lab show that KATP channels formed exclusively of SUR2/Kir6.2 cause delayed fatigue and development of unstimulated force in isolated EDL skeletal muscles. This suggests similar contractile deficits will be present in ABCC9-dependent intellectual disability myopathy syndrome and KCNJ11-dependent neonatal diabetes. https://hubs.la/Q04hl3Qc0

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