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Paweorn Angsutararux, Amal K. Dutta, Martina Marras, Carlota Abella, Rebecca L. Mellor, Jingyi Shi, Jeanne M. Nerbonne, Jonathan R. Silva
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.
Callum M. Ives, Neil J. Thomson, Ulrich Zachariae
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.
Grigory Maksaev, Peng Yuan, Colin G. Nichols
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.
Article | Myofilament Function 2022
Willem J. De Lange, Emily T. Farrell, Jonathan J. Hernandez, Alana Stempien, Caroline R. Kreitzer, Derek R. Jacobs, Dominique L. Petty, Richard L. Moss, Wendy C. Crone, J. Carter Ralphe
Similar to HCM-causing truncation mutations, CRISPR-mediated cMyBP-C ablation in iPSC-derived human engineered cardiac tissue constructs causes cMyBP-C haploinsufficiency in the heterozygous state. While cMyBP-C ablation causes early hypercontractility, developing Ca2+-handling abnormalities leads to progressive contractile dysfunction.
Han-Zhong Feng, Xupei Huang, Jian-Ping Jin
This article reports that restrictive deletion of the N-terminal extension of cardiac troponin I as seen in adaptation to heart failure enhances Frank-Starling response of the heart by increasing myofilament sensitivity to passive tension rather than resting sarcomere length.
Francisco Jaque-Fernandez, Bruno Allard, Laloé Monteiro, Aude Lafoux, Corinne Huchet, Enrique Jaimovich, Christine Berthier, Vincent Jacquemond
Probenecid, an FDA-approved gout medication of therapeutic interest for other disease conditions, depresses sarcoplasmic reticulum Ca2+ release and contractile activation in mouse skeletal muscle. The effects are unrelated to its capacity to block ATP release through pannexin-1 channels.
Astghik Abrahamyan, Jodene Eldstrom, Harutyun Sahakyan, Nare Karagulyan, Liana Mkrtchyan, Tatev Karapetyan, Ernest Sargsyan, Matthias Kneussel, Karen Nazaryan, Jürgen R. Schwarz, David Fedida, Vitya Vardanyan
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.

Related Articles from Rockefeller University Press

Issue Cover
Current Issue
Volume 155,
Issue 3,
6 March 2023
Reviews & Opinions
Rene Barro-Soria
External potassium inhibits KCNQ1 channel through a mechanism involving increased occupancy of the filter S0 site by K+o.
Commentary | Myofilament Function 2022
David Y. Barefield
Reduced expression of MYBPC3 causes early dysfunction in human cell culture models prior to reduced cMyBP-C levels.
Research News
Ben Short
JGP study reveals that segregation of signals within sensory cilia allows Ca2+ to play opposing roles in olfactory signal transduction.

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