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JGP study suggests that, by altering microtubule dynamics, persistent PKA activation promotes the delivery of Nav1.5 channels to intercalated discs.


Bernas et al. show that persistent PKA activation increases INa by directing NaV1.5 to the myocyte surface, activating CREB1, upregulating EB1, and reorganizing microtubules. Their study suggests that persistent PKA activation may protect impulse propagation in a chronically stressed heart.

NaV1.7, a voltage-gated sodium channel, plays a crucial role in pain perception and is specifically targeted by PTx2, which serves as a template for designing pain therapeutics. In this study, Ngo et al. employed computational modeling to evaluate the state-dependent binding of PTx2 to NaV1.7.

Nicotinic acetylcholine receptors (AChRs) play critical roles in muscle contraction and cognition. Kumari et al. elucidate the mechanism of AChR gate opening and show why mutations at the gate result in constitutive channel openings that cause congenital disorders.

Inactivation of calcium channels is an important feedback mechanism that limits excessive calcium influx into cells. This study identifies asymmetric conformational changes in the selectivity filter as critical for orchestrating channel inactivation. Destabilizing the selectivity filter could reverse deficits in inactivation linked to Timothy syndrome.


Longden and Lederer propose a detailed electro-metabolic signaling hypothesis, describing a set of mechanisms that may operate in a diverse array of systems to precisely match local energy demand with supply via capillary electrical signaling to control blood flow.

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