A multi-species chemical screening platform reveals a conserved role for p38 inhibition in modulating ryanodine receptor-related phenotypes and is adaptable to a range of neuromuscular disorders.

A mouse model of human muscle myopathy is used to provide mechanistic insight, identify possible biomarkers of disease, and suggest possible therapeutic strategies to alleviate muscle weakness.

Quantitative proteomic analysis shows that recessive Ryr1 mutations not only decrease the content of RyR1 protein in muscle, but also affect the content of many other proteins involved in a variety of biological processes.

The Caenorhabditis elegans presynapse contains two pools of synaptic vesicles at the active zone, coupled to either neuronal-type or muscle-type calcium channels, and to different docking machinery.

Physiological and biochemical studies show that the treatment of a transgenic mouse model carrying recessive Ryr1 mutations with a combination of class II histone deacetylase inhibitors and DNA methyl transferase inhibitors significantly improves skeletal muscle function.

Ca²⁺-dependent nuclear entry of Ca²⁺/calmodulin-dependent protein kinase-1 in sensory neurons, taking place with a relatively slow kinetics, contributes to couple long-lasting sensory stimulations with signaling in the nucleus over a timescale relevant for sensory history-dependent plasticity.

A potassium channel, as a nonconducting function, organizes compartmentalized neuronal calcium signaling microdomains via structural and functional coupling of plasma membrane and endoplasmic reticulum calcium channels.

The Ca²⁺-driven functional coupling of CaV1.2 channels is a mechanism of channel memory that may modulate the amplification of Ca²⁺ influx.

In C. elegans, presenilin functions, independent of its gamma-secretase proteolytic activity, to regulate mitochondrial metabolism by controlling ER-mitochondrial calcium transfer and, even in the absence of Abeta signaling, loss of this activity leads to neurodegeneration.

Synapses employ distinct acute and chronic signaling processes in order to maintain physiologically appropriate levels of function.