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Astrocytic ER calcium release and gap junction communication exhibit circadian modulation driven by HERPUD1, highlighting the importance of astrocytic circadian rhythms in brain function.

Orai1 channels activate intermittently in motile T cells, generating calcium transients, detected by a novel genetically encoded indicator and inducing pauses that favor antigen scanning.

Spontaneous fusion of vesicles at synapses is regulated independently of fusion triggered by action potentials, adding to evidence that the two types of fusion have distinct functions.

Colorectal tumors down-regulate the mitochondrial Na+/Ca2+/Li+ exchanger (NCLX) to alter mitochondrial Ca2+ signaling and initiate transcriptional and metabolic reprogramming that drives tumor chemo-resistance and metastasis.

The role of lysosomal Ca²⁺ flux associated with K⁺ efflux, a well-known event in inflammasome activation in metabolic inflammation and inflammasome activation, has been presented.

Synaptic glutamate release is potentiated by short metabolic failure whereas longer durations of energy depletion lead to a postsynaptic failure of synaptic transmission.

Cytosolic S100A8/A9 enhances Ca²⁺ availability at LFA-1 adhesion sites, facilitating neutrophil recruitment and extravasation by supporting proper integrin signaling and cytoskeletal rearrangement.

Eugenol has the potential as a novel exercise mimetic, and TRPV1 may represent a promising target for the development of exercise mimetics.

Cell-wide Ca²⁺ signals that regulate numerous cellular functions comprise dual Ca²⁺ release modes through IP₃ receptors, punctate transients mediated by clustered receptors and spatiotemporally diffuse release through functionally distinct receptors.

Excitotoxicity driven by NMDA receptor hyper-activation does not involve DAPK1-dependent events in vitro or in vivo, and previously described DAPK1-NMDAR disrupting peptides act by blocking the NMDA receptor.