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A systematic review and meta-analysis show that calcium supplementation significantly improves bone mass, implying that preventive calcium supplementation in young people (age ≤35 years) may be a shift in the window of intervention for osteoporosis.

Genetic and electrophysiology experiments provide the first direct evidence that protein kinase C is a calcium-sensing protein in post-tetanic potentiation, a form of synaptic plasticity that supports short-term memory.

By restricting actin polymerization to the perimeter of the immune synapse and promoting depolymerization, calcium influx drives centripetal actin flow, which confines CRAC channels and the endoplasmic reticulum to the synapse center.

Calcium influx during acute cell stimulation triggers a global actin reset in mammalian cells, which is linked to plasma membrane repair and transcription and has implications for our understanding of cell migration, cancer, inflammation and cell stress response.

Novel components in the pathway from malignant hyperthermia to diabetes include promotion of a kinase that impedes glycogen synthesis, increased lysis of junctophilin1 and gene regulatory actions by a junctophilin fragment, surprisingly predicted to oppose the effects of elevated calcium.

Outward calcium ion currents desensitize the human PKD2-L1 ion channel via a mechanism that is independent of cytosolic motifs.

The calcium-dependent signaling pathway during ABA-dependent stomatal closure requires the calcium-independent pathway, and calcium signaling specificity is mediated by PP2C protein phosphatases.

The delayed-onset of asynchronous transmitter release seen in neurons that fire repeatedly is triggered by a different source of calcium from that which triggers synchronous transmitter release.

Inhibition enhances the spatial specificity of high calcium influx for cooperatively stimulated synapses, suggesting that inhibitory inputs may regulate both synapse-specific and heterosynaptic plasticity to support learning and memory.

Quantitative experiments and analysis determine the limit of excitation power of 1300-nm three-photon microscopy, and the imaging depth where three-photon outperforms two-photon for calcium imaging in the mouse brain.