α-SNAP mediated rearrangement of Stim1 and Orai1 molecules within CRAC channel clusters is required for store-operated calcium entry.

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.

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

A multidisciplinary platform featured by patient-derived RPEs is established to study the disease-causing mechanisms of BEST1 mutations, and demonstrates gene-supplemented rescue of the mutation-caused deficiency in Ca²⁺-dependent Cl^- current in human RPE.

In response to tissue damage, reactive oxygen species can be sensed by cation channels TRPA1/RyR to cause increases of cytosolic Ca²⁺ in intestinal stem cells, activating Ras/MAPK activity and stimulating stem cell proliferation in Drosophila.

A near-infrared light-stimulable optogenetic platform enables remote and wireless manipulation of calcium signaling and immune responses both in vitro and in vivo to achieve tailored function.

An intracellular ion channel may have a central role in the release of cytokines by macrophages.

Mutations in TIN2, a component of shelterin that keeps telomere length in check, lead to cancer-predisposition by disabling the telomere tumor suppressor pathway.

Adult Scleraxis-lineage cells are not required for successful tendon healing but are required for maintenance of tendon homeostasis.

The genome of a tiny tomato pest reveals mechanisms that underlie metazoan genome reduction.