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