Loss-of-function mutations in stromal interaction molecule 1 (STIM1) impair the activation of Ca2+ release–activated Ca2+ (CRAC) channels and store-operated Ca2+ entry (SOCE), resulting in a disease syndrome called CRAC channelopathy that is characterized by severe dental enamel defects. The cause of these enamel defects has remained unclear given a lack of animal models. We generated
Miriam Eckstein, Martin Vaeth, Cinzia Fornai, Manikandan Vinu, Timothy G. Bromage, Meerim K. Nurbaeva, Jessica L. Sorge, Paulo G. Coelho, Youssef Idaghdour, Stefan Feske, Rodrigo S. Lacruz
STIM1 and STIM2 mediate store-operated Ca2+ entry in ameloblast cells.