May 9, 2005 | Jack Roos, Paul J. DiGregorio, Andriy V. Yeromin, Kari Ohlsen, Maria Lioudyna, Shenyuan Zhang, Olga Safrina, J. Ashot Kozak, Steven L. Wagner, Michael D. Cahalan, Gonül Velicelebi, and Kenneth A. Stauderman
The study investigates the role of *Stim* (STIM1 in humans) in store-operated Ca²⁺ (SOC) channel function. Using an RNA interference (RNAi)-based screen, the authors identified *Stim* as a critical component of SOC influx in *Drosophila* S2 cells and human Jurkat T cells. RNAi-mediated knockdown of *Stim* significantly reduced thapsigargin (TG)-dependent Ca²⁺ entry and CRAC current activity in both cell types. Overexpression of STIM1 in HEK293 cells modestly enhanced TG-induced Ca²⁺ entry. These findings suggest that STIM1, a conserved protein from *Drosophila* to mammalian cells, plays an essential role in SOC influx and may be a common component of SOC and CRAC channels. The study also discusses potential models for how STIM1 affects SOC influx and CRAC channel function, including its role as a Ca²⁺ sensor or coupler linking store depletion to channel activation.The study investigates the role of *Stim* (STIM1 in humans) in store-operated Ca²⁺ (SOC) channel function. Using an RNA interference (RNAi)-based screen, the authors identified *Stim* as a critical component of SOC influx in *Drosophila* S2 cells and human Jurkat T cells. RNAi-mediated knockdown of *Stim* significantly reduced thapsigargin (TG)-dependent Ca²⁺ entry and CRAC current activity in both cell types. Overexpression of STIM1 in HEK293 cells modestly enhanced TG-induced Ca²⁺ entry. These findings suggest that STIM1, a conserved protein from *Drosophila* to mammalian cells, plays an essential role in SOC influx and may be a common component of SOC and CRAC channels. The study also discusses potential models for how STIM1 affects SOC influx and CRAC channel function, including its role as a Ca²⁺ sensor or coupler linking store depletion to channel activation.