At the cellular level, one major calcium signaling pathway is known as store-operated calcium entry, or SOCE. In this pathway, the endoplasmic reticulum—a major intracellular calcium store—acts like a sensor-and-supply system. When calcium levels inside the endoplasmic reticulum fall, the protein stromal interaction molecule 1 (STIM1) detects the change and activates ORAI channels in the plasma membrane. ORAI1 forms the pore of the calcium release-activated calcium channel, or CRAC channel, allowing calcium from outside the cell to enter the cytosol and trigger downstream signaling.

Understanding how this pathway works—and how it can be controlled when it doesn’t—is the focus of research led by Yubin Zhou, director of the Center for Translational Cancer Research at the Texas A&M Health Institute of Biosciences and Technology and professor in the Texas A&M Naresh K. Vashisht College of Medicine.