Abstract
Store-operated Ca(2+) entry (SOCE) is a major mechanism controlling Ca(2+) signaling and Ca(2+)-dependent functions and has been implicated in immunity, cancer, and organ development. SOCE-dependent cytosolic Ca(2+) signals are affected by mitochondrial Ca(2+) transport through several competing mechanisms. However, how these mechanisms interact in shaping Ca(2+) dynamics and regulating Ca(2+)-dependent functions remains unclear. In a recent issue, Yoast et al. shed light on these questions by defining multiple roles of the mitochondrial Ca(2+) uniporter in regulating SOCE, Ca(2+) dynamics, transcription, and lymphocyte activation.