In B cells, changes in intracellular concentration of Ca(2+) drive signal transduction to initiate changes in gene expression and various cellular events, including apoptosis and differentiation. B cell receptor engagement causes a transient Ca(2+) flux from the endoplasmic reticulum Ca(2+) store, followed by a continuous increase in intracellular Ca(2+) concentration, mainly resulting from store-operated Ca(2+) entry (SOCE). The recent identification of stromal interaction molecule (STIM) and Orai as essential components for SOCE has allowed researchers to probe further the role of Ca(2+) signals in B cell biology. Here, we summarize the B cell signaling pathways that lead to SOCE, the role of Ca(2+) signals in B cell regulatory function, and how a breakdown in the balance of Ca(2+) signals is associated with immune-related disease.
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