Store-operated calcium entry in mast cells (SOCE (in mast cells))

Store-operated calcium entry (SOCE) is a critical cellular mechanism that mediates sustained calcium influx into mast cells following antigen stimulation. This process is essential for key functions such as degranulation—the release of histamine and other inflammatory mediators—cytokine production, and chemotaxis. The canonical molecular machinery involves depletion of endoplasmic reticulum Ca²⁺ stores sensed by STIM1 proteins, which then interact with plasma membrane Orai1 channels to trigger extracellular Ca²⁺ entry. This sustained elevation in cytosolic Ca²⁺ is obligatory for full activation and effector functions of mast cells during allergic reactions and inflammation[1][2][4]. Pharmacological inhibition or genetic disruption of this pathway can suppress allergic responses but may also compromise broader immune function. Note on correctness: "Calcium influx in mast cells" describes a physiological process rather than a single molecular target; it encompasses several components including STIM1, Orai1/CRACM1 channels, TRPC channels, etc.[2][4]. For structured data purposes—especially drug discovery—it is more accurate to refer specifically to "Store-operated calcium entry" or "Calcium-release activated calcium channel protein 1 (Orai1)" when discussing therapeutic targets. Thus, "calcium influx in mast cells" does not refer to one discrete molecule/receptor but rather a multi-component signaling event.

Other names

Calcium-release activated calcium channel in mast cellsCRAC channel in mast cellsOrai1-mediated calcium influx in mast cellsStore-operated calcium influx (mast cell)Mast cell SOCE

Drugs targeting this pathway typically act as inhibitors of store-operated calcium entry by blocking the function or formation of the CRAC channel complex, thereby suppressing downstream events such as degranulation and cytokine release from mast cells.