Abstract
Store-mediated Ca 2 + entry (SMCE) is the main pathway for Ca 2 + influx in platelets and other nonexcitable cells, yet how depletion of the intracellular Ca 2 + stores leads to the activation of Ca 2 + entry across the plasma membrane remains unclear. Recent work in platelets favors a secretionlike conformational coupling mechanism involving the Ca 2 + -permeable channel protein, Trp1, in the plasma membrane and the type-II inositol 1,4,5-trisphosphate receptor in the membrane of the Ca 2 + store, which is located in the endoplasmic reticulum. Extracellular signal-regulated kinases (ERKs) are common participants in a broad variety of signal transduction pathways in human platelets, and inactivation of the ERK cascade has been shown to reduce Ca 2 + entry stimulated by thapsigargin or thrombin. The role of ERK in SMCE into human platelets was found to be independent of the cytoskeleton and a downstream effector of the small guanosine-triphosphate-binding protein Ras.
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