Introduction

Abstract

More than two decades have elapsed since the discovery of capacitative Ca 2+ entry, also known as store-operated Ca 2+ entry (SOCE), by J.W. Putney, Jr. in 1986. SOCE was first reported as a mechanism for receptor-regulated Ca 2+ influx controlled by inositol 1,4,5-trisphosphate that allows refilling of the intracellular Ca 2+ compartments once agonist stimulation has finished. In fact, the term capacitative calcium entry was originally meant to describe the cyclic loading and discharge of a Ca 2+ store, similar to an electrical circuit, where charging of a capacitor is associated with flow of a capacitative current. The initial hypothesis, which limited the role of SOCE to the refilling of the intracellular Ca 2+ pools after or during agonist stimulation, was soon modified by the same research group providing evidence to the idea that store refilling did not involve a direct Ca 2+ -route into the endoplasmic reticulum, but rather resulted from a sequential Ca 2+ entry into the cytoplasm and subsequent accumulation in the Ca 2+ stores by SERCA pumps. This new concept of SOCE significantly broadened the functional implications of SOCE in Ca 2+ signaling as this mechanism serves as a Ca 2+ source for agonist-stimulated Ca 2+ mobilization (Putney 2007).