Store-Operated Calcium Channel and Cancer
Journal Title: International Journal of Cancer Studies & Research (IJCR) - Year 2012, Vol 1, Issue 1
Abstract
The increase of intracellular Ca2+ concentration is an important mechanism that regulates a variety of physiological processes ranging from exocytosis to gene regulation and cell proliferation [1]. Calcium release from intracellular stores (mainly endoplasmic reticulum, ER) or calcium entry through calcium channels can be used by cells to evoke a higher level of cytosolic Ca2+ concentration. In non-excitable cells, a major pathway for Ca2+ influx is via store-operated Ca2+ channels (also known as capacitative calcium entry) [2]. The concept of Store-operated calcium (SOC) channel was first proposed by James Putney in 1986 [3]. In this model, the depletion of intracellular calcium stores triggers calcium entry across the plasma membrane. In 1992, Hoth & Penner identified the presence of this a Ca2+ release-activated Ca2+ current (CRAC) [4]. Using RNA interference (RNAi)-based approaches, STIM1, an intracellular calcium sensor, was found in 2005 [5, 6].
Authors and Affiliations
Wei-Chiao Chang
Keywords
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- DOI 10.19070/2167-9118-120003e
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