Open AccessActivation and regulation of store‐operated calcium entry
Author(s) -
Smyth Jeremy T.,
Hwang SungYong,
Tomita Takuro,
DeHaven Wayne I.,
Mercer Jason C.,
Putney James W.
Publication year - 2010
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2010.01168.x
Subject(s) - stim1 , endoplasmic reticulum , orai1 , microbiology and biotechnology , intracellular , chemistry , function (biology) , biophysics , membrane , calcium signaling , calcium , biology , biochemistry , organic chemistry
• Introduction • ICRAC• Orais • STIM1 • STIM2 • STIM1, STIM2 and Ca 2+ oscillations • TRPCs and SOCE • ConclusionsThe process of store‐operated Ca 2+ entry (SOCE), whereby Ca 2+ influx across the plasma membrane is activated in response to depletion of intracellular Ca 2+ stores in the endoplasmic reticulum (ER), has been under investigation for greater than 25 years; however, only in the past 5 years have we come to understand this mechanism at the molecular level. A surge of recent experimentation indicates that STIM molecules function as Ca 2+ sensors within the ER that, upon Ca 2+ store depletion, rearrange to sites very near to the plasma membrane. At these plasma membrane‐ER junctions, STIM interacts with and activates SOCE channels of the Orai family. The molecular and biophysical data that have led to these findings are discussed in this review, as are several controversies within this rapidly expanding field.