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- W4313379020 abstract "Abstract The main source of calcium in T cells is through a mechanism known as store-operated calcium entry (SOCE). STIM1 and STIM2 serve as ER calcium sensors that, upon store depletion, activate calcium release-activated calcium (CRAC) channels (Orai1-3,CRACM1-3) in the plasma membrane. In the absence of sustained calcium influx through CRAC channels, numerous lymphocyte functions are severely compromised, as demonstrated in patients suffering from SCID. Agonist-induced calcium oscillations in many cell types are triggered by calcium release from intracellular stores and driven by SOCE. However, their relative roles in agonist-mediated calcium oscillations remain ambiguous. We here report that while both STIM1 and STIM2 contribute to store-refilling during calcium oscillations in T cells, RBL and HEK cells, they do so dependent on the level of store depletion. Molecular silencing of STIM2 by siRNA or inhibition by G418 selectively suppresses SOCE and agonist-mediated calcium oscillations at low levels of store depletion, without interfering with STIM1-mediated signals induced by full store depletion. Thus, STIM2 is preferentially activated by low-level physiological agonist concentrations that cause mild reductions in ER calcium levels. We conclude that with increasing agonist concentrations, SOCE is mediated initially by endogenous STIM2 and incrementally by STIM1, enabling differential modulation of calcium entry over a range of stimulus intensities and levels of store depletion." @default.
- W4313379020 created "2023-01-06" @default.
- W4313379020 creator A5054563731 @default.
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- W4313379020 date "2013-05-01" @default.
- W4313379020 modified "2023-09-30" @default.
- W4313379020 title "STIM2 drives calcium oscillations through store-operated calcium entry caused by mild store depletion (P1160)" @default.
- W4313379020 doi "https://doi.org/10.4049/jimmunol.190.supp.190.5" @default.
- W4313379020 hasPublicationYear "2013" @default.
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