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First published online March 5, 2008

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Reversal of SOCE fortune

Depletion of intracellular Ca²⁺ stores leads to the activation of Ca²⁺-permeable channels in the plasma membrane, a reversible process known as store-operated Ca²⁺ entry (SOCE). The Ca²⁺ that enters through the store-operated channels can then be pumped into stores within the ER to replenish them. Depleted Ca²⁺ stores in the ER stimulate the ER Ca²⁺ sensor Stim1 to rearrange from tubular structures throughout the ER to punctate structures near the plasma membrane, where it activates the SOCE channels. On page 762, James W. Putney, Jr and colleagues investigate the poorly understood mechanism and determinants of the localisation and reversal of Stim1 puncta formation. They show that SOCE is tightly coupled to the formation of Stim1 puncta, because the basis for SOCE termination is the reversal of punctate Stim1 localisation, which, in turn, is dependent on SOCE-dependent store refilling. In addition, they report on the role of the pharmacologic agent ML-9 as a potential antagonist of Stim1-dependent SOCE. These findings provide a molecular basis for the self-regulating nature of the SOCE process.

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Ca²⁺-store-dependent and -independent reversal of Stim1 localization and function

Jeremy T. Smyth, Wayne I. DeHaven, Gary S. Bird, and James W. Putney, Jr
JCS 2008 121: 762-772. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?