Stromal interacting molecule one (STIM1) is currently known to be a calcium sensor protein located in the endoplasmic reticulum (ER). Depletion of the ER calcium store triggers translocation of STIM1 into subplasmalemmal puncta where it activates calcium channels and initiates store operated calcium entry (SOCE). We show that inhibition of ATP production induced a slow calcium leak from the ER that was followed by formation of subplasmalemmal STIM1 puncta. Depletion of cytosolic ATP also initiated the loss of phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) from the plasma membrane. Although STIM1 puncta formed by inhibition of ATP synthesis co-localised with clusters of ORAI1 channels these complexes were inefficient to facilitate calcium influx. Restoration of ER calcium levels in the absence of ATP permitted STIM1 re-translocation from subplasmalemmal puncta to the ER. Therefore we suggest that dynamic re-arrangement of STIM1 and the formation of STIM1-ORAI1 complexes is an ATP independent process that can occur under conditions of PI(4,5)P2 depletion.
University College Dublin (2009) Proc Physiol Soc 15, PC44
Poster Communications: ATP independent translocation of STIM1 and formation of STIM1-Orai1 complexes
C. M. Walsh1, G. Lur1, M. Chvanov1, L. P. Haynes1, S. G. Voronina1, O. V. Gerasimenko1, O. H. Petersen1, O. H. Petersen1, R. D. Burgoyne1, A. V. Tepikin1
1. The Physiological Laboratory, University of Liverpool, Liverpool, United Kingdom.
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