Identification of the coupling between skeletal muscle store-operated Ca2+ entry and the inositol trisphosphate receptor
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Edited by Clara Franzini-Armstrong, University of Pennsylvania School of Medicine, Philadelphia, PA, and approved January 9, 2003 (received for review October 18, 2002)
Abstract
Examination of store-operated Ca2+ entry (SOC) in single, mechanically skinned skeletal muscle cells by confocal microscopy shows that the inositol 1,4,5-trisphosphate (IP3) receptor acts as a sarcoplasmic reticulum [Ca2+] sensor and mediates SOC by physical coupling without playing a key role in Ca2+ release from internal stores, as is the case with various cell types in which SOC was investigated previously. The results have broad implications for understanding the mechanism of SOC that is essential for cell function in general and muscle function in particular. Moreover, the study ascribes an important role to the IP3 receptors in skeletal muscle, the role of which with respect to Ca2+ homeostasis was ill defined until now.
Footnotes
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↵ * Present address: Department of Molecular Biophysics and Physiology, Rush University, Chicago, IL 60612.
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↵ † To whom correspondence should be addressed at: Department of Zoology, La Trobe University, Plenty Road, Bundoora, Victoria 3086, Australia. E-mail: g.stephenson{at}zoo.latrobe.edu.au.
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This paper was submitted directly (Track II) to the PNAS office.
- Abbreviations:
- SOC,
- store-operated Ca2+ entry;
- IP3,
- inositol 1,4,5-trisphosphate;
- IP3R,
- IP3 receptor;
- RyR,
- ryanodine receptor;
- E-C,
- excitation–contraction;
- t,
- tubular;
- SR,
- sarcoplasmic reticulum;
- DHPR,
- dihydropyridine receptor
- Copyright © 2003, The National Academy of Sciences
