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The actin cytoskeleton in store-mediated calcium entry.
1Department of Physiology, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK.
The Journal of Physiology
|July 15, 2000
Summary
The actin cytoskeleton regulates calcium (Ca2+) entry into cells by controlling the proximity of the endoplasmic reticulum to the plasma membrane. Remodelling of this cytoskeleton is key to activating Ca2+ influx.
Area of Science:
- Cellular Biology
- Molecular Physiology
- Biochemistry
Background:
- Store-mediated calcium (Ca2+) entry is crucial for cellular functions, involving endoplasmic reticulum (ER) and plasma membrane (PM) interactions.
- Existing models propose direct or indirect coupling mechanisms between the ER and PM for Ca2+ influx.
Purpose of the Study:
- To investigate the role of the cytoskeleton in regulating store-mediated Ca2+ entry.
- To explore a secretion-like coupling model for Ca2+ influx.
Main Methods:
- Review of recent advances in understanding Ca2+ signaling.
- Analysis of cytoskeletal regulation in ER-PM coupling.
- Examination of the roles of small GTPases and phosphoinositides.
Main Results:
- The actin cytoskeleton acts as an inhibitor of Ca2+ entry by preventing ER-PM coupling.
- Cytoskeletal remodeling is essential for activating store-mediated Ca2+ entry.
- Small GTPases and phosphoinositides may regulate Ca2+ entry via cytoskeletal remodeling.
Conclusions:
- Store-mediated Ca2+ entry is regulated by a secretion-like mechanism involving reversible ER-PM trafficking.
- The actin cytoskeleton plays a critical inhibitory role, with its remodeling being a key activation step.
- Small GTPases and phosphoinositides are implicated in this pathway through cytoskeletal modulation.