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Does a decrease in subplasmalemmal Ca2+ explain how store-operated Ca2+ channels are opened?

G J Barritt1

  • 1Department of Medical Biochemistry, School of Medicine, Faculty of Health Sciences, Flinders University, Adelaide, Australia. Greg.Barritt@flinders.edu.au

Cell Calcium
|May 7, 1998
PubMed
Summary
This summary is machine-generated.

Store-operated calcium channels (SOCs) activate when calcium depletes from the endoplasmic reticulum (ER). This study proposes localized subplasmalemmal calcium reduction activates SOCs, explaining cellular calcium regulation.

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Area of Science:

  • Cellular Biology
  • Physiology
  • Biochemistry

Background:

  • Store-activated calcium inflow, or capacitative calcium entry, is crucial for non-excitable and some excitable cells.
  • The precise mechanisms and structures of store-operated calcium channels (SOCs) and their activation by ER calcium depletion remain unclear.

Purpose of the Study:

  • To propose and discuss a hypothesis for the activation mechanism of SOCs.
  • To explain how a decrease in subplasmalemmal calcium concentration activates SOCs.

Main Methods:

  • Literature review and hypothesis development.
  • Discussion of existing observations on calcium feedback inhibition and subplasmalemmal spaces.
  • Analysis of agonist and thapsigargin actions on SOCs.

Main Results:

  • Hypothesizes that reduced calcium in the subplasmalemmal space, rather than the ER lumen, activates SOCs.
  • Explains SOC activation by agonists and thapsigargin through this localized calcium depletion model.
  • Considers the role of thapsigargin-insensitive SERCAs in the proposed mechanism.

Conclusions:

  • The subplasmalemmal calcium concentration decrease is proposed as the key activator of SOCs.
  • This hypothesis offers a framework for understanding capacitative calcium entry.
  • Further research is needed to validate the proposed mechanism and its limitations.