IP3 Receptor-Dependent Cytoplasmic Ca2+ Signals Are Tightly Controlled by Cavβ3

Anouar Belkacemi1, Xin Hui2, Barbara Wardas1

  • 1Institut für Experimentelle und Klinische Pharmakologie und Toxikologie der Universität des Saarlandes, 66421 Homburg, Germany.

Cell Reports
|February 2, 2018
PubMed

Insights

The Cavβ3 subunit acts as a brake on calcium release by interacting with IP3 receptors. Its absence accelerates wound healing, highlighting its role in calcium signal control.

Area of Science:

  • Cellular Biology
  • Molecular Physiology

Background:

  • Voltage-gated calcium channels (Cavs) are crucial for calcium (Ca2+) entry in excitable cells.
  • Cav β subunits modulate channel function and membrane trafficking.

Purpose of the Study:

  • To investigate the role of Cavβ3 in regulating intracellular calcium release.
  • To explore the mechanism by which Cavβ3 affects calcium signaling.

Main Methods:

  • Studied the effect of Cavβ3 on calcium release stimulated by phospholipase C-coupled receptors.
  • Investigated the interaction between Cavβ3 and inositol 1,4,5-trisphosphate (IP3) receptors.
  • Assessed fibroblast migration and skin wound closure in the presence and absence of Cavβ3.

Main Results:

  • Cavβ3 significantly reduces Ca2+ release downstream of IP3 formation.
  • This function requires the SH3-HOOK domain of Cavβ3 and involves direct interaction with IP3 receptors.
  • Absence of Cavβ3 enhances fibroblast migration and accelerates wound healing in vivo.

Conclusions:

  • Cavβ3 plays a novel role in controlling intracellular Ca2+ release, independent of its canonical function in Cavs.
  • This β subunit acts as a brake on Ca2+ signaling, contributing to cellular homeostasis and physiological processes like wound repair.

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