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IP3 receptors and Ca2+ entry.

Nagendra Babu Thillaiappan1, Pragnya Chakraborty2, Gaiti Hasan3

  • 1Department of Pharmacology, Tennis Court Road, Cambridge CB2 1PD, United Kingdom.

Biochimica Et Biophysica Acta. Molecular Cell Research
|November 19, 2018
PubMed
Summary
This summary is machine-generated.

Inositol 1,4,5-trisphosphate receptors (IP3Rs) regulate intracellular calcium (Ca2+) release. This review explores how IP3Rs influence store-operated Ca2+ entry (SOCE) and direct Ca2+ influx in cells.

Keywords:
Ca(2+) entryCa(2+) puffCa(2+) signalEndoplasmic reticulumIP(3) receptorRyanodine receptorSTIMStore-operated Ca(2+) entry

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Area of Science:

  • Cellular Biology
  • Molecular Physiology
  • Calcium Signaling

Background:

  • Inositol 1,4,5-trisphosphate receptors (IP3Rs) are key intracellular Ca2+ release channels.
  • IP3R activation by IP3 and Ca2+ facilitates rapid Ca2+ flux from the ER to the cytosol.
  • Cytosolic Ca2+ increases regulate cellular effectors and organelle Ca2+ uptake, while ER Ca2+ depletion triggers store-operated Ca2+ entry (SOCE).

Purpose of the Study:

  • To review the structural basis of IP3R activation.
  • To examine the interaction between STIM, Orai, and IP3Rs in SOCE.
  • To explore the role of IP3Rs in regulating SOCE and direct Ca2+ entry.

Main Methods:

  • Literature review of existing research on IP3Rs and Ca2+ signaling.
  • Analysis of structural and functional data related to IP3R activation and SOCE.
  • Synthesis of evidence regarding IP3R localization and function in Ca2+ entry.

Main Results:

  • IP3Rs are strategically positioned to regulate SOCE.
  • Evidence suggests IP3Rs can modulate SOCE independently of ER Ca2+ depletion.
  • IP3Rs located in the plasma membrane can directly mediate Ca2+ influx in certain cell types.

Conclusions:

  • IP3Rs play a multifaceted role in cellular Ca2+ homeostasis.
  • Understanding IP3R function is crucial for deciphering Ca2+ signaling pathways.
  • IP3Rs are implicated in both indirect and direct mechanisms of cellular Ca2+ entry.