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Related Experiment Videos

Ca2+ release induced by cyclic ADP-ribose.

A Galione1, A White

  • 1University Department of Pharmacology, Oxford, UK.

Trends in Cell Biology
|December 1, 1994
PubMed
Summary
This summary is machine-generated.

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Cyclic ADP-ribose (cADPR) is a potent calcium-releasing agent synthesized from NAD+. It regulates calcium release from the endoplasmic reticulum, potentially acting as a key cellular messenger.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Pharmacology

Background:

  • Cyclic ADP-ribose (cADPR) is recognized as a highly effective agent for mobilizing intracellular calcium (Ca2+).
  • This molecule is ubiquitously found across various cell types.
  • Its synthesis involves the precursor nicotinamide adenine dinucleotide (NAD+) and ADP-ribosyl cyclases.

Purpose of the Study:

  • To elucidate the role of cADPR in calcium signaling pathways.
  • To investigate the mechanism by which cADPR modulates calcium release.
  • To explore cADPR's potential function as an endogenous second messenger.

Main Methods:

  • Investigating the synthesis of cADPR from NAD+ via ADP-ribosyl cyclases.
  • Analyzing the binding of cADPR to Ca2+ channels located on the endoplasmic reticulum.

Related Experiment Videos

  • Studying the potentiation of Ca2+ release by elevated cytoplasmic Ca2+ concentrations.

    • Main Results:

    • cADPR activates a Ca2+ release mechanism by binding to Ca2+ channels in the endoplasmic reticulum membrane.
    • The Ca2+ release triggered by cADPR is enhanced by increased intracellular Ca2+ levels.
    • Evidence suggests cADPR acts as a regulator of Ca2+-induced Ca2+ release.

    Conclusions:

    • cADPR is a potent endogenous regulator of intracellular calcium.
    • The findings support the hypothesis that cADPR functions as a critical Ca2+-mobilizing second messenger.
    • Further research into cADPR signaling is warranted for understanding cellular calcium homeostasis.