FEBS Letters
Volume 582, Issue 25 , Pages 3614-3618, 29 October 2008

Ascorbic acid is a regulator of the intracellular cAMP concentration: Old molecule, new functions?

Edited by Judit Ovádi

  • F. Kaya

      Affiliations

    • INSERM UMR EA4263, Medical Genetics, Faculté de Médecine de la Timone, 27 Bd. J. Moulin, 13385 Marseille cedex 5, France
  • ,
  • S. Belin

      Affiliations

    • INSERM UMR EA4263, Medical Genetics, Faculté de Médecine de la Timone, 27 Bd. J. Moulin, 13385 Marseille cedex 5, France
  • ,
  • Gr. Diamantidis

      Affiliations

    • Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece
  • ,
  • M. Fontes

      Affiliations

    • INSERM UMR EA4263, Medical Genetics, Faculté de Médecine de la Timone, 27 Bd. J. Moulin, 13385 Marseille cedex 5, France
    • Corresponding Author InformationCorresponding author.

Received 6 July 2008; received in revised form 11 September 2008; accepted 18 September 2008. published online 01 October 2008.

Abstract 

Recently, using an animal model of Charcot-Marie-Tooth human disorder, we showed that ascorbic acid (AA) represses PMP22 gene expression by acting on intracellular cAMP concentrations. In this work, we present kinetics data on the inhibitory effect of AA upon adenylate cyclase activity. The data show that this molecule acts as a competitive inhibitor of the enzyme, a finding that opens new pharmacological avenues.

Keywords: Ascorbic acid, Adenylate cyclase, Gene expression, CMT disorder

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PII: S0014-5793(08)00776-X

doi:10.1016/j.febslet.2008.09.040

FEBS Letters
Volume 582, Issue 25 , Pages 3614-3618, 29 October 2008