Ascorbic acid is a regulator of the intracellular cAMP concentration: old molecule, new functions?
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.
INSERM UMR EA4263, Medical Genetics, Faculté de Médecine de la Timone, 13385 Marseille cedex 5, France.
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D000067956:Adenylyl Cyclase Inhibitors; D000262:Adenylyl Cyclases / Q000235:genetics; D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology* / Q000502:physiology; D002460:Cell Line; D000242:Cyclic AMP / Q000037:antagonists & inhibitors* / Q000096:biosynthesis; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects; D007527:Isoenzymes / Q000037:antagonists & inhibitors / Q000235:genetics; D007700:Kinetics; D051379:Mice
D000067956:Adenylyl Cyclase Inhibitors; D004791:Enzyme Inhibitors; D007527:Isoenzymes; D000242:Cyclic AMP; D000262:Adenylyl Cyclases; D001205:Ascorbic Acid