Regulation of Synthesis of cADPR and NAADP



The discovery of the Ca2+ mobilizing properties of cyclic adenosine diphosphate-ribose (cADPR), a cyclic metabolite of NAD [1], and product of enzyme activities termed ADP-ribosyl cyclases [2], has engendered a number of studies aimed at investigating the regulation of synthesis of this molecule. This is important since for cADPR to satisfy the criteria of a second messenger as originally laid down by Sutherland [3], its intracellular levels must be regulated and, in particular, by signals acting at cell surface receptors [4]. Our understanding of the regulation of cADPR synthesis, although still incomplete, has come from two types of approach. The first is the biochemical studies of regulation of ADP-ribosyl cyclase activities, and the second from the development of techniques to quantify changes in cell and tissue levels of cADPR in intact cells and tissues [4]. Endogenous levels in cells and tissues are approximately in the tens of pmol/mg protein, which coincide broadly with the concentration-response relationship range for cADPR-induced Ca2+ release. The first evidence for clues as to possible regulatory mechanisms of cADPR synthesis came from studies investigating the pathway for cGMP-induced Ca2+ mobilization in sea urchin eggs [5].


Nitric Oxide Nitric Oxide Hypoxic Pulmonary Vasoconstriction Nicotinic Acid Adenine Dinucleotide Phosphate CD38 Knockout Mouse 
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© Springer Science+Business Media New York 2002

Authors and Affiliations

  1. 1.Department of PharmacologyOxford UniversityOxfordUK

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