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Chemical Compound Review

nadide     [[(2R,3S,4R,5R)-5-(5- aminocarbonylpyridin...

Synonyms: COZYMASE, Enzopride, Nadidum, coenzyme I, DPN, ...
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Disease relevance of nadide


High impact information on nadide

  • This sensitivity of LTRPC2 to redox state modifiers was attributable to an agonistic binding of nicotinamide adenine dinucleotide (beta-NAD+) to the MutT motif [5].
  • BFA had no effect on cell surface binding and endocytosis of a functional fluorescent CT analog or on the dose dependency of CT induced 32P-NAD ribosylation of Gs alpha in vitro [6].
  • Similar to our observations with pierisin-1 and -2, crude extracts from the clams Meretrix lamarckii, Ruditapes philippinarum, and Corbicula japonica incubated with calf thymus DNA and beta-NAD resulted in production of N(2)-(ADP-ribos-1-yl)-2'-deoxyguanosine [7].
  • ADP-ribosylation with 32P-NAD and PTX of choroid plexus revealed an intense labeling at the 40 kDa level in addition to the known PTX-substrates at 41 kDa (Gi alpha) and 39 kDa (Go alpha) [8].
  • To test whether the redox state might have an effect on AMPK activity, we examined the effect of beta-NAD and NADH on this enzyme [9].

Chemical compound and disease context of nadide

  • Furthermore, pertussis toxin treatment of membrane fragments from these cells did not result in labeling of the 41,000-dalton alpha-subunit of Ni with ADP ribose from [32P] NAD, indicating maximal ADP ribosylation of Ni by prior treatment of cells with pertussis toxin [10].

Biological context of nadide

  • 2. In inside-out recordings, beta-NAD+ (0.05-1.0 mM) induced the appearance of a channel characterized by extremely slow kinetics, with mean open times in the range of seconds [11].
  • Exposure of the labelled proteins to phosphodiesterase yielded 32P-AMP, and hydrolysis with NaOH yielded 32P-NAD+ [12].
  • Botulinum neurotoxin A (BoNTA, 0.1 micromol/l) abolished the evoked release of NE, ATP, and beta-NAD at 4 Hz, suggesting that at low levels of neural activity, release of these neurotransmitters results from N-ethylmaleimide-sensitive factor attachment protein receptor/synaptosomal-associated protein of 25 kDa-mediated exocytosis [13].
  • Our data indicated that lipopolysaccharide (1mg/kgb.w., i.p.)-evoked systemic inflammation enhanced PARP-1 activity in the mouse brain, leading to the lowering of beta-NAD(+) concentration, to translocation of apoptosis inducing factor from mitochondria to the nucleus, and to enhanced lipid peroxidation [14].
  • The cyclase converts beta-NAD to cADPR, a calcium mobilizing second messenger involved in fertilization, insulin secretion, and muscle contraction [15].

Anatomical context of nadide

  • In conclusion, we detected constitutive and nerve-evoked overflow of beta-NAD, cADPR, and ADPR in vascular and non-vascular smooth muscles, beta-NAD being the prevailing compound [16].
  • We report here that incubation of beta-NAD+ with cell-free extracts of several rat tissues (including pituitary gland) generates a product which releases intracellular Ca2+ stores in permeabilized rat pituitary GH4C1 cells [17].
  • Both of these electrical changes could be induced by perfusion, through a patch pipette, of nanomolar concentrations of cADPR or its precursor, beta-NAD, into unfertilized oocytes [18].
  • MMS produces more cell membrane damage than MNNG at equitoxic doses. beta-NAD+ is the substrate for ADP-ribosylation and normally does not freely diffuse into cells. beta-NAD+ had no significant effect on SCE induction in intact cells or in cells treated with either 3AB or alkylating agent alone [19].
  • 1. Whole-cell voltage-clamp recordings were used to study the characteristics of a non-selective cation current, activated by intracellular beta-NAD+, present in CRI-G1 insulin-secreting cells [20].

Associations of nadide with other chemical compounds

  • ADP-ribosyl cyclase catalyzes the synthesis of two structurally and functionally different Ca2+ releasing molecules, cyclic ADP-ribose (cADPR) from beta-NAD and nicotinic acid-adenine dinucleotide phosphate (NAADP) from beta-NADP [18].
  • Microinjection of beta-NAD+ into fura-2-loaded beta-cells did not increase [Ca2+]i nor did it alter the cells' subsequent [Ca2+]i response to glucose [21].
  • 6. The flavin fluorescence is partially quenched, and the visible and near-ultraviolet circular dichroism spectrum is changed by beta-NAD+ [22].
  • Capsaicin (10 micromol/l) increased both the resting and EFS-evoked overflow of beta-NAD+ [23].
  • The EFS-evoked release of beta-NAD+ was frequency dependent and is reduced in the presence of tetrodotoxin (TTX; 0.3 micromol/l), omega-conotoxin GVIA (50 nmol/l), and botulinum neurotoxin A (BoNT/A; 100 nmol/l), but remained unchanged in the presence of guanethidine (3 micromol/l), omega-agatoxin IVA (50 nmol/l), or charbachol (1 micromol/l) [23].

Gene context of nadide

  • Sir2 enzymes have been shown to couple substrate deacetylation and beta-NAD(+) cleavage to the formation of O-acetyl-ADP-ribose, a newly described metabolite [24].
  • Cyclic adenosine diphosphate ribose (cADPR) is a potent endogenous calcium-mobilizing agent synthesized from beta-NAD+ by ADP-ribosyl cyclases in sea urchin eggs and in several mammalian cells (Galione, A., and White, A. (1994) Trends Cell Biol. 4, 431 436) [25].
  • To provide evidence for the identification of the 170-kDa band as DNA topoisomerase II, the enzyme was immunoprecipitated from isolated nuclei incubated with 32P-NAD and a labeled peptide of 170 kDa was observed [26].
  • The tissue superfusates collected during EFS also contained the beta-NAD+ metabolite ADPR (0.35 +/- 0.2 fmol/mg tissue) but not cyclic ADPR (cADPR) [23].
  • We determined the capacity of kidney and its components for synthesis of cADPR from beta-NAD, that is catalyzed by enzyme ADP-ribosyl cyclase, and enzymatic inactivation that is catalyzed by cADPR-glycohydrolase [27].

Analytical, diagnostic and therapeutic context of nadide

  • The level of alpha s as measured both by ADP-ribosylation with cholera toxin in the presence of 32P-NAD and by immunoblotting with specific antibody to alpha s decreased by 3-fold in cells grown in media supplemented with LPDS compared with control [28].
  • A detailed HPLC fraction analysis determined that nicotinamide adenine dinucleotide (beta-NAD+; 7.0 +/- 0.7 fmol/mg tissue) is the primary nucleotide that contributes to the formation of eADPR [23].
  • Isolated nuclei or nucleoli were labeled with 32P-NAD; then the nucleolar proteins were analyzed by 1-dimensional and 2-dimensional polyacrylamide gel electrophoresis (PAGE) and modified proteins were detected by autoradiography [29].
  • A robust analytical method, using reversed-phase high-performance liquid chromatography with gradient elution and photodiode-array detection, was used to measure six purines and beta-NAD+ in acid-soluble extracts of samples taken from six different regions of human term placenta [30].
  • A consistently moderate inhibition was found when fragments were previously incubated with toxin in the presence of beta-NAD but not in its absence of after treatment with non-activated toxin [31].


  1. Presence of a functional inhibitory GTP-binding regulatory component, Gi, linked to adenylate cyclase in adipocytes of ob/ob mice. Greenberg, A.S., Taylor, S.I., Londos, C. J. Biol. Chem. (1987) [Pubmed]
  2. Involvement of Gi in the inhibition of adenylate cyclase by cannabimimetic drugs. Howlett, A.C., Qualy, J.M., Khachatrian, L.L. Mol. Pharmacol. (1986) [Pubmed]
  3. A rapid and versatile method for cloning viroids or other circular plant pathogenic RNAs. Lakshman, D.K., Tavantzis, S.M., Boucher, A., Singh, R.P. Anal. Biochem. (1992) [Pubmed]
  4. Human mutation affecting hormone-sensitive adenylate cyclase. Bourne, H.R., Farfel, Z., Brickman, A.S., Kaslow, H.R., Brothers, V.M. Prog. Clin. Biol. Res. (1981) [Pubmed]
  5. LTRPC2 Ca2+-permeable channel activated by changes in redox status confers susceptibility to cell death. Hara, Y., Wakamori, M., Ishii, M., Maeno, E., Nishida, M., Yoshida, T., Yamada, H., Shimizu, S., Mori, E., Kudoh, J., Shimizu, N., Kurose, H., Okada, Y., Imoto, K., Mori, Y. Mol. Cell (2002) [Pubmed]
  6. Entry of cholera toxin into polarized human intestinal epithelial cells. Identification of an early brefeldin A sensitive event required for A1-peptide generation. Lencer, W.I., de Almeida, J.B., Moe, S., Stow, J.L., Ausiello, D.A., Madara, J.L. J. Clin. Invest. (1993) [Pubmed]
  7. Purification and molecular cloning of a DNA ADP-ribosylating protein, CARP-1, from the edible clam Meretrix lamarckii. Nakano, T., Matsushima-Hibiya, Y., Yamamoto, M., Enomoto, S., Matsumoto, Y., Totsuka, Y., Watanabe, M., Sugimura, T., Wakabayashi, K. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  8. Apical localization of the alpha subunit of GTP-binding protein Go in choroidal and ciliated ependymocytes. Péraldi, S., Nguyen Than Dao, B., Brabet, P., Homburger, V., Rouot, B., Toutant, M., Bouille, C., Assenmacher, I., Bockaert, J., Gabrion, J. J. Neurosci. (1989) [Pubmed]
  9. Biochemical regulation of mammalian AMP-activated protein kinase activity by NAD and NADH. Rafaeloff-Phail, R., Ding, L., Conner, L., Yeh, W.K., McClure, D., Guo, H., Emerson, K., Brooks, H. J. Biol. Chem. (2004) [Pubmed]
  10. Agonist-induced down-regulation of muscarinic cholinergic and alpha 2-adrenergic receptors after inactivation of Ni by pertussis toxin. Thomas, J.M., Hoffman, B.B. Endocrinology (1986) [Pubmed]
  11. Characterization of a nicotinamide-adenine dinucleotide-dependent cation channel in the CRI-G1 rat insulinoma cell line. Herson, P.S., Dulock, K.A., Ashford, M.L. J. Physiol. (Lond.) (1997) [Pubmed]
  12. Inhibition of chemotaxis in A7r5 rat smooth muscle cells by a novel panel of inhibitors. Saxty, B.A., Yadollahi-Farsani, M., Kefalas, P., Paul, S., MacDermot, J. Br. J. Pharmacol. (1998) [Pubmed]
  13. Nicotinamide adenine dinucleotide is released from sympathetic nerve terminals via a botulinum neurotoxin A-mediated mechanism in canine mesenteric artery. Smyth, L.M., Breen, L.T., Mutafova-Yambolieva, V.N. Am. J. Physiol. Heart Circ. Physiol. (2006) [Pubmed]
  14. Poly(ADP-ribose) polymerase-1 inhibition protects the brain against systemic inflammation. Czapski, G.A., Cakala, M., Gajkowska, B., Strosznajder, J.B. Neurochem. Int. (2006) [Pubmed]
  15. Regulation of CD 38 expression and function by steroid hormones in myometrium. Dogan, S., Deshpande, D.A., White, T.A., Walseth, T.F., Kannan, M.S. Mol. Cell. Endocrinol. (2006) [Pubmed]
  16. Release of beta-nicotinamide adenine dinucleotide upon stimulation of postganglionic nerve terminals in blood vessels and urinary bladder. Smyth, L.M., Bobalova, J., Mendoza, M.G., Lew, C., Mutafova-Yambolieva, V.N. J. Biol. Chem. (2004) [Pubmed]
  17. Novel mechanism of intracellular calcium release in pituitary cells. Koshiyama, H., Lee, H.C., Tashjian, A.H. J. Biol. Chem. (1991) [Pubmed]
  18. Calcium signaling by cyclic ADP-ribose, NAADP, and inositol trisphosphate are involved in distinct functions in ascidian oocytes. Albrieux, M., Lee, H.C., Villaz, M. J. Biol. Chem. (1998) [Pubmed]
  19. Potentiation of alkylation-induced sister chromatid exchange frequency by 3-aminobenzamide is mediated by intracellular loss of NAD+. Schwartz, J.L. Carcinogenesis (1986) [Pubmed]
  20. Reduced glutathione inhibits beta-NAD+-activated non-selective cation currents in the CRI-G1 rat insulin-secreting cell line. Herson, P.S., Ashford, M.L. J. Physiol. (Lond.) (1999) [Pubmed]
  21. Insulin exocytosis and glucose-mediated increase in cytoplasmic free Ca2+ concentration in the pancreatic beta-cell are independent of cyclic ADP-ribose. Webb, D.L., Islam, M.S., Efanov, A.M., Brown, G., Köhler, M., Larsson, O., Berggren, P.O. J. Biol. Chem. (1996) [Pubmed]
  22. Modulation of the oxidation-reduction potential of the flavin in lipoamide dehydrogenase from Escherichia coli by alteration of a nearby charged residue, K53R. Maeda-Yorita, K., Russell, G.C., Guest, J.R., Massey, V., Williams, C.H. Biochemistry (1994) [Pubmed]
  23. beta-NAD is a novel nucleotide released on stimulation of nerve terminals in human urinary bladder detrusor muscle. Breen, L.T., Smyth, L.M., Yamboliev, I.A., Mutafova-Yambolieva, V.N. Am. J. Physiol. Renal Physiol. (2006) [Pubmed]
  24. Structural identification of 2'- and 3'-O-acetyl-ADP-ribose as novel metabolites derived from the Sir2 family of beta -NAD+-dependent histone/protein deacetylases. Jackson, M.D., Denu, J.M. J. Biol. Chem. (2002) [Pubmed]
  25. Nitric oxide-induced mobilization of intracellular calcium via the cyclic ADP-ribose signaling pathway. Willmott, N., Sethi, J.K., Walseth, T.F., Lee, H.C., White, A.M., Galione, A. J. Biol. Chem. (1996) [Pubmed]
  26. ADP-ribosylation of nonhistone proteins in HeLa cells: modification of DNA topoisomerase II. Scovassi, A.I., Mariani, C., Negroni, M., Negri, C., Bertazzoni, U. Exp. Cell Res. (1993) [Pubmed]
  27. Cyclic ADP-ribose metabolism in rat kidney: high capacity for synthesis in glomeruli. Chini, E.N., Klener, P., Beers, K.W., Chini, C.C., Grande, J.P., Dousa, T.P. Kidney Int. (1997) [Pubmed]
  28. Effects of low density lipoproteins and mevinolin on sympathetic responsiveness in cultured chick atrial cells. Regulation of beta-adrenergic receptors and alpha s. Barnett, J.V., Haigh, L.S., Marsh, J.D., Galper, J.B. J. Biol. Chem. (1989) [Pubmed]
  29. ADP-ribosylation of nucleolar proteins in HeLa tumor cells. Leitinger, N., Wesierska-Gadek, J. J. Cell. Biochem. (1993) [Pubmed]
  30. Determination of concentrations of adenosine and other purines in human term placenta by reversed-phase high-performance liquid chromatography with photodiode-array detection: evidence for pathways of purine metabolism in the placenta. Maguire, M.H., Szabo, I., Slegel, P., King, C.R. J. Chromatogr. (1992) [Pubmed]
  31. The effect of cholera toxin on human red cell Ca-ATPase. Romero, P.J., Weitzman, C. Biochem. Biophys. Res. Commun. (1991) [Pubmed]
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