ArticleThe Biochemical journal1996
Nicotinamide inhibits cyclic ADP-ribose-mediated calcium signalling in sea urchin eggs.
Article in The Biochemical journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 84 citations in OpenAlex.
- A network-based modeling framework reveals the core signal transduction network underlying high carbon dioxide-induced stomatal closure in guard cells.PLoS biology · 2024Article
- The NaProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Therapeutic Potential of Emerging NAD+-Increasing Strategies for Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- NADBiomolecules · 2020Review
- Beneficial effects of nicotinamide on hypertensive mice with impaired endothelial nitric oxide function.Journal of experimental nephrology · 2020Article
- Diverse therapeutic efficacies and more diverse mechanisms of nicotinamide.Metabolomics : Official journal of the Metabolomic Society · 2019Review
- The Influence of Nicotinamide on Health and Disease in the Central Nervous System.International journal of tryptophan research : IJTR · 2018Review
- Glaucoma as a Metabolic Optic Neuropathy: Making the Case for Nicotinamide Treatment in Glaucoma.Journal of glaucoma · 2017Review
- Nicotinamide and WLDFrontiers in neuroscience · 2017Article
- CD38 mediates angiotensin II-induced intracellular Ca(2+) release in rat pulmonary arterial smooth muscle cells.American journal of respiratory cell and molecular biology · 2015Article
- Cyclic ADP ribose-dependent Ca2+ release by group I metabotropic glutamate receptors in acutely dissociated rat hippocampal neurons.PloS one · 2011Article
- The calcium-mobilizing messenger nicotinic acid adenine dinucleotide phosphate participates in sperm activation by mediating the acrosome reaction.The Journal of biological chemistry · 2010Article
- Nicotinamidase modulation of NAD+ biosynthesis and nicotinamide levels separately affect reproductive development and cell survival in C. elegans.Development (Cambridge, England) · 2009Article
- Interactions between circadian and hormonal signalling in plants.Plant molecular biology · 2009Review
- Ca(2+) signaling occurs via second messenger release from intraorganelle synthesis sites.Current biology : CB · 2008Article
- H2O 2-stimulated Ca2+ influx via TRPM2 is not the sole determinant of subsequent cell death.Pflugers Archiv : European journal of physiology · 2008Article
- cADP-ribose potentiates cytosolic Ca2+ elevation and Ca2+ entry via L-type voltage-activated Ca2+ channels in NG108-15 neuronal cells.The Biochemical journal · 2000Article
- Abscisic acid-induced stomatal closure mediated by cyclic ADP-ribose.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- NAD and axon degeneration: from the Wlds gene to neurochemistry.Cell adhesion & migrationReview
- Niacinamide and Neuroprotection: The Glaucoma Holy Grail.Journal of current glaucoma practiceArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cyclic ADP ribose (cADPR) is a potent Ca(2+)-releasing agent, and putative second messenger, the endogenous levels of which are tightly regulated by synthetic (ADP-ribosyl cyclases) and degradative (cADPR hydrolase) enzymes. These enzymes have been characterized in a number of mammalian and invertebrate tissues and their activities are often found on a single polypeptide. beta-NAD+, cGMP and nitric oxide (NO) have been reported to mobilize Ca2+ in the sea urchin egg via the cADPR-mediated pathway. We now report that in sea urchin egg homogenates, nicotinamide inhibits the Ca(2+)-mobilizing action of beta-NAD+, cGMP and NO, but has no effect on cADPR-induced Ca2+ release. Moreover, nicotinamide inhibits cGMP-induced regenerative Ca2+ waves in the intact sea urchin egg. By successfully separating the cADPR-metabolizing machinery from that which releases Ca2+, we have shown that nicotinamide inhibits cADPR-mediated Ca2+ signalling at the level of cADPR generation. Importantly, nicotinamide had no effect upon the hydrolysis of cADPR, and its selective action on cyclase activity was supported by its inhibition of purified Aplysia ADP-ribosyl cyclase, which does not exhibit detectable hydrolytic activity. The action of nicotinamide in blocking Ca2+ release by beta-NAD+, cGMP and NO strongly suggests that these agents act as modulators of cADPR synthesis rather than to sensitize calcium release channels to cADPR.
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