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Article: Mechanisms of calcium signaling by cyclic ADP-ribose and NAADP
Title | Mechanisms of calcium signaling by cyclic ADP-ribose and NAADP |
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Authors | |
Issue Date | 1997 |
Citation | Physiological Reviews, 1997, v. 77 n. 4, p. 1133-1164 How to Cite? |
Abstract | Cells possess various mechanisms for transducing external signals to intracellular responses. The discovery of inositol 1,4,5-trisphosphate (IP 3) as a messenger for mobilizing internal Ca 2+ stores has centralized Ca 2+ mobilization among signaling mechanisms. Results reviewed in this article establish that, in addition to IP 3, the internal Ca 2+ stores can be mobilized by at least two other molecules, cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP), via totally independent mechanisms. Cyclic ADP-ribose is a newly discovered cyclic nucleotide derived from NAD, but, unlike adenosine 3',5'-cyclic monophosphate, its main signaling function is modulation of Ca 2+-induced Ca 2+ release, a major mechanism of Ca 2+ mobilization in addition to the IP 3 pathway. Evidence shows that cADPR may in fact be responsible for mediating the Ca 2+-mobilizing activity of the gaseous messenger nitric oxide. Cells responsive to cADPR are widespread and include species from plant to mammal, indicating the generality of cADPR as a signaling molecule. In addition to cADPR, NAADP, a metabolite of NADP, can also mobilize Ca 2+ stores. The release mechanism and the stores on which NAADP acts are distinct from cADPR and IP 3. Nicotinic acid adenine dinucleotide phosphate may play a role in generating Ca 2+ oscillations, since liberation of NAADP in live cells by photolyzing its caged analog produces long-lasting Ca 2+ oscillations. These two new Ca 2+ agonists are intimately related, since the same metabolic enzymes can, under appropriate conditions, synthesize either one, suggesting a unified mechanism may regulate both pathways. Elucidation of these two new Ca 2+ mobilization pathways is likely to have an important impact on our understanding of cellular signaling mechanisms. |
Persistent Identifier | http://hdl.handle.net/10722/171722 |
ISSN | 2023 Impact Factor: 29.9 2023 SCImago Journal Rankings: 10.821 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, HC | en_US |
dc.date.accessioned | 2012-10-30T06:16:36Z | - |
dc.date.available | 2012-10-30T06:16:36Z | - |
dc.date.issued | 1997 | en_US |
dc.identifier.citation | Physiological Reviews, 1997, v. 77 n. 4, p. 1133-1164 | en_US |
dc.identifier.issn | 0031-9333 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171722 | - |
dc.description.abstract | Cells possess various mechanisms for transducing external signals to intracellular responses. The discovery of inositol 1,4,5-trisphosphate (IP 3) as a messenger for mobilizing internal Ca 2+ stores has centralized Ca 2+ mobilization among signaling mechanisms. Results reviewed in this article establish that, in addition to IP 3, the internal Ca 2+ stores can be mobilized by at least two other molecules, cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP), via totally independent mechanisms. Cyclic ADP-ribose is a newly discovered cyclic nucleotide derived from NAD, but, unlike adenosine 3',5'-cyclic monophosphate, its main signaling function is modulation of Ca 2+-induced Ca 2+ release, a major mechanism of Ca 2+ mobilization in addition to the IP 3 pathway. Evidence shows that cADPR may in fact be responsible for mediating the Ca 2+-mobilizing activity of the gaseous messenger nitric oxide. Cells responsive to cADPR are widespread and include species from plant to mammal, indicating the generality of cADPR as a signaling molecule. In addition to cADPR, NAADP, a metabolite of NADP, can also mobilize Ca 2+ stores. The release mechanism and the stores on which NAADP acts are distinct from cADPR and IP 3. Nicotinic acid adenine dinucleotide phosphate may play a role in generating Ca 2+ oscillations, since liberation of NAADP in live cells by photolyzing its caged analog produces long-lasting Ca 2+ oscillations. These two new Ca 2+ agonists are intimately related, since the same metabolic enzymes can, under appropriate conditions, synthesize either one, suggesting a unified mechanism may regulate both pathways. Elucidation of these two new Ca 2+ mobilization pathways is likely to have an important impact on our understanding of cellular signaling mechanisms. | en_US |
dc.language | eng | en_US |
dc.relation.ispartof | Physiological Reviews | en_US |
dc.subject.mesh | Adp-Ribosyl Cyclase | en_US |
dc.subject.mesh | Adenosine Diphosphate Ribose - Agonists - Analogs & Derivatives - Antagonists & Inhibitors - Chemistry - Metabolism - Physiology | en_US |
dc.subject.mesh | Amino Acid Sequence | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Antigens, Cd | en_US |
dc.subject.mesh | Antigens, Cd38 | en_US |
dc.subject.mesh | Antigens, Differentiation - Metabolism | en_US |
dc.subject.mesh | Calcium - Physiology | en_US |
dc.subject.mesh | Calmodulin - Physiology | en_US |
dc.subject.mesh | Cyclic Adp-Ribose | en_US |
dc.subject.mesh | Hl-60 Cells | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Membrane Glycoproteins | en_US |
dc.subject.mesh | Molecular Sequence Data | en_US |
dc.subject.mesh | Nad+ Nucleosidase - Metabolism | en_US |
dc.subject.mesh | Nadp - Analogs & Derivatives - Biosynthesis - Chemistry - Physiology | en_US |
dc.subject.mesh | Nitric Oxide - Pharmacology | en_US |
dc.subject.mesh | Pc12 Cells | en_US |
dc.subject.mesh | Rats | en_US |
dc.subject.mesh | Sea Urchins | en_US |
dc.subject.mesh | Signal Transduction | en_US |
dc.subject.mesh | Tretinoin - Pharmacology | en_US |
dc.title | Mechanisms of calcium signaling by cyclic ADP-ribose and NAADP | en_US |
dc.type | Article | en_US |
dc.identifier.email | Lee, HC:leehc@hku.hk | en_US |
dc.identifier.authority | Lee, HC=rp00545 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.pmid | 9354813 | - |
dc.identifier.scopus | eid_2-s2.0-0345609814 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0345609814&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 77 | en_US |
dc.identifier.issue | 4 | en_US |
dc.identifier.spage | 1133 | en_US |
dc.identifier.epage | 1164 | en_US |
dc.identifier.isi | WOS:A1997YC32000006 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Lee, HC=26642959100 | en_US |
dc.identifier.issnl | 0031-9333 | - |