{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T12:16:19Z","timestamp":1777810579241,"version":"3.51.4"},"reference-count":55,"publisher":"SAGE Publications","issue":"10","license":[{"start":{"date-parts":[[1998,10,1]],"date-time":"1998-10-01T00:00:00Z","timestamp":907200000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Dent Res"],"published-print":{"date-parts":[[1998,10]]},"abstract":"<jats:p>\n                    Cyclic ADP-ribose (cADPR), a novel putative messenger of the ryanodine receptor, was examined regarding its ability to mobilize Ca2+ from intracellular Ca2+ stores in isolated cells of parotid and submandibular glands of the dog. cADPR induced a rapid and transient Ca2+ release in the digitonin-permeabilized cells of salivary glands. cADPR-induced Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release was inhibited by ryanodine receptor antagonists ruthenium red, ryanodine, benzocaine, and imperatoxin inhibitor but not by the inositol 1,4,5-trisphosphate (IP\n                    <jats:sub>3<\/jats:sub>\n                    )-receptor antagonist heparin. Thapsigargin, at a concentration of 3 to 30 \u03bcM, inhibited IP\n                    <jats:sub>3<\/jats:sub>\n                    -induced Ca2+ release, while higher concentrations were required to inhibit cADPR-induced Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release. Cross-potentiation was observed between cADPR and ryanodine or SrCl2, suggesting that cADPR sensitizes the Ca2+-induced Ca2+ release mechanism. Cyclic AMP plays a stimulatory role on cADPR- and IP3-induced Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release in digitonin-permeabilized cells. Calmodulin also potentiated cADPR-induced Ca2+ release, but inhibited IP\n                    <jats:sub>3<\/jats:sub>\n                    -induced Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release. Acetylcholine and ryanodine caused the rise in intracellular free Ca2+ concentration ([Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    ) in intact submandibular and parotid cells. Caffeine did not produce any increase in Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release or [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    rise in any preparation. ADP-ribosyl cyclase activity was found in the centrifuged particulate fractions of the salivary glands. These results suggest that cADPR serves as an endogenous modulator of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release from Ca2+ pools through a caffeine-insensitive ryanodine receptor channel, which are different from IP\n                    <jats:sub>3<\/jats:sub>\n                    -sensitive pools in canine salivary gland cells. This system is positively regulated by cyclic AMP and calmodulin.\n                  <\/jats:p>","DOI":"10.1177\/00220345980770100801","type":"journal-article","created":{"date-parts":[[2009,1,8]],"date-time":"2009-01-08T19:39:42Z","timestamp":1231443582000},"page":"1807-1816","source":"Crossref","is-referenced-by-count":13,"title":["Cyclic ADP-ribose Induces Ca2+ Release from Caffeine-insensitive Ca2+ Pools in Canine Salivary Gland Cells"],"prefix":"10.1177","volume":"77","author":[{"given":"H.","family":"Yamaki","sequence":"first","affiliation":[{"name":"Department of Removable Prosthodontics"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Morita","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Hiroshima University School of Dentistry, Kasumi 1-2-3, Minami-ku, Hiroshima 734-8553, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Kitayama","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Hiroshima University School of Dentistry, Kasumi 1-2-3, Minami-ku, Hiroshima 734-8553, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Y.","family":"Imai","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Hiroshima University School of Dentistry, Kasumi 1-2-3, Minami-ku, Hiroshima 734-8553, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Itadani","sequence":"additional","affiliation":[{"name":"Department of Removable Prosthodontics"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Y.","family":"Akagawa","sequence":"additional","affiliation":[{"name":"Department of Removable 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