cyclic adp​ribose

Cyclic ADP-ribose (cADPR) is an effective calcium mobilization second messenger, which is synthesized from NAD + by ADP-ribosyl cyclase. Cyclic ADP-ribose mainly increases cytosolic calcium through Ryanodine receptor-mediated endoplasmic reticulum release

Cyclic ADP-ribose (cADP-ribose) is an endogenous metabolite of NAD+ that mobilizes the release of stored Ca2+ in the endoplasmic reticulum via ryanodine receptors in various cell types.[1],[2],[3],[4],[5] This second messenger is generated via the cADP-ribose synthases CD38 and CD157.[6],[5],[7] cADP-Ribose may also trigger the cell surface Ca2+ influx channel TRPM2 in a temperature-dependent manner.[8] In vitro, cADP-ribose modulates Ca2+ signaling in rat and mouse cardiomyocytes treated with isoproterenol , and treatment with this metabolite at 100 μM under heat stress conditions induces the release of oxytocin from the mouse hypothalamus.[9],[4]

Cyclic ADP-ribose ammonium (cADPR ammonium) is a powerful calcium mobilization second messenger synthesized from NAD+ by an ADP-ribosyl cyclase. It primarily raises cytosolic calcium levels through Ryanodine receptor-mediated release from the endoplasmic reticulum, while also facilitating extracellular influx through the opening of TRPM2 channels [1][2][3].

Cyclic ADP-ribose (cADP-ribose) is a calcium mobilizing nucleotide that is biosynthesized from NAD+ by cADP-ribose synthases, including CD38. cADP-Ribose appears to activate calcium channels in intracellular membranes, which in turn activate ryanodine receptors. 8-bromo-cADP-Ribose is a stable, cell-permeable analog that blocks calcium release evoked by cADP-ribose in sea urchin egg homogenates with an IC50 value of 1.7 μM. It is commonly used to investigate intracellular signaling through cADP-ribose in isolated cells and tissues.

8-Br-7-CH-cADPR disodium (7-Deaza-8-bromo-cADPR) 是一种有效的cADPR拮抗剂，该化合物能够部分抑制sTIR二聚化引起的钙浓度升高，并显著降低紫杉醇诱导的轴突变性。

8-Br-7-CH-cADPR (7-Deaza-8-bromo-cADPR) 是一种cADPR有效拮抗剂。该化合物能部分抑制sTIR二聚化引发的钙离子升高。此外，8-Br-7-CH-cADPR 对于降低紫杉醇诱导的轴突变性也有显著效果。

8-Br-cADPR为cADPR的高效拮抗剂,能有效减轻肾损伤并降低caspase-3与TRPM2的表达水平.