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. 2021 Oct 11;97(8):423–461. doi: 10.2183/pjab.97.022

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© 2021 The Japan Academy

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 6. — The CD38-cADPR signal system for insulin secretion by glucose stimulation in β-cells (adapted from Ref. 94). Shown in red is the regulatory pathway for glucose-induced insulin secretion via the CD38-cADPR signal system. ATP competes with cADPR for the binding site (Lys-129, see also Section 5.2), inhibiting the cADPR hydrolysis which causes the accumulation of cADPR. cADPR binds to FKBP12.6 to release Ca²⁺, dissociating FKBP12.6 from RyR. CaM kinase II phosphorylates RyR to sensitize and activate the Ca²⁺ channel (Pi, phosphorylation). Ca²⁺, released from intracellular stores and/or supplied from extracellular sources, further activates CaM kinase II and amplifies the process. In this way, Ca²⁺-induced Ca²⁺ release may be explained.²⁸⁸⁾ The conventional insulin secretion mechanism by Ca²⁺ influx from extracellular sources is shown in black. CaM, calmodulin; RyR, ryanodine receptor; ADPR, ADP-ribose; A-kinase, cyclic AMP-dependent protein kinase.