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. 2022 May 6;36(13-15):920–952. doi: 10.1089/ars.2021.0113

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© Petr Ježek et al., 2022; Published by Mary Ann Liebert, Inc.

This Open Access article is distributed under the terms of the Creative Commons License [CC-BY] (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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FIG. 1. — Redox signaling triggers GSIS in parallel with ATP. (A) Hypothetical model based on Plecita-Hlavata et al. (194), in which only K_ATP is redox-regulated; K_ATP closure is only possible when H₂O₂ and ATP are elevated. (B) Extended hypothetical model, in which TRPM2 is also redox-activated. For an explanation, see the Introduction section and the Plasma Membrane Depolarization in Pancreatic β-Cells section. G6PDH, glucose-6-phosphate dehydrogenase; GSIS, glucose-stimulated insulin secretion; K_ATP, ATP-sensitive K⁺ channel; TRPM, transient receptor potential melastin.