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pylori -infected gastric tissue by provoking a semimature state of DCs, which was dependent on glutamate produced as result of GT activity (Oertli et al., 2013

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Glucagon binds to GCGR on pancreatic -cells, and the activated receptor then binds to the G protein G, leading to the activation of adenylate cyclase (AC) and the formation of cAMP, which results in increased blood glucose levels[5]

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