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Knutson, V

AsiG subsequently targets PDAC cells that overexpress CD71 receptors and release siG in response to the high concentration of intracellular glutathione (GSH) upon disulfide bond breakage

In addition, when the proportions of S-OPA1 and L-OPA1, which mediate mitochondrial fusion are out of balance, mitochondrial fusion in osteoblasts is inhibited, and abnormal mitochondria produce large amounts of mtROS, thereby inducing osteoblast apoptosis [265]

Neuroinflammation 18 , 106 (2021)

To explore alternative mechanismsespecially its reported effect on intestinal glucose uptakewe aimed to minimize the confounding influence of incretin signaling