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This may be related to sequestration of CoA within mitochondria, depletion of mitochondrial DNA, increased production of ROS, and alterations in gene expression [2]

Concentrations of the peptide up to 500 ng/mL failed to increase proliferation of mouse C2C12 cells or primary human skeletal muscle myoblasts, failed to inhibit myoblast differentiation, and failed to activate the signaling responses previously attributed to it, even as mature IGF-1 and full-length IGF-1Eb produced robust responses in the same assays