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10.1001/jama.2018.7614 JAMA 56 XiangD.LuJ.WeiC.CaiX.WangY.LiangY.et al (2020)

This observation was mechanistically determined to be in part due to A 142 binding directly to COX1 and inducing loss of enzymatic activity of the greater mitochondrial electron transport chain complex 4 (C4), of which COX1 is an integral part

It helps clinicians confirm exposure, identify unexpected toxic agents, and rule out alternative diagnoses (Ghandi et al., 2024)

Activation of this pathway results in protein synthesis, hypertrophy and inhibition of the key ubiquitin ligase atrogin-1 by inactivating Foxo factors[82], IGF-IR also phosphorylates Shc, which subsequently activates the RAS/Raf/MEK pathway leading to cell proliferation and mitogenesis[2]