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As recently deciphered, JNK emerges as a key culprit in APAP-induced hepatocellular death and liver damaged caused by a Sab-dependent mechanism that involves inactivation of intramitochondrial Src in the MIM, which in turn inhibits electron transport, increases ROS, and sustains JNK activation (Win et al., 2016)
Journal of Investigative Dermatology, 1999 PubMed The tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+ stimulates matrix metalloproteinase-2 expression by fibroblast cultures Simon A, Emonard H, Hornebeck W, Maquart FX Life Sciences, 2000 PubMed Expression of glycosaminoglycans and small proteoglycans in wounds: modulation by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+ Simon A, Wegrowski Y, Bontemps Y, Maquart FX Journal of Investigative Dermatology, 2000 PubMed These papers establish GHK-Cu's documented effect on matrix metalloproteinase activity and extracellular matrix components in wound-healing models
