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Zuo et al., 2015)

A GIP receptor agonist exhibits beta-cell anti-apoptotic actions in rat models of diabetes resulting in improved beta-cell function and glycemic control

Interestingly, overexpression of the c-KIT tyrosine kinase, a key regulator of melanocytes, has been described in a great number of mucosal melanoma cases (from 39 to 88% depending on the study) and could be a marker or even a target for KIT inhibitors for the treatment of metastatic mucosal melanomas [3, 31]

Individual red and green channels of RBG images from the main figures are shown in Supplementary Fig

Documented mechanisms include: Gene expression modulation published research has measured GHK-Cu influence on the expression of over 4,000 genes related to repair, regeneration, antioxidant systems, and cellular aging Copper-dependent enzyme cofactor activity copper is required for several antioxidant enzymes (most notably superoxide dismutase), and GHK-Cu participates in copper delivery to these systems Collagen synthesis upregulation fibroblast cultures exposed to GHK-Cu produce measurably more Type I collagen than control conditions Glycosaminoglycan synthesis hyaluronic acid and related GAGs increase in research models Fibroblast proliferation and migration measured in cell culture studies Anti-inflammatory effects pro-inflammatory cytokine modulation in research models DNA repair pathway engagement research has documented effects on genes involved in cellular DNA repair The multi-pathway, multi-target nature of GHK-Cus mechanism is what makes the compound interesting in research contexts it doesnt fit the one receptor, one effect model of most synthetic peptides