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On the basis of these observations, and as suggested by our model in which HPV-16 E7 occupies the space between Cys 47 and Cys 101 of GSTP1 and prevents both intramolecular and intermolecular disulfide formation, we propose that HPV-16 E7 binding might protect GSTP1 against inactivation via oxidative attacks at Cys 47 and/or Cys 101

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GHK-Cu shows optimal effects at surprisingly low concentrations because at higher concentrations it also ramps up collagen-degrading enzymes

There was no statistically significant difference in the frequency of side effects between groups (logRR=0.36