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There are two main limitations of the redox array: firstly, a positive signal on the array could also be due to a biotinylated protein that binds to the antibody specific ligand thus resulting in a false positive signal

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Next, these membranes were washed three times with TBST, and were incubate with the goat anti-rabbit IgG antibody (Abclonal, Wuhan, China) diluted 1: 10,000 for 1 h followed by triple washing with TBST

But if androgen receptor density is such a dominant driver of anabolic response, how do you reconcile this with the fact that chronic low-grade inflammation (particularly via IL-6/STAT3 and TNF-/NF-B signaling) can suppress AR nuclear translocation even when receptor count is high and that in some individuals this blunts hypertrophy more dramatically than CAG-repeat length or hormone levels themselves?