If i stand correct: wnt agonist works the same way as wnt's, they need the LRP5/6 + frizzled receptor to phosphorylze GSK3b, so that B-cetanin can be trans located to the nuclies, and genes such as tcf(important for hair growth), can be activated.
now in aga we many inhibitors one of the is DKK1 which block the above mentioned receptor where wnt does its work. GSk3b inhibitors like vpa or more selective 6BIO , don't need the frizzeled + lrp5-6 receptors, it enters the cell, and immediately starts gsk3b phosphorylation of GSK3 that leads to b-cetanin accumulation and translocation to the nuclies(what we need). so it is a shortcut and it overrules the inhibitory effect of dkk1. it is why i believe that gsk3b inhibitors have more potential in vivo.
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