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This, in turn, could either lead to supplementation in the event of deficient endogenous Wnt signaling with the supplemental Wnts doubling as agonists or prompt the restoration of Wnt signaling if the endogenous function is completely absent (which could be investigated in knockout models)

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Mitchell CB, Black B, Sun F, Chrzanowski W, Cooper-White J, Maisonneuve B, et al
