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It has been reported that pyrvinium pamoate (PyrPam), an FDA (U.S. Food and Drug Administration)-approved anthelminthic drug, is a potent inhibitor of Wnt signalling by a mechanism which implies the direct activation of protein kinase CK1α. In the present paper, we provide data ruling out any direct stimulatory effect of PyrPam on CK1, by showing that the catalytic activity of CK1α and those of its isoforms δ and γ1 are not significantly affected by PyrPam when tested with the aid of specific peptide and protein substrates. Accordingly, cell treatment with PyrPam has no significant effect on the phosphorylation of β-catenin Ser⁴⁵. By contrast, the phosphorylation of β-catenin Thr⁴¹ is increased upon cell treatment with PyrPam, through a mechanism that implies the upstream dephosphorylation of Akt/PKB (protein kinase B) and of GSK3 (glycogen synthase kinase 3). It can be concluded from the present study that …