Guizhong Liu

TL;DR: Unlike Wnt antagonists, which exert their effects by molecular mimicry of Fz or Wnt sequestration through other mechanisms, Dkk-1 specifically inhibits canonical Wnt signalling by binding to the LRP6 component of the receptor complex.

TL;DR: It is demonstrated here that prototype canonical Wnt3a and noncanonical Wnt5a ligands specifically trigger completely unrelated endogenous coreceptors-LRP5/6 and Ror1/2, respectively-through a common mechanism that involves their Wnt-dependent coupling to the Frizzled (Fzd) coreceptor and recruitment of shared components.

TL;DR: These findings establish the involvement of autocrine Wnt signaling in human cancer cells and identify breast and ovarian tumor lines with upregulation of the uncomplexed transcriptionally active form of beta-catenin without mutations afflicting downstream components.

TL;DR: Data is presented suggesting that HFz6 activates the transforming growth factor-β-activated kinase-NEMO-like kinase pathway that blocks TCF/lymphoid enhancer factor binding to target promoters, thereby inhibiting the ability of β-catenin to activate transcription of Wnt target genes.

TL;DR: It is demonstrated here that wild-type LRP6 forms an inactive dimer through interactions mediated by epidermal growth factor repeat regions within the extracellular domain, establishing a novel mechanism for receptor activation which is opposite to the general paradigm of ligand-induced receptor oligomerization.