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Randall T. Moon

Researcher at University of Washington

Publications -  305
Citations -  54792

Randall T. Moon is an academic researcher from University of Washington. The author has contributed to research in topics: Wnt signaling pathway & Signal transduction. The author has an hindex of 119, co-authored 305 publications receiving 51964 citations. Previous affiliations of Randall T. Moon include Marine Biological Laboratory & Howard Hughes Medical Institute.

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WNT signalling pathways as therapeutic targets in cancer

TL;DR: This work has shown that WNTs and their downstream effectors regulate various processes that are important for cancer progression, including tumour initiation, tumour growth, cell senescence, cell death, differentiation and metastasis, and improved drug-discovery platforms and new technologies have facilitated the discovery of agents that can alter WNT signalling in preclinical models.
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WNT and β-catenin signalling: diseases and therapies

TL;DR: WNT signalling has been studied primarily in developing embryos, but WNTs also have important functions in adults, and aberrant signalling by WNT pathways is linked to a range of diseases, most notably cancer.
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A second canon. Functions and mechanisms of beta-catenin-independent Wnt signaling.

TL;DR: Recent developments in both the functions and mechanisms of noncanonical Wnt signaling are reviewed, and some challenges and difficulties the field faces are outlined.
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The axis-inducing activity, stability, and subcellular distribution of beta-catenin is regulated in Xenopus embryos by glycogen synthase kinase 3.

TL;DR: It is demonstrated thatosphorylation of beta-catenin in vivo requires an in vitro amino-terminal Xgsk-3 phosphorylation site, which is conserved in the Drosophila protein armadillo, which provides a basis for understanding the interaction between XgSk-3 and beta-catsin in the establishment of the dorsal-ventral axis in early Xenopus embryos.
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Proximal events in Wnt signal transduction

TL;DR: Intriguingly, the transmembrane receptor Tyr kinases Ror2 and Ryk, as well as Frizzled receptors that act independently of LRP5 or LRP6, function as receptors for Wnt and activate β-catenin-independent pathways, which leads to changes in cell movement and polarity and to the antagonism of the β- catenin pathway.