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Chu, Qian

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Chu

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Chu, Qian
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    I. Targeted β-catenin Ubiquitination and Degradation Using Bifunctional Stapled Peptides II. Studies on Cell Penetration by Stapled Peptides
    (2014-02-25) Chu, Qian; Verdine, Gregory L.; Liu, David; Saghatelian, Alan
    Hydrocarbon-stapled alpha-helical peptides represent a relatively new class of synthetic peptidomimetics capable of inhibiting protein-protein interactions. It has been shown that hydrocarbon "staples" spanning one or two helical turns in a peptide increase alpha-helical content and protease resistance, enhance target binding affinity, and promote cell penetration. This technology has been applied to the development of cell-permeable ligands targeting several intracellular targets. This dissertation describes efforts to further the development of stapled peptide technology.
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    Inhibition of Oncogenic Wnt Signaling through Direct Targeting of β-Catenin
    (Proceedings of the National Academy of Sciences, 2012) Grossmann, Tom N.; Yeh, Johannes Johannes; Bowman, Brian R.; Chu, Qian; Moellering, Raymond E.; Verdine, Gregory
    Aberrant activation of signaling by the Wnt pathway is strongly implicated in the onset and progression of numerous types of cancer. Owing to the persistent dependence of these tumors on Wnt signaling for growth and survival, inhibition of this pathway is considered an attractive mechanism-based therapeutic approach. Oncogenic activation of Wnt signaling can ensue from a variety of distinct aberrations in the signaling pathway, but most share the common feature of causing increased cellular levels of β-catenin by interfering with its constitutive degradation. β-Catenin serves as a central hub in Wnt signaling by engaging in crucial protein–protein interactions with both negative and positive effectors of the pathway. Direct interference with these protein–protein interactions is a biologically compelling approach toward suppression of β-catenin hyperactivity, but such interactions have proven intransigent with respect to small-molecule targeting. Hence β-catenin remains an elusive target for translational cancer therapy. Here we report the discovery of a hydrocarbon-stapled peptide that directly targets β-catenin and interferes with its ability to serve as a transcriptional coactivator for T-cell factor (TCF) proteins, the downstream transcriptional regulators of the Wnt pathway.