In vivo target protein degradation induced by PROTACs based on E3 ligase DCAF15
Author:
Funder
National Natural Science Foundation of China
Publisher
Springer Science and Business Media LLC
Subject
Cancer Research,Genetics
Link
http://www.nature.com/articles/s41392-020-00245-0.pdf
Reference5 articles.
1. Sun, X. et al. PROTACs: great opportunities for academia and industry. Signal Transduct. Target Ther.4, 64 (2019).
2. Han, T. et al. Anticancer sulfonamides target splicing by inducing RBM39 degradation via recruitment to DCAF15. Science356, eaal3755 (2017).
3. Zhang, X., Crowley, V. M., Wucherpfennig, T. G., Dix, M. M. & Cravatt, B. F. Electrophilic PROTACs that degrade nuclear proteins by engaging DCAF16. Nat. Chem. Biol.15, 737–746 (2019).
4. Zoppi, V. et al. Iterative design and optimization of initially inactive proteolysis targeting chimeras (PROTACs) Identify VZ185 as a potent, fast, and selective von Hippel-Lindau (VHL) based dual degrader probe of BRD9 and BRD7. J. Med Chem.62, 699–726 (2019).
5. Du, X. et al. Structural basis and kinetic pathway of RBM39 recruitment to DCAF15 by a sulfonamide molecular glue E7820. Structure27, 1625–1633. e3 (2019).
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