Journal article
Quantitative proteomic analysis of EZH2 inhibition in acute myeloid leukemia reveals the targets and pathways that precede the induction of cell death
Jarrod J Sandow, Giuseppe Infusini, Aliaksei Z Holik, Gabriela Brumatti, Tessa V Averink, Paul G Ekert, Andrew I Webb
PROTEOMICS CLINICAL APPLICATIONS | WILEY-V C H VERLAG GMBH | Published : 2017
Abstract
PURPOSE: Chromosomal translocation of the mixed lineage leukemia (MLL) locus generates fusion proteins that drive acute myeloid leukemia (AML) resulting in atypical histone methyltransferase activity and alterations in the epigenetic regulation of gene expression. Targeting histone regulators, such as Enhancer of Zeste Homologue 2 (EZH2), has shown promise in AML. Profiling differential protein expression following inhibition of epigenetic regulators in AML may help to identify novel targets for therapeutics. EXPERIMENTAL DESIGN: Murine models of AML combined with quantitative SILAC analysis were used to identify differentially expressed proteins following inhibition of EZH2 activity using 3..
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Awarded by NHMRC project
Funding Acknowledgements
This work was supported by NHMRC project grants # 1025594, # 1081376. GB is supported by Victorian Cancer Agency, Mid-career fellowship. This work was made possible through Victorian State Government Operational Infrastructure Support, and L. E. W. Carty Charitable Fund and Ian Rollo Currie Estate Foundation for infrastructure support.