Inhibition of Zinc-Dependent Histone Deacetylases with a Chemically Triggered Electrophile
- ACS Chem Biol. 2016 Jul 15;11(7):1844-51. doi: 10.1021/acschembio.6b00012.
- 1. Center for the Science of Therapeutics, Broad Institute , Cambridge, Massachusetts 02142, United States.
- 2. Department of Chemistry and Chemical Biology, Harvard University , Cambridge, Massachusetts 02138, United States.
- 3. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology , Cambridge, Massachusetts 02139, United States.
- 4. Department of Biological Engineering, Massachusetts Institute of Technology , Cambridge, Massachusetts 02139, United States.
- 5. Division of Hematology/Oncology, Boston Children's Hospital , Boston, Massachusetts 02116, United States.
- 6. Department of Biochemistry, Albert Einstein College of Medicine , Bronx, New York 10461, United States.
Unbiased binding assays involving small-molecule microarrays were used to identify compounds that display unique patterns of selectivity among members of the zinc-dependent histone deacetylase family of Enzymes. A novel, hydroxyquinoline-containing compound, BRD4354, was shown to preferentially inhibit activity of HDAC5 and HDAC9 in vitro. Inhibition of deacetylase activity appears to be time-dependent and reversible. Mechanistic studies suggest that the compound undergoes zinc-catalyzed decomposition to an ortho-quinone methide, which covalently modifies nucleophilic cysteines within the proteins. The covalent nature of the compound-enzyme interaction has been demonstrated in experiments with biotinylated probe compound and with electrospray ionization-mass spectrometry.
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