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SMYD3-Mediated H2A.Z.1 Methylation Promotes Cell Cycle and Cancer Proliferation
2016
Cancer Research
SMYD3 methyltransferase is nearly undetectable in normal human tissues but highly expressed in several cancers, including breast cancer, although its contributions to pathogenesis in this setting are unclear. Here we report that histone H2A.Z.1 is a substrate of SMYD3 that supports malignancy. SMYD3-mediated dimethylation of H2A.Z.1 at lysine 101 (H2A.Z.1K101me2) increased stability by preventing binding to the removal chaperone ANP32E and facilitating its interaction with histone H3. Moreover,
doi:10.1158/0008-5472.can-16-0500
pmid:27569210
fatcat:dnpab6gok5fp7hz73soypmyiq4