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Smyd3 regulates cancer cell phenotypes and catalyzes histone H4 lysine 5 methylation
Authors:Glenn S. Van Aller  Nicolas Reynoird  Olena Barbash  Michael Huddleston  Shichong Liu  Anne-Flore Zmoos  Patrick McDevitt  Robert Sinnamon  BaoChau Le  Gloria Mas  Roland Annan  Julien Sage  Benjamin A. Garcia  Peter J. Tummino  Or Gozani  Ryan G. Kruger
Affiliation:1.GlaxoSmithKline; Collegeville, PA USA;2.Department of Biolog; Stanford University; Stanford, CA USA;3.Department of Molecular Biology; Princeton University; Princeton NJ USA;4.Department of Pediatrics; Stanford School of Medicine; Stanford, CA USA;5.Department of Biology; Stanford University; Stanford, CA USA
Abstract:
Smyd3 is a lysine methyltransferase implicated in chromatin and cancer regulation. Here we show that Smyd3 catalyzes histone H4 methylation at lysine 5 (H4K5me). This novel histone methylation mark is detected in diverse cell types and its formation is attenuated by depletion of Smyd3 protein. Further, Smyd3-driven cancer cell phenotypes require its enzymatic activity. Thus, Smyd3, via H4K5 methylation, provides a potential new link between chromatin dynamics and neoplastic disease.
Keywords:cancer   epigenetics   lysine   methylation   oncogene   oncology   Smyd3
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