LSD1 demethylates repressive histone marks to promote androgen-receptor-dependent transcription

By E. Metzger, Melanie Wissmann, Na Yin, J. Müller, Robert Schneider, Antoine H. F. M. Peters, T. Günther, R. Buettner, R. Schüle. Nature, 2005

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Epigenetic Modifications as Therapeutic Targets (2010, background): “LSD1 targets the activating H3K4 mono- and dimethylation mark but can also target the repressive H3K9 dimethylation (H3K9me2) mark when complexed with the androgen recepto”
The X-linked mental retardation gene SMCX/JARID1C defines a family of histone H3 lysine 4 demethylases. (2007, neutral): “However, the recent discovery of a large number of histone demethylases indicates that demethylases play a central role in the regulation of histone methylation dynamics (Cloos et al., 2006; Fodor et al., 2006; Klose et al., 2006b; Metzger et al., 2005; Shi et al., 2004; Tsukada et al., 2006; Whetst”
Histone lysine demethylases: emerging roles in development, physiology and disease (2007, background): “and of transcription mediated by nuclear receptors (the androgen and oestrogen receptors, AR and ER) in mammal”
JmjC-domain-containing proteins and histone demethylation (2006, background): “org/uniprot/O60341">LSD1 (Lysine specific demethylase 1) was the founding member of a second class of enzymes that directly reverse histone H3K4 or H3K9 modifications by an oxidative demethylation reaction in which flavin is a cofacto”
SUV39H2 methylates and stabilizes LSD1 by inhibiting polyubiquitination in human cancer cells (2015, background): “LSD1 is involved in both transcriptional gene repression and activation through its demethylation of H3K4 and H3K9 [1, 5].”