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Epigenetic Regulation by Lysine Demethylase 5 (KDM5) Enzymes in Cancer
Department of Pathology, Yale University School of Medicine, New Haven, CT, USA
* Author to whom correspondence should be addressed.
Received: 30 January 2011; in revised form: 7 March 2011 / Accepted: 8 March 2011 / Published: 16 March 2011
Abstract: Similar to genetic alterations, epigenetic aberrations contribute significantly to tumor initiation and progression. In many cases, these changes are caused by activation or inactivation of the regulators that maintain epigenetic states. Here we review our current knowledge on the KDM5/JARID1 family of histone demethylases. This family of enzymes contains a JmjC domain and is capable of removing tri- and di- methyl marks from lysine 4 on histone H3. Among these proteins, RBP2 mediates drug resistance while JARID1B is required for melanoma maintenance. Preclinical studies suggest inhibition of these enzymes can suppress tumorigenesis and provide strong rationale for development of their inhibitors for use in cancer therapy.
Keywords: KDM5; JARID1; RBP2; PLU1; SMCX; SMCY; LID; histone demethylase; cancer stem cell; drug resistance
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MDPI and ACS Style
Blair, L.P.; Cao, J.; Zou, M.R.; Sayegh, J.; Yan, Q. Epigenetic Regulation by Lysine Demethylase 5 (KDM5) Enzymes in Cancer. Cancers 2011, 3, 1383-1404.
Blair LP, Cao J, Zou MR, Sayegh J, Yan Q. Epigenetic Regulation by Lysine Demethylase 5 (KDM5) Enzymes in Cancer. Cancers. 2011; 3(1):1383-1404.
Blair, Lauren P.; Cao, Jian; Zou, Mike Ran; Sayegh, Joyce; Yan, Qin. 2011. "Epigenetic Regulation by Lysine Demethylase 5 (KDM5) Enzymes in Cancer." Cancers 3, no. 1: 1383-1404.