Class I lysine deacetylases promote glucocorticoid-induced transcriptional repression through functional interaction with LSD1

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• 作者：Nina M. Patrick^a ; ^b ; Chanel A. Griggs^b ; Ali L. Icenogle^b ; Maryam M. Gilpatrick^b ; Vineela Kadiyala^b ; ^c ; ¹ ; Rosa Jaime-Frias^b ; Catharine L. Smith ; PhD^b ; ^{csmith@pharmacy.arizona.edu}
• 关键词：KDAC ; lysine deacetylase ; KDACi ; lysine deacetylase inhibitor ; KAT ; lysine acetyltransferase ; GR ; glucocorticoid receptor ; VPA ; valproic acid ; NR ; nuclear receptor ; Dex ; dexamethasone ; GAPDH ; glyceraldehyde 3-phosphate dehydrogenase ; HDAC ; histone deacetylase ; HDACi ; HDAC inhibitor ; HAT ; histone acetyltransferase ; RT-qPCR ; real time quantitative polymerase chain reaction ; Ct ; threshold cycle ; siRNA ; small interfering RNA ; LSD1 ; lysine-specific demethylase 1 ; AR ; androgen receptor ; CoREST ; co-rep
• 刊名：The Journal of Steroid Biochemistry and Molecular Biology
• 出版年：2017
• 出版时间：March 2017
• 年：2017
• 卷：167
• 期：Complete
• 页码：1-13
• 全文大小：2657 K
• 卷排序：167

文摘

Lysine deacetylases (KDACs or HDACs) are required for glucocorticoid-mediated transcriptional repression in a gene-selective fashion. KDACs promote transcriptional repression through suppression of LSD1 complex activity at selected target promoters. Pharmacological modulation of KDACs or LSD1 in treatment of disease could significantly impact glucocorticoid-regulated transcription and alter cellular response.