共查询到20条相似文献,搜索用时 31 毫秒
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The SUMO E3 ligase RanBP2 promotes modification of the HDAC4 deacetylase 总被引:13,自引:0,他引:13
Kirsh O Seeler JS Pichler A Gast A Müller S Miska E Mathieu M Harel-Bellan A Kouzarides T Melchior F Dejean A 《The EMBO journal》2002,21(11):2682-2691
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《Bioorganic & medicinal chemistry》2019,27(22):115087
Epigenetic control plays an important role in gene regulation through chemical modifications of DNA and post-translational modifications of histones. An essential post-translational modification is the histone acetylation/deacetylation-process which is regulated by histone acetyltransferases (HATs) and histone deacetylases (HDACs). The mammalian zinc dependent HDAC family is subdivided into three classes: class I (HDACs 1-3, 8), class II (IIa: HDACs 4, 5, 7, 9; IIb: HDACs 6, 10) and class IV (HDAC 11). In this review, recent studies on the biological role and regulation of class IIa HDACs as well as their contribution in neurodegenerative diseases, immune disorders and cancer will be presented. Furthermore, the development, synthesis, and future perspectives of selective class IIa inhibitors will be highlighted. 相似文献
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Li J Staver MJ Curtin ML Holms JH Frey RR Edalji R Smith R Michaelides MR Davidsen SK Glaser KB 《Life sciences》2004,74(22):2693-2705
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Cardiac hypertrophy is a form of global remodeling, although the initial step
seems to be an adaptation to increased hemodynamic demands. The characteristics
of cardiac hypertrophy include the functional reactivation of the arrested fetal
gene program, where histone deacetylases (HDACs) are closely linked in the
development of the process. To date, mammalian HDACs are divided into four
classes: I, II, III, and IV. By structural similarities, class II HDACs are then
subdivided into IIa and IIb. Among class I and II HDACs, HDAC2, 4, 5, and 9 have
been reported to be involved in hypertrophic responses; HDAC4, 5, and 9 are
negative regulators, whereas HDAC2 is a pro-hypertrophic mediator. The molecular
function and regulation of class IIa HDACs depend largely on the
phosphorylation-mediated cytosolic redistribution, whereas those of HDAC2 take
place primarily in the nucleus. In response to stresses, posttranslational
modification (PTM) processes, dynamic modifications after the translation of
proteins, are involved in the regulation of the activities of those
hypertrophy-related HDACs. In this article, we briefly review 1) the activation
of HDAC2 in the development of cardiac hypertrophy and 2) the PTM of HDAC2 and
its implications in the regulation of HDAC2 activity. [BMB Reports 2015; 48(3):
131-138] 相似文献
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Wang AH Kruhlak MJ Wu J Bertos NR Vezmar M Posner BI Bazett-Jones DP Yang XJ 《Molecular and cellular biology》2000,20(18):6904-6912
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Histone deacetylase 8 safeguards the human ever-shorter telomeres 1B (hEST1B) protein from ubiquitin-mediated degradation
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Lee H Sengupta N Villagra A Rezai-Zadeh N Seto E 《Molecular and cellular biology》2006,26(14):5259-5269
Histone deacetylases (HDACs) are enzymes that regulate the functions of histones as well as nonhistones by catalyzing the removal of acetyl groups from lysine residues. HDACs regulate many biological processes, including the cell division cycle and tumorigenesis. Although recent studies have implicated HDAC8 in tumor cell proliferation, the molecular mechanisms linking HDAC8 to cell growth remain unknown. Here, we report that the human ortholog of the yeast ever-shorter telomeres 1B (EST1B) binds HDAC8. This interaction is regulated by protein kinase A-mediated HDAC8 phosphorylation and protects human EST1B (hEST1B) from ubiquitin-mediated degradation. Phosphorylated HDAC8 preferentially recruits Hsp70 to a complex that inhibits the CHIP (C-terminal heat shock protein interacting protein) E3 ligase-mediated degradation of hEST1B. Importantly, HDAC8 regulation of hEST1B protein stability modulates total telomerase enzymatic activity. Our findings reveal a novel mechanism by which HDAC8 contributes to tumorigenesis by regulating telomerase activity. 相似文献
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Chiara V. Segré Silvia Senese Sara Loponte Stefano Santaguida Paolo Soffientini Gabriela Grigorean 《MABS-AUSTIN》2016,8(1):37-42
Histone deacetylases (HDACs) are modification enzymes that regulate a plethora of biological processes. HDAC1, a crucial epigenetic modifier, is deregulated in cancer and subjected to a variety of post-translational modifications. Here, we describe the generation of a new monoclonal antibody that specifically recognizes a novel highly dynamic prophase phosphorylation of serine 406-HDAC1, providing a powerful tool for detecting early mitotic cells. 相似文献
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Histone deacetylases (HDACs) play important roles in fundamental cellular processes, and HDAC inhibitors are emerging as promising cancer therapeutics. p73, a member of the p53 family, plays a critical role in tumor suppression and neural development. Interestingly, p73 produces two classes of proteins with opposing functions: the full-length TAp73 and the N-terminally truncated ΔNp73. In the current study, we sought to characterize the potential regulation of p73 by HDACs and found that histone deacetylase 1 (HDAC1) is a key regulator of TAp73 protein stability. Specifically, we showed that HDAC1 inhibition by HDAC inhibitors or by siRNA shortened the half-life of TAp73 protein and subsequently decreased TAp73 expression under normal and DNA damage-induced conditions. Mechanistically, we found that HDAC1 knockdown resulted in hyperacetylation and inactivation of heat shock protein 90, which disrupted the interaction between heat shock protein 90 and TAp73 and thus promoted the proteasomal degradation of TAp73. Functionally, we found that down-regulation of TAp73 was required for the enhanced cell migration mediated by HDAC1 knockdown. Together, we uncover a novel regulation of TAp73 protein stability by HDAC1-heat shock protein 90 chaperone complex, and our data suggest that TAp73 is a critical downstream mediator of HDAC1-regulated cell migration. 相似文献