Beside the MEF2 axis: Unconventional functions of HDAC4

被引：33
作者：
Clocchiatti, Andrea [1 ,2 ]
Di Giorgio, Eros [1 ,2 ]
Demarchi, Francesca [3 ]
Brancolini, Claudio [1 ,2 ]
机构：
[1] Univ Udine, Dipartimento Sci Med & Biol, I-33100 Udine, Italy
[2] Univ Udine, MATI Ctr Excellence, I-33100 Udine, Italy
[3] Lab Nazl CIB, I-34012 Trieste, Italy
来源：
CELLULAR SIGNALLING | 2013年 / 25卷 / 01期
关键词：
Histone deacetylase; MEF2; HIF; STAT1; FOXOs; Foxp3; Sumoylation; Metabolism; Muscle; LXB; II HISTONE DEACETYLASES; CONTROLS CHONDROCYTE HYPERTROPHY; FOXO TRANSCRIPTION FACTORS; GENE-EXPRESSION; MUSCLE ATROPHY; HYPOXIA; ACETYLATION; BINDING; ACTIVATION; PROMOTES;
D O I：
10.1016/j.cellsig.2012.10.002
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
The class Ila deacetylase HDAC4 is unequivocally known as a negative regulator of MEF2-dependent transcription. In the past years several works have allowed us to understand how different signals, mirroring specific environmental circumstances keep in check the repressive action of HDAC4 against MEF2s. At the same time, pieces of evidence have gradually accumulated about HDAC4 activities emancipated from MEF2s. The aim of this review is to discuss about these "unconventional functions" of HDAC4. (C) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码：269 / 276
页数：8
相关论文
共 83 条
[1]   MEF2C transcription factor controls chondrocyte hypertrophy and bone development [J].
Arnold, Michael A. ;
Kim, Yuri ;
Czubryt, Michael P. ;
Phan, Dillon ;
McAnally, John ;
Qi, Xiaoxia ;
Shelton, John M. ;
Richardson, James A. ;
Bassel-Duby, Rhonda ;
Olson, Eric N. .
DEVELOPMENTAL CELL, 2007, 12 (03) :377-389
[2]   Selective repression of MEF2 activity by PKA-dependent proteolysis of HDAC4 [J].
Backs, Johannes ;
Worst, Barbara C. ;
Lehmann, Lorenz H. ;
Patrick, David M. ;
Jebessa, Zegeye ;
Kreusser, Michael M. ;
Sun, Qiang ;
Chen, Lan ;
Heft, Claudia ;
Katus, Hugo A. ;
Olson, Eric N. .
JOURNAL OF CELL BIOLOGY, 2011, 195 (03) :403-415
[3]   Signaling pathways in skeletal muscle remodeling [J].
Bassel-Duby, Rhonda ;
Olson, Eric N. .
ANNUAL REVIEW OF BIOCHEMISTRY, 2006, 75 :19-37
[4]   Histone/protein deacetylases control Foxp3 expression and the heat shock response of T-regulatory cells [J].
Beier, Ulf H. ;
Akimova, Tatiana ;
Lu, Yujie ;
Wang, Liqing ;
Hancock, Wayne W. .
CURRENT OPINION IN IMMUNOLOGY, 2011, 23 (05) :670-678
[5]   Loss of Epigenetic Modification Driven by the Foxp3 Transcription Factor Leads to Regulatory T Cell Insufficiency [J].
Bettini, Matthew L. ;
Pan, Fan ;
Bettini, Maria ;
Finkelstein, David ;
Rehg, Jerold E. ;
Floess, Stefan ;
Bell, Bryan D. ;
Ziegler, Steven F. ;
Huehn, Jochen ;
Pardoll, Drew M. ;
Vignali, Dario A. A. .
IMMUNITY, 2012, 36 (05) :717-730
[6]  
Bodily J.M., 2010, CANCER RES, P1187
[7]   Structural and functional analysis of the human HDAC4 catalytic domain reveals a regulatory structural zinc-binding domain [J].
Bottomley, Matthew J. ;
Lo Surdo, Paola ;
Di Giovine, Paolo ;
Cirillo, Agostino ;
Scarpelli, Rita ;
Ferrigno, Federica ;
Jones, Philip ;
Neddermann, Petra ;
De Francesco, Raffaele ;
Steinkuhler, Christian ;
Gallinari, Paola ;
Carfi, Andrea .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2008, 283 (39) :26694-26704
[8]   Functional characterization of an amino-terminal region of HDAC4 that possesses MEF2 binding and transcriptional repressive activity [J].
Chan, JKL ;
Sun, LG ;
Yang, XJ ;
Zhu, G ;
Wu, ZG .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (26) :23515-23521
[9]   Histone deacetylase 7 maintains vascular integrity by repressing matrix metalloproteinase 10 [J].
Chang, Shurong ;
Young, Bryan D. ;
Li, Shijie ;
Qi, Xiaoxia ;
Richardson, James A. ;
Olson, Eric N. .
CELL, 2006, 126 (02) :321-334
[10]   Role of MEKK2-MEK5 in the regulation of TNF-α gene expression and MEKK2-MKK7 in the activation of c-Jun N-terminal kinase in mast cells [J].
Chayama, K ;
Papst, PJ ;
Garrington, TP ;
Pratt, JC ;
Ishizuka, T ;
Webb, S ;
Ganiatsas, S ;
Zon, LI ;
Sun, WY ;
Johnson, GL ;
Gelfand, EW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (08) :4599-4604
123456789