The many roles of histone deacetylases in development and physiology: implications for disease and therapy (original) (raw)
Cheung, W. L., Briggs, S. D. & Allis, C. D. Acetylation and chromosomal functions. Curr. Opin. Cell Biol.12, 326–333 (2000). ArticleCASPubMed Google Scholar
Grunstein, M. Histone acetylation in chromatin structure and transcription. Nature389, 349–352 (1997). ArticleCASPubMed Google Scholar
Clayton, A. L., Hazzalin, C. A. & Mahadevan, L. C. Enhanced histone acetylation and transcription: a dynamic perspective. Mol. Cell23, 289–296 (2006). ArticleCASPubMed Google Scholar
Shahbazian, M. D. & Grunstein, M. Functions of site-specific histone acetylation and deacetylation. Annu. Rev. Biochem.76, 75–100 (2007). ArticleCASPubMed Google Scholar
Ruthenburg, A. J., Li, H., Patel, D. J. & Allis, C. D. Multivalent engagement of chromatin modifications by linked binding modules. Nature Rev. Mol. Cell Biol.8, 983–994 (2007). ArticleCAS Google Scholar
Rundlett, S. E. et al. HDA1 and RPD3 are members of distinct yeast histone deacetylase complexes that regulate silencing and transcription. Proc. Natl Acad. Sci. USA93, 14503–14508 (1996). ArticleCASPubMedPubMed Central Google Scholar
Wang, A., Kurdistani, S. K. & Grunstein, M. Requirement of Hos2 histone deacetylase for gene activity in yeast. Science298, 1412–1414 (2002). ArticleCASPubMed Google Scholar
De Nadal, E. et al. The MAPK Hog1 recruits Rpd3 histone deacetylase to activate osmoresponsive genes. Nature427, 370–374 (2004). ArticleCASPubMed Google Scholar
Nusinzon, I. & Horvath, C. M. Histone deacetylases as transcriptional activators? Role reversal in inducible gene regulation. Sci. STKE296, re11 (2005). Google Scholar
Glaser, K. B. et al. Gene expression profiling of multiple histone deacetylase (HDAC) inhibitors: defining a common gene set produced by HDAC inhibition in T24 and MDA carcinoma cell lines. Mol. Cancer Ther.2, 151–163 (2003). CASPubMed Google Scholar
Montgomery, R. L. et al. Histone deacetylases 1 and 2 redundantly regulate cardiac morphogenesis, growth, and contractility. Genes Dev.21, 1790–1802 (2007). Reports the first conditional knockout of a class I HDAC. ArticleCASPubMedPubMed Central Google Scholar
Lahm, A. et al. Unraveling the hidden catalytic activity of vertebrate class IIa histone deacetylases. Proc. Natl Acad. Sci. USA104, 17335–17340 (2007). Describes the mechanism for the loss of enzymatic activity in class IIa HDACs. ArticleCASPubMedPubMed Central Google Scholar
Schwer, B. & Verdin, E. Conserved metabolic regulatory functions of sirtuins. Cell. Metab.7, 104–112 (2008). ArticleCASPubMed Google Scholar
Longo, V. D. & Kennedy, B. K. Sirtuins in aging and age-related disease. Cell126, 257–268 (2006). ArticleCASPubMed Google Scholar
Guarente, L. Sirtuins as potential targets for metabolic syndrome. Nature444, 868–874 (2006). ArticleCASPubMed Google Scholar
Bordone, L. & Guarente, L. Calorie restriction, SIRT1 and metabolism: understanding longevity. Nature Rev. Mol. Cell Biol.6, 298–305 (2005). ArticleCAS Google Scholar
Taunton, J., Hassig, C. A. & Schreiber, S. L. A mammalian histone deacetylase related to the yeast transcriptional regulator Rpd3p. Science272, 408–411 (1996). A seminal paper describing the cloning of the first mammalian HDAC. ArticleCASPubMed Google Scholar
Yang, X. J. & Seto, E. The Rpd3/Hda1 family of lysine deacetylases: from bacteria and yeast to mice and men. Nature Rev. Mol. Cell Biol.9, 206–218 (2008). An elegant review about the classical HDAC family. ArticleCAS Google Scholar
Kurdistani, S. K. & Grunstein, M. Histone acetylation and deacetylation in yeast. Nature Rev. Mol. Cell Biol.4, 276–284 (2003). ArticleCAS Google Scholar
Yang, X. J. & Seto, E. Collaborative spirit of histone deacetylases in regulating chromatin structure and gene expression. Curr. Opin. Genet. Dev.13, 143–153 (2003). ArticleCASPubMed Google Scholar
Vega, R. B. et al. Protein kinases C and D mediate agonist-dependent cardiac hypertrophy through nuclear export of histone deacetylase 5. Mol. Cell Biol.24, 8374–8385 (2004). ArticleCASPubMedPubMed Central Google Scholar
McKinsey, T. A., Zhang, C. L., Lu, J. & Olson, E. N. Signal-dependent nuclear export of a histone deacetylase regulates muscle differentiation. Nature408, 106–111 (2000). The first study to show that class IIa HDACs are signal-responsive modulators of gene expression. ArticleCASPubMedPubMed Central Google Scholar
Lu, J., McKinsey, T. A., Nicol, R. L. & Olson, E. N. Signal-dependent activation of the MEF2 transcription factor by dissociation from histone deacetylases. Proc. Natl Acad. Sci. USA97, 4070–4075 (2000). ArticleCASPubMedPubMed Central Google Scholar
Passier, R. et al. CaM kinase signaling induces cardiac hypertrophy and activates the MEF2 transcription factor in vivo. J. Clin. Invest.105, 1395–1406 (2000). ArticleCASPubMedPubMed Central Google Scholar
Lu, J., McKinsey, T. A., Zhang, C. L. & Olson, E. N. Regulation of skeletal myogenesis by association of the MEF2 transcription factor with class II histone deacetylases. Mol. Cell6, 233–244 (2000). ArticleCASPubMed Google Scholar
Youn, H. D., Grozinger, C. M. & Liu, J. O. Calcium regulates transcriptional repression of myocyte enhancer factor 2 by histone deacetylase 4. J. Biol. Chem.275, 22563–22567 (2000). ArticleCASPubMed Google Scholar
Wang, A. H. et al. HDAC4, a human histone deacetylase related to yeast HDA1, is a transcriptional corepressor. Mol. Cell Biol.19, 7816–7827 (1999). ArticleCASPubMedPubMed Central Google Scholar
Zhang, C. L. et al. Class II histone deacetylases act as signal-responsive repressors of cardiac hypertrophy. Cell110, 479–488 (2002). Describes the first knockout of a class IIa HDAC. ArticleCASPubMedPubMed Central Google Scholar
Chang, S. et al. Histone deacetylases 5 and 9 govern responsiveness of the heart to a subset of stress signals and play redundant roles in heart development. Mol. Cell Biol.24, 8467–8476 (2004). ArticleCASPubMedPubMed Central Google Scholar
Vega, R. B. et al. Histone deacetylase 4 controls chondrocyte hypertrophy during skeletogenesis. Cell119, 555–566 (2004). ArticleCASPubMed Google Scholar
Chang, S. et al. Histone deacetylase 7 maintains vascular integrity by repressing matrix metalloproteinase 10. Cell126, 321–334 (2006). Reports the first conditional class IIa HDAC knockout. ArticleCASPubMed Google Scholar
Fischle, W. et al. Enzymatic activity associated with class II HDACs is dependent on a multiprotein complex containing HDAC3 and SMRT/N-CoR. Mol. Cell9, 45–57 (2002). The first definitive report showing that class IIa HDAC enzymatic activity is due to the copurification of class I HDACs. ArticleCASPubMed Google Scholar
Jones, P. et al. Probing the elusive catalytic activity of vertebrate class IIa histone deacetylases. Bioorg. Med. Chem. Lett.18, 1814–1819 (2008). ArticleCASPubMed Google Scholar
Zhang, C. L., McKinsey, T. A., Lu, J. R. & Olson, E. N. Association of COOH-terminal-binding protein (CtBP) and MEF2-interacting transcription repressor (MITR) contributes to transcriptional repression of the MEF2 transcription factor. J. Biol. Chem.276, 35–39 (2001). ArticleCASPubMed Google Scholar
Zhang, C. L., McKinsey, T. A. & Olson, E. N. Association of class II histone deacetylases with heterochromatin protein 1: potential role for histone methylation in control of muscle differentiation. Mol. Cell Biol.22, 7302–7312 (2002). ArticleCASPubMedPubMed Central Google Scholar
Zhang, C. L., McKinsey, T. A. & Olson, E. N. The transcriptional corepressor MITR is a signal-responsive inhibitor of myogenesis. Proc. Natl Acad. Sci. USA98, 7354–7359 (2001). ArticleCASPubMedPubMed Central Google Scholar
Dressel, U. et al. A dynamic role for HDAC7 in MEF2-mediated muscle differentiation. J. Biol. Chem.276, 17007–17013 (2001). ArticleCASPubMed Google Scholar
Bottomley, M. J. et al. Structural and functional analysis of the human HDAC4 catalytic domain reveals a regulatory structural zinc-binding domain. J. Biol. Chem.283, 26694–26704 (2008). ArticleCASPubMedPubMed Central Google Scholar
Schuetz, A. et al. Human HDAC7 harbors a class IIa histone deacetylase-specific zinc binding motif and cryptic deacetylase activity. J. Biol. Chem.283, 11355–11363 (2008). ArticleCASPubMedPubMed Central Google Scholar
Zhang, Y. et al. Mice lacking histone deacetylase 6 have hyperacetylated tubulin but are viable and develop normally. Mol. Cell Biol.28, 1688–1701 (2008). Describes the first knockout of a class IIb HDAC. ArticleCASPubMedPubMed Central Google Scholar
Fischer, D. D. et al. Isolation and characterization of a novel class II histone deacetylase, HDAC10. J. Biol. Chem.277, 6656–6666 (2002). ArticleCASPubMed Google Scholar
Guardiola, A. R. & Yao, T. P. Molecular cloning and characterization of a novel histone deacetylase HDAC10. J. Biol. Chem.277, 3350–3356 (2002). ArticleCASPubMed Google Scholar
Tang, X. et al. Acetylation-dependent signal transduction for type I interferon receptor. Cell131, 93–105 (2007). ArticleCASPubMed Google Scholar
Kovacs, J. J. et al. HDAC6 regulates Hsp90 acetylation and chaperone-dependent activation of glucocorticoid receptor. Mol. Cell18, 601–607 (2005). ArticleCASPubMed Google Scholar
Hubbert, C. et al. HDAC6 is a microtubule-associated deacetylase. Nature417, 455–458 (2002). ArticleCASPubMed Google Scholar
Gao, L., Cueto, M. A., Asselbergs, F. & Atadja, P. Cloning and functional characterization of HDAC11, a novel member of the human histone deacetylase family. J. Biol. Chem.277, 25748–25755 (2002). ArticleCASPubMed Google Scholar
Liu, H., Hu, Q., Kaufman, A., D'Ercole, A. J. & Ye, P. Developmental expression of histone deacetylase 11 in the murine brain. J. Neurosci. Res.86, 537–543 (2008). ArticleCASPubMedPubMed Central Google Scholar
Lagger, G. et al. Essential function of histone deacetylase 1 in proliferation control and CDK inhibitor repression. EMBO J.21, 2672–2681 (2002). Reports the first knockout of a class I HDAC ArticleCASPubMedPubMed Central Google Scholar
Zupkovitz, G. et al. Negative and positive regulation of gene expression by mouse histone deacetylase 1. Mol. Cell Biol.26, 7913–7928 (2006). ArticleCASPubMedPubMed Central Google Scholar
Yamaguchi, M. et al. Histone deacetylase 1 regulates retinal neurogenesis in zebrafish by suppressing Wnt and Notch signaling pathways. Development132, 3027–3043 (2005). ArticleCASPubMed Google Scholar
Cunliffe, V. T. Histone deacetylase 1 is required to repress Notch target gene expression during zebrafish neurogenesis and to maintain the production of motoneurones in response to hedgehog signalling. Development131, 2983–2995 (2004). ArticleCASPubMed Google Scholar
Cunliffe, V. T. & Casaccia-Bonnefil, P. Histone deacetylase 1 is essential for oligodendrocyte specification in the zebrafish CNS. Mech. Dev.123, 24–30 (2006). ArticleCASPubMed Google Scholar
Pillai, R., Coverdale, L. E., Dubey, G. & Martin, C. C. Histone deacetylase 1 (HDAC-1) required for the normal formation of craniofacial cartilage and pectoral fins of the zebrafish. Dev. Dyn.231, 647–654 (2004). ArticleCASPubMed Google Scholar
Nambiar, R. M., Ignatius, M. S. & Henion, P. D. Zebrafish colgate/hdac1 functions in the non-canonical Wnt pathway during axial extension and in Wnt-independent branchiomotor neuron migration. Mech. Dev.124, 682–698 (2007). ArticleCASPubMedPubMed Central Google Scholar
Farooq, M. et al. Histone deacetylase 3 (hdac3) is specifically required for liver development in zebrafish. Dev. Biol.317, 336–353 (2008). ArticleCASPubMed Google Scholar
Trivedi, C. M. et al. Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3 beta activity. Nature Med.13, 324–331 (2007). ArticleCASPubMed Google Scholar
Voss, A. K., Thomas, T. & Gruss, P. Efficiency assessment of the gene trap approach. Dev. Dyn.212, 171–180 (1998). ArticleCASPubMed Google Scholar
Chen, F. et al. Hop is an unusual homeobox gene that modulates cardiac development. Cell110, 713–723 (2002). ArticleCASPubMed Google Scholar
Kook, H. et al. Cardiac hypertrophy and histone deacetylase-dependent transcriptional repression mediated by the atypical homeodomain protein Hop. J. Clin. Invest.112, 863–871 (2003). ArticleCASPubMedPubMed Central Google Scholar
Shin, C. H. et al. Modulation of cardiac growth and development by HOP, an unusual homeodomain protein. Cell110, 725–735 (2002). ArticleCASPubMed Google Scholar
Kuwahara, K. et al. The neuron-restrictive silencer element-neuron-restrictive silencer factor system regulates basal and endothelin 1-inducible atrial natriuretic peptide gene expression in ventricular myocytes. Mol. Cell Biol.21, 2085–2097 (2001). ArticleCASPubMedPubMed Central Google Scholar
Nakagawa, Y. et al. Class II HDACs mediate CaMK-dependent signaling to NRSF in ventricular myocytes. J. Mol. Cell Cardiol.41, 1010–1022 (2006). ArticleCASPubMed Google Scholar
Kuwahara, K. et al. NRSF regulates the fetal cardiac gene program and maintains normal cardiac structure and function. EMBO J.22, 6310–6321 (2003). ArticleCASPubMedPubMed Central Google Scholar
Montgomery, R. L. et al. Maintenance of cardiac energy metabolism by histone deacetylase 3 in mice. J. Clin. Invest.118, 3588–3597 (2008). ArticleCASPubMedPubMed Central Google Scholar
Bhaskara, S. et al. Deletion of histone deacetylase 3 reveals critical roles in S phase progression and DNA damage control. Mol. Cell30, 61–72 (2008). ArticleCASPubMedPubMed Central Google Scholar
Knutson, S. K. et al. Liver-specific deletion of histone deacetylase 3 disrupts metabolic transcriptional networks. EMBO J.27, 1017–1028 (2008). ArticleCASPubMedPubMed Central Google Scholar
Trivedi, C. M., Lu, M. M., Wang, Q. & Epstein, J. A. Transgenic over-expression of Hdac3 in the heart produces increased postnatal cardiac myocyte proliferation but does not induce hypertrophy. J. Biol. Chem.283, 26484–26489 (2008). ArticleCASPubMedPubMed Central Google Scholar
Cohen, M. M. Jr. The new bone biology: pathologic, molecular, and clinical correlates. Am. J. Med. Genet. A140, 2646–2706 (2006). ArticlePubMedCAS Google Scholar
Arnold, M. A. et al. MEF2C transcription factor controls chondrocyte hypertrophy and bone development. Dev. Cell12, 377–89 (2007). ArticleCASPubMed Google Scholar
Song, K. et al. The transcriptional coactivator CAMTA2 stimulates cardiac growth by opposing class II histone deacetylases. Cell125, 453–466 (2006). ArticleCASPubMed Google Scholar
McKinsey, T. A. & Olson, E. N. Toward transcriptional therapies for the failing heart: chemical screens to modulate genes. J. Clin. Invest.115, 538–546 (2005). ArticleCASPubMedPubMed Central Google Scholar
Backs, J. & Olson, E. N. Control of cardiac growth by histone acetylation/deacetylation. Circ. Res.98, 15–24 (2006). ArticleCASPubMed Google Scholar
Kim, Y. et al. The MEF2D transcription factor mediates stress-dependent cardiac remodeling in mice. J. Clin. Invest.118, 124–32 (2008). ArticleCASPubMed Google Scholar
Backs, J., Song, K., Bezprozvannaya, S., Chang, S. & Olson, E. N. CaM kinase II selectively signals to histone deacetylase 4 during cardiomyocyte hypertrophy. J. Clin. Invest.116, 1853–1864 (2006). ArticleCASPubMedPubMed Central Google Scholar
Bassel-Duby, R. & Olson, E. N. Signaling pathways in skeletal muscle remodeling. Annu. Rev. Biochem.75,19-37 (2006).
Kim, M. S. et al. Protein kinase D1 stimulates MEF2 activity in skeletal muscle and enhances muscle performance. Mol. Cell Biol.28, 3600–3609 (2008). ArticleCASPubMedPubMed Central Google Scholar
Potthoff, M. J. et al. Histone deacetylase degradation and MEF2 activation promote the formation of slow-twitch myofibers. J. Clin. Invest.117, 2459–2467 (2007). ArticleCASPubMedPubMed Central Google Scholar
Mejat, A. et al. Histone deacetylase 9 couples neuronal activity to muscle chromatin acetylation and gene expression. Nature Neurosci.8, 313–321 (2005). ArticleCASPubMed Google Scholar
Haberland, M. et al. Regulation of HDAC9 gene expression by MEF2 establishes a negative-feedback loop in the transcriptional circuitry of muscle differentiation. Mol. Cell Biol.27, 518–525 (2007). ArticleCASPubMed Google Scholar
Lindsey, M. L., Mann, D. L., Entman, M. L. & Spinale, F. G. Extracellular matrix remodeling following myocardial injury. Ann. Med.35, 316–326 (2003). ArticleCASPubMed Google Scholar
Jiang, Y., Goldberg, I. D. & Shi, Y. E. Complex roles of tissue inhibitors of metalloproteinases in cancer. Oncogene21, 2245–2252 (2002). ArticleCASPubMed Google Scholar
Lee, A. Y. et al. Quantitative analysis of histone deacetylase-1 selective histone modifications by differential mass spectrometry. J. Proteome Res. 31 Oct 2008 (doi:10.1021/pr800510p). ArticleCASPubMed Google Scholar
Jones, P. et al. 2-Trifluoroacetylthiophenes, a novel series of potent and selective class II histone deacetylase inhibitors. Bioorg. Med. Chem. Lett.18, 3456–3461 (2008). ArticleCASPubMed Google Scholar
Bolden, J. E., Peart, M. J. & Johnstone, R. W. Anticancer activities of histone deacetylase inhibitors. Nature Rev. Drug Discov.5, 769–784 (2006). ArticleCAS Google Scholar
Duvic, M. et al. Phase 2 trial of oral vorinostat (suberoylanilide hydroxamic acid, SAHA) for refractory cutaneous T-cell lymphoma (CTCL). Blood109, 31–39 (2007). ArticleCASPubMedPubMed Central Google Scholar
Xu, W. S., Parmigiani, R. B. & Marks, P. A. Histone deacetylase inhibitors: molecular mechanisms of action. Oncogene26, 5541–5552 (2007). ArticleCASPubMed Google Scholar
Marks, P. A. Discovery and development of SAHA as an anticancer agent. Oncogene26, 1351–1356 (2007). ArticleCASPubMed Google Scholar
Marks, P. A. & Breslow, R. Dimethyl sulfoxide to vorinostat: development of this histone deacetylase inhibitor as an anticancer drug. Nature Biotechnol.25, 84–90 (2007). ArticleCAS Google Scholar
Karagiannis, T. C. & El-Osta, A. Modulation of cellular radiation responses by histone deacetylase inhibitors. Oncogene25, 3885–3893 (2006). ArticleCASPubMed Google Scholar
Zimmermann, S. et al. Reduced body size and decreased intestinal tumor rates in HDAC2-mutant mice. Cancer Res.67, 9047–9054 (2007). ArticleCASPubMed Google Scholar
Fischer, A., Sananbenesi, F., Wang, X., Dobbin, M. & Tsai, L. H. Recovery of learning and memory is associated with chromatin remodelling. Nature447, 178–182 (2007). ArticleCASPubMed Google Scholar
Reddy, P. et al. Histone deacetylase inhibition modulates indoleamine 2,3-dioxygenase-dependent DC functions and regulates experimental graft-versus-host disease in mice. J. Clin. Invest.118, 2562–2573 (2008). CASPubMedPubMed Central Google Scholar
Kong, Y. et al. Suppression of class I and II histone deacetylases blunts pressure-overload cardiac hypertrophy. Circulation113, 2579–2588 (2006). ArticleCASPubMedPubMed Central Google Scholar
Granger, A. et al. Histone deacetylase inhibition reduces myocardial ischemia-reperfusion injury in mice. FASEB J.22, 3549–3560 (2008). ArticleCASPubMedPubMed Central Google Scholar
Zhang, B. et al. HDAC inhibitor increases histone H3 acetylation and reduces microglia inflammatory response following traumatic brain injury in rats. Brain Res.1226, 181–191 (2008). ArticleCASPubMedPubMed Central Google Scholar
Williams, J. A. et al. Valproic acid prevents brain injury in a canine model of hypothermic circulatory arrest: a promising new approach to neuroprotection during cardiac surgery. Ann. Thorac. Surg.81, 2235–2241; discussion 2241–2242 (2006). ArticlePubMed Google Scholar
Almeida, A. M. et al. Targeted therapy for inherited GPI deficiency. N. Engl. J. Med.356, 1641–1647 (2007). Describes the 'cure' of an inherited genetic disorder using an HDAC inhibitor. ArticleCASPubMed Google Scholar
Kim, S. C. et al. Substrate and functional diversity of lysine acetylation revealed by a proteomics survey. Mol. Cell23, 607–618 (2006). An elegant screen for the 'acetylome'. ArticleCASPubMed Google Scholar
Mann, B. S., Johnson, J. R., Cohen, M. H., Justice, R. & Pazdur, R. FDA approval summary: vorinostat for treatment of advanced primary cutaneous T-cell lymphoma. Oncologist12, 1247–1252 (2007). This study highlights the first US Food and Drug Administration (FDA) approval of an HDAC inhibitor. ArticleCASPubMed Google Scholar
Olsen, E. A. et al. Phase IIb multicenter trial of vorinostat in patients with persistent, progressive, or treatment refractory cutaneous T-cell lymphoma. J. Clin. Oncol.25, 3109–3115 (2007). ArticleCASPubMed Google Scholar
Luhrs, H. et al. Butyrate inhibits NF-kappaB activation in lamina propria macrophages of patients with ulcerative colitis. Scand. J. Gastroenterol.37, 458–466 (2002). ArticleCASPubMed Google Scholar
Atweh, G. F. et al. Sustained induction of fetal hemoglobin by pulse butyrate therapy in sickle cell disease. Blood93, 1790–1797 (1999). CASPubMed Google Scholar
Chung, Y. L., Lee, M. Y., Wang, A. J. & Yao, L. F. A therapeutic strategy uses histone deacetylase inhibitors to modulate the expression of genes involved in the pathogenesis of rheumatoid arthritis. Mol. Ther.8, 707–717 (2003). ArticleCASPubMed Google Scholar
Choi, J. H. et al. Trichostatin A attenuates airway inflammation in mouse asthma model. Clin. Exp. Allergy35, 89–96 (2005). ArticleCASPubMed Google Scholar
Camelo, S. et al. Transcriptional therapy with the histone deacetylase inhibitor trichostatin A ameliorates experimental autoimmune encephalomyelitis. J. Neuroimmunol.164, 10–21 (2005). ArticleCASPubMed Google Scholar
Glauben, R. et al. Histone hyperacetylation is associated with amelioration of experimental colitis in mice. J. Immunol.176, 5015–5022 (2006). ArticleCASPubMed Google Scholar
Antos, C. L. et al. Dose-dependent blockade to cardiomyocyte hypertrophy by histone deacetylase inhibitors. J. Biol. Chem.278, 28930–28937 (2003). ArticleCASPubMed Google Scholar
Reddy, P. et al. Histone deacetylase inhibitor suberoylanilide hydroxamic acid reduces acute graft-versus-host disease and preserves graft-versus-leukemia effect. Proc. Natl Acad. Sci. USA101, 3921–3926 (2004). ArticleCASPubMedPubMed Central Google Scholar
Leoni, F. et al. The histone deacetylase inhibitor ITF2357 reduces production of pro-inflammatory cytokines in vitro and systemic inflammation in vivo. Mol. Med.11, 1–15 (2005). ArticleCASPubMedPubMed Central Google Scholar
Minetti, G. C. et al. Functional and morphological recovery of dystrophic muscles in mice treated with deacetylase inhibitors. Nature Med.12, 1147–1150 (2006). ArticleCASPubMed Google Scholar
Mishra, N., Reilly, C. M., Brown, D. R., Ruiz, P. & Gilkeson, G. S. Histone deacetylase inhibitors modulate renal disease in the MRL-lpr/lpr mouse. J. Clin. Invest.111, 539–552 (2003). ArticleCASPubMedPubMed Central Google Scholar
Avila, A. M. et al. Trichostatin A increases SMN expression and survival in a mouse model of spinal muscular atrophy. J. Clin. Invest.117, 659–671 (2007). ArticleCASPubMedPubMed Central Google Scholar
Sailhamer, E. A. et al. Acetylation: a novel method for modulation of the immune response following trauma/hemorrhage and inflammatory second hit in animals and humans. Surgery144, 204–216 (2008). ArticlePubMed Google Scholar