Altered acetylation in polyglutamine disease: an opportunity for therapeutic intervention? - PubMed (original) (raw)
Altered acetylation in polyglutamine disease: an opportunity for therapeutic intervention?
J Paul Taylor et al. Trends Mol Med. 2002 May.
Abstract
Recent investigations into polyglutamine diseases suggest that aberrant transcriptional regulation might be central to the molecular pathogenesis, perhaps because of inappropriate interaction between mutant proteins and important nuclear factors. Several groups have reported an interaction of mutant polyglutamine with histone acetylases, implicating defective acetylation as a cause of abnormal transcription. An important recent observation is that reversal of the acetylation defect with histone deacetylase inhibitors ameliorates polyglutamine toxicity in yeast, mammalian cell culture, and animal models. These encouraging findings suggest that a novel strategy--pharmacological restoration of histone acetylation-- could prove effective in treating this group of devastating illnesses.
Similar articles
- Altered protein acetylation in polyglutamine diseases.
Bodai L, Pallos J, Thompson LM, Marsh JL. Bodai L, et al. Curr Med Chem. 2003 Dec;10(23):2577-87. doi: 10.2174/0929867033456530. Curr Med Chem. 2003. PMID: 14529472 Review. - Polyglutamine disease: acetyltransferases awry.
Hughes RE. Hughes RE. Curr Biol. 2002 Feb 19;12(4):R141-3. doi: 10.1016/s0960-9822(02)00709-1. Curr Biol. 2002. PMID: 11864588 Review. - Aberrant histone acetylation, altered transcription, and retinal degeneration in a Drosophila model of polyglutamine disease are rescued by CREB-binding protein.
Taylor JP, Taye AA, Campbell C, Kazemi-Esfarjani P, Fischbeck KH, Min KT. Taylor JP, et al. Genes Dev. 2003 Jun 15;17(12):1463-8. doi: 10.1101/gad.1087503. Genes Dev. 2003. PMID: 12815067 Free PMC article. - Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila.
Steffan JS, Bodai L, Pallos J, Poelman M, McCampbell A, Apostol BL, Kazantsev A, Schmidt E, Zhu YZ, Greenwald M, Kurokawa R, Housman DE, Jackson GR, Marsh JL, Thompson LM. Steffan JS, et al. Nature. 2001 Oct 18;413(6857):739-43. doi: 10.1038/35099568. Nature. 2001. PMID: 11607033 - [Molecular biology of polyglutamine diseases].
Owecki M, Kozubski W. Owecki M, et al. Postepy Hig Med Dosw. 2002;56(6):779-88. Postepy Hig Med Dosw. 2002. PMID: 12661407 Review. Polish.
Cited by
- Meclofenamic Acid Reduces Reactive Oxygen Species Accumulation and Apoptosis, Inhibits Excessive Autophagy, and Protects Hair Cell-Like HEI-OC1 Cells From Cisplatin-Induced Damage.
Li H, Song Y, He Z, Chen X, Wu X, Li X, Bai X, Liu W, Li B, Wang S, Han Y, Xu L, Zhang D, Li J, Chai R, Wang H, Fan Z. Li H, et al. Front Cell Neurosci. 2018 May 23;12:139. doi: 10.3389/fncel.2018.00139. eCollection 2018. Front Cell Neurosci. 2018. PMID: 29875633 Free PMC article. - Developing treatment for spinal and bulbar muscular atrophy.
Fischbeck KH. Fischbeck KH. Prog Neurobiol. 2012 Dec;99(3):257-61. doi: 10.1016/j.pneurobio.2012.05.012. Epub 2012 Jun 2. Prog Neurobiol. 2012. PMID: 22668795 Free PMC article. Review. - Aminoglycoside-induced histone deacetylation and hair cell death in the mouse cochlea.
Chen FQ, Schacht J, Sha SH. Chen FQ, et al. J Neurochem. 2009 Mar;108(5):1226-36. doi: 10.1111/j.1471-4159.2009.05871.x. Epub 2009 Jan 29. J Neurochem. 2009. PMID: 19141081 Free PMC article. - Reflections on the diseases linked to mutations of the androgen receptor.
Poletti A, Negri-Cesi P, Martini L. Poletti A, et al. Endocrine. 2005 Dec;28(3):243-62. doi: 10.1385/ENDO:28:3:243. Endocrine. 2005. PMID: 16388114 Review. - Ataxin 1, a SCA1 neurodegenerative disorder protein, is functionally linked to the silencing mediator of retinoid and thyroid hormone receptors.
Tsai CC, Kao HY, Mitzutani A, Banayo E, Rajan H, McKeown M, Evans RM. Tsai CC, et al. Proc Natl Acad Sci U S A. 2004 Mar 23;101(12):4047-52. doi: 10.1073/pnas.0400615101. Epub 2004 Mar 11. Proc Natl Acad Sci U S A. 2004. PMID: 15016912 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical
Molecular Biology Databases