Name | HDAC |
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Synonyms | HD7; HDAC 7; HDAC7; HD7B; HD9; HDAC; HDAC 9; HDAC7B… |
Name | SMA |
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CAS | sodium 2-chloroacetate |
PubMed | Abstract | RScore(About this table) | |
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17998807 | Gray SG, Dangond F: Rationale for the use of histone deacetylase inhibitors as a dual therapeutic modality in multiple sclerosis. Epigenetics. 2006 Apr-Jun;1(2):67-75. Epub 2006 Mar 5. Mutations in genes that encode HDAC-binding proteins cause neurological disorders, such as MeCP2 mutations in Rett's syndrome. |
5(0,0,0,5) | Details |
18537606 | Echaniz-Laguna A, Bousiges O, Loeffler JP, Boutillier AL: Histone deacetylase inhibitors: therapeutic agents and research tools for deciphering motor neuron diseases. Curr Med Chem. 2008;15(13):1263-73. Histone deacetylase (HDAC) inhibition as a therapeutic regimen in motor neuron diseases (MND) is generating intense interest in both the scientific and medical areas, with a number of potent compounds having demonstrated good safety profiles and hints of clinical activity on animal models. The use of HDACi and possible mechanisms of action will be reviewed in three MND, i.e. amyotrophic lateral sclerosis (ALS), spinal muscular atrophy (SMA) and spinal and bulbar muscular atrophy (SBMA), diseases among which clinical trials with HDACi are currently perfomed (ALS, SMA). |
2(0,0,0,2) | Details |
19700647 | Guo W, Shan B, Klingsberg RC, Qin X, Lasky JA: Abrogation of TGF-beta1-induced fibroblast-myofibroblast differentiation by histone deacetylase inhibition. Am J Physiol Lung Cell Mol Physiol. 2009 Nov;297(5):L864-70. Epub 2009 Aug 21. In the current study, we investigated the molecular link between TGF-beta1-mediated myofibroblast differentiation and histone deacetylase (HDAC) activity. |
2(0,0,0,2) | Details |
17610967 | Glenisson W, Castronovo V, Waltregny D: Histone deacetylase 4 is required for TGFbeta1-induced myofibroblastic differentiation. Biochim Biophys Acta. 2007 Oct;1773(10):1572-82. Epub 2007 Jun 12. Herein, we sought to investigate the role of histone deacetylases (HDAC) in TGFbeta1-induced MF differentiation. |
2(0,0,0,2) | Details |
19640900 | Pang M, Kothapally J, Mao H, Tolbert E, Ponnusamy M, Chin YE, Zhuang S: Inhibition of histone deacetylase activity attenuates renal fibroblast activation and interstitial fibrosis in obstructive nephropathy. Am J Physiol Renal Physiol. 2009 Oct;297(4):F996-F1005. Epub 2009 Jul 29. In this study, we investigated the effect of trichostatin A (TSA), a specific histone deacetylase (HDAC) inhibitor, on the activation of renal interstitial fibroblasts in a rat renal interstitial fibroblast line (NRK-49F) and the development of renal fibrosis in a murine model of unilateral ureteral obstruction (UUO). alpha-Smooth muscle actin (alpha-SMA) and fibronectin, two hallmarks of fibroblast activation, were highly expressed in cultured NRK-49F cells, and their expression was inhibited in the presence of TSA. |
2(0,0,0,2) | Details |
18971205 | Hauke J, Riessland M, Lunke S, Eyupoglu IY, Blumcke I, El-Osta A, Wirth B, Hahnen E: Survival motor neuron gene 2 silencing by DNA methylation correlates with spinal muscular atrophy disease severity and can be bypassed by histone deacetylase inhibition. Hum Mol Genet. 2009 Jan 15;18(2):304-17. Epub 2008 Oct 29. We identified histone deacetylase (HDAC) inhibitors including vorinostat and romidepsin which are able to bypass SMN2 gene silencing by DNA methylation, while others such as and phenylbutyrate do not, due to HDAC isoenzyme specificities. |
1(0,0,0,1) | Details |
18345520 | Dayangac-Erden D, Topaloglu H, Erdem-Yurter H: A preliminary report on spinal muscular atrophy lymphoblastoid cell lines: are they an appropriate tool for drug screening?. Adv Ther. 2008 Mar;25(3):274-9. METHODS: In this preliminary study, we investigated the effect of phenylbutyrate, a histone deacetylase (HDAC) inhibitor, on SMN2 expression in two SMA type III Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines to understand the suitability of lymphoblastoid cell lines in drug screening. |
1(0,0,0,1) | Details |