ABCD2 p.Ala30Pro
Predicted by SNAP2: | C: N (66%), D: D (63%), E: N (66%), F: N (82%), G: N (93%), H: N (82%), I: N (93%), K: N (72%), L: N (97%), M: N (93%), N: N (82%), P: N (66%), Q: N (82%), R: N (93%), S: N (93%), T: N (93%), V: N (93%), W: D (66%), Y: N (78%), |
Predicted by PROVEAN: | C: N, D: D, E: N, F: N, G: N, H: D, I: N, K: N, L: N, M: N, N: N, P: D, Q: N, R: N, S: N, T: N, V: N, W: N, Y: N, |
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[hide] Histone deacetylase inhibitors: possible implicati... Expert Opin Investig Drugs. 2008 Feb;17(2):169-84. Hahnen E, Hauke J, Trankle C, Eyupoglu IY, Wirth B, Blumcke I
Histone deacetylase inhibitors: possible implications for neurodegenerative disorders.
Expert Opin Investig Drugs. 2008 Feb;17(2):169-84., [PMID:18230051]
Abstract [show]
During the past six years numerous studies identified histone deacetylase (HDAC) inhibitors as candidate drugs for the treatment of neurodegenerative disorders. Two major neuroprotective mechanisms of HDAC inhibitors have been identified, namely the transcriptional activation of disease-modifying genes and the correction of perturbations in histone acetylation homeostasis, which have been shown to be intimately involved in the neurodegenerative pathomechanisms of Huntington's, Parkinson's and Kennedy disease, amyotropic lateral sclerosis, Rubinstein-Taybi syndrome as well as stroke. Based on the promising in vitro and in vivo analyses, clinical trials have been initiated to evaluate the safety and efficacy of HDAC inhibitors for the treatment of devastating diseases such as Huntington's disease, amyotropic lateral sclerosis and spinal muscular atrophy. Here, the authors summarize and discuss the findings on the emerging field of epigenetic therapy strategies in neurodegenerative disorders.
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No. Sentence Comment
280 Even though no direct binding of α-synuclein to histone acetyltransferases was found, wild-type as well as mutant α-synuclein proteins (A30P, A53T) inhibit histone acetylation mediated by CBP, p300 and P/CAF in vitro.
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ABCD2 p.Ala30Pro 18230051:280:148
status: NEW