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Selective toxicity by HDAC3 in neurons: regulation by Akt and GSK3beta

Although it is well established that pharmacological inhibitors of classical histone deacetylases (HDACs) are protective in various in vivo models of neurodegenerative disease, the identity of the neurotoxic HDAC(s) that these inhibitors target to exert their protective effects has not been resolved... Full description

Journal Title: The Journal of neuroscience : the official journal of the Society for Neuroscience 02 February 2011, Vol.31(5), pp.1746-51
Main Author: Bardai, Farah H
Other Authors: D'Mello, Santosh R
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1529-2401 ; PMID: 21289184 Version:1 ; DOI: 10.1523/JNEUROSCI.5704-10.2011
Link: http://pubmed.gov/21289184
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recordid: medline21289184
title: Selective toxicity by HDAC3 in neurons: regulation by Akt and GSK3beta
format: Article
creator:
  • Bardai, Farah H
  • D'Mello, Santosh R
subjects:
  • Glycogen Synthase Kinase 3 -- Metabolism
  • Histone Deacetylases -- Pharmacology
  • Neurons -- Drug Effects
  • Proto-Oncogene Proteins C-Akt -- Metabolism
ispartof: The Journal of neuroscience : the official journal of the Society for Neuroscience, 02 February 2011, Vol.31(5), pp.1746-51
description: Although it is well established that pharmacological inhibitors of classical histone deacetylases (HDACs) are protective in various in vivo models of neurodegenerative disease, the identity of the neurotoxic HDAC(s) that these inhibitors target to exert their protective effects has not been resolved. We find that HDAC3 is a protein with strong neurotoxic activity. Forced expression of HDAC3 induces death of otherwise healthy rat cerebellar granule neurons, whereas shRNA-mediated suppression of its expression protects against low-potassium-induced neuronal death. Forced expression of HDAC3 also promotes the death of rat cortical neurons and hippocampally derived HT22 cells, but has no effect on the viability of primary kidney fibroblasts or the HEK293 and HeLa cell lines. This suggests that the toxic effect of HDAC3 is cell selective and that neurons are sensitive to it. Neurotoxicity by HDAC3 is inhibited by treatment with IGF-1 as well as by the expression of a constitutively active form...
language: eng
source:
identifier: E-ISSN: 1529-2401 ; PMID: 21289184 Version:1 ; DOI: 10.1523/JNEUROSCI.5704-10.2011
fulltext: fulltext
issn:
  • 15292401
  • 1529-2401
url: Link


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titleSelective toxicity by HDAC3 in neurons: regulation by Akt and GSK3beta
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subjectGlycogen Synthase Kinase 3 -- Metabolism ; Histone Deacetylases -- Pharmacology ; Neurons -- Drug Effects ; Proto-Oncogene Proteins C-Akt -- Metabolism
descriptionAlthough it is well established that pharmacological inhibitors of classical histone deacetylases (HDACs) are protective in various in vivo models of neurodegenerative disease, the identity of the neurotoxic HDAC(s) that these inhibitors target to exert their protective effects has not been resolved. We find that HDAC3 is a protein with strong neurotoxic activity. Forced expression of HDAC3 induces death of otherwise healthy rat cerebellar granule neurons, whereas shRNA-mediated suppression of its expression protects against low-potassium-induced neuronal death. Forced expression of HDAC3 also promotes the death of rat cortical neurons and hippocampally derived HT22 cells, but has no effect on the viability of primary kidney fibroblasts or the HEK293 and HeLa cell lines. This suggests that the toxic effect of HDAC3 is cell selective and that neurons are sensitive to it. Neurotoxicity by HDAC3 is inhibited by treatment with IGF-1 as well as by the expression of a constitutively active form...
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abstractAlthough it is well established that pharmacological inhibitors of classical histone deacetylases (HDACs) are protective in various in vivo models of neurodegenerative disease, the identity of the neurotoxic HDAC(s) that these inhibitors target to exert their protective effects has not been resolved. We find that HDAC3 is a protein with strong neurotoxic activity. Forced expression of HDAC3 induces death of otherwise healthy rat cerebellar granule neurons, whereas shRNA-mediated suppression of its expression protects against low-potassium-induced neuronal death. Forced expression of HDAC3 also promotes the death of rat cortical neurons and hippocampally derived HT22 cells, but has no effect on the viability of primary kidney fibroblasts or the HEK293 and HeLa cell lines. This suggests that the toxic effect of HDAC3 is cell selective and that neurons are sensitive to it. Neurotoxicity by HDAC3 is inhibited by treatment with IGF-1 as well as by the expression of a constitutively active form...
doi10.1523/JNEUROSCI.5704-10.2011
pmid21289184
date2011-02-02