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Min, Kyung-Tai
Molecular & Cellular Neurobiology Lab(Min Lab)
Research Interests
  • adult neurogenesis; axon development; axon regeneration; protein stability; protein synthesis; Down syndrome; Alzheimer's disease;
  • learning and memory; mitochondria dynamics

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Aberrant histone acetylation, altered transcription, and retinal degeneration in a Drosophila model of polyglutamine disease are rescued by CREB-binding protein

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Title
Aberrant histone acetylation, altered transcription, and retinal degeneration in a Drosophila model of polyglutamine disease are rescued by CREB-binding protein
Author
Taylor, JPTaye, AACampbell, CKazemi-Esfarjani, PFischbeck, KHMin, Kyung-Tai
Keywords
CREB-binding protein (CBP); Drosophila; Gene expression analysis; Histone acetylation; Polyglutamine; Retinal degeneration
Issue Date
2003-06
Publisher
COLD SPRING HARBOR LAB PRESS
Citation
GENES & DEVELOPMENT, v.17, no.12, pp.1463 - 1468
Abstract
Sequestration of the transcriptional coactivator CREB-binding protein (CBP), a histone acetyltransferase, has been implicated in the pathogenesis of polyglutamine expansion neurodegenerative disease. We used a Drosophila model to demonstrate that polyglutamine-induced neurodegeneration is accompanied by a defect in histone acetylation and a substantial alteration in the transcription profile. Furthermore, we demonstrate complete functional and morphological rescue by up-regulation of endogenous Drosophila CBP (dCBP). Rescue of the degenerative phenotype is associated with eradication of polyglutamine aggregates, recovery of histone acetylation, and normalization of the transcription profile. These findings suggest that histone acetylation is an early target of polyglutamine toxicity and indicate that transcriptional dysregulation is an important part of the pathogenesis of polyglutamine-induced neurodegeneration.
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DOI
10.1101/gad.1087503
ISSN
0890-9369
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BME_Journal Papers
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