Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/66685
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Type: Journal article
Title: Perturbation of the Akt/Gsk3-beta signalling pathway is common to Drosophila expressing expanded untranslated CAG, CUG and AUUCU repeat RNAs
Author: van Eyk, C.
O'Keefe, L.
Lawlor, K.
Samaraweera, S.
McLeod, C.
Price, G.
Venter, D.
Richards, R.
Citation: Human Molecular Genetics, 2011; 20(14):2783-2794
Publisher: Oxford Univ Press
Issue Date: 2011
ISSN: 0964-6906
1460-2083
Statement of
Responsibility: 
Clare L. van Eyk, Louise V. O'Keefe, Kynan T. Lawlor, Saumya E. Samaraweera, Catherine J. McLeod, Gareth R. Price, Deon J. Venter and Robert I. Richards
Abstract: Recent evidence supports a role for RNA as a common pathogenic agent in both the ‘polyglutamine’ and ‘untranslated’ dominant expanded repeat disorders. One feature of all repeat sequences currently associated with disease is their predicted ability to form a hairpin secondary structure at the RNA level. In order to investigate mechanisms by which hairpin-forming repeat RNAs could induce neurodegeneration, we have looked for alterations in gene transcript levels as hallmarks of the cellular response to toxic hairpin repeat RNAs. Three disease-associated repeat sequences—CAG, CUG and AUUCU—were specifically expressed in the neurons of Drosophila and resultant common transcriptional changes assessed by microarray analyses. Transcripts that encode several components of the Akt/Gsk3-β signalling pathway were altered as a consequence of expression of these repeat RNAs, indicating that this pathway is a component of the neuronal response to these pathogenic RNAs and may represent an important common therapeutic target in this class of diseases.
Keywords: Animals; Drosophila melanogaster; Neurodegenerative Diseases; Glycogen Synthase Kinase 3; Drosophila Proteins; RNA; Signal Transduction; Gene Expression; Repetitive Sequences, Nucleic Acid; Proto-Oncogene Proteins c-akt; Glycogen Synthase Kinase 3 beta
Rights: © The Author 2011. Copyright © 2011 Oxford University Press This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
RMID: 0020111159
DOI: 10.1093/hmg/ddr177
Grant ID: http://purl.org/au-research/grants/nhmrc/207830
http://purl.org/au-research/grants/nhmrc/453674
http://purl.org/au-research/grants/nhmrc/627183
Appears in Collections:Molecular and Biomedical Science publications

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