Journal
NATURE COMMUNICATIONS
Volume 4, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms2514
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Funding
- Volkswagen Stiftung
- AtaxiaUK
- Tenovus Scotland
- Medical University Innsbruck [IFTZ-03]
- Austrian Science Fund [FWF-SFB021, TRP233]
- Tiroler Zukunftsstiftung
- Austrian Science Fund (FWF) [TRP 233] Funding Source: researchfish
- Austrian Science Fund (FWF) [TRP233] Funding Source: Austrian Science Fund (FWF)
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Expansion of CAG repeats is a common feature of various neurodegenerative disorders, including Huntington's disease. Here we show that expanded CAG repeats bind to a translation regulatory protein complex containing MID1, protein phosphatase 2A and 40S ribosomal S6 kinase. Binding of the MID1-protein phosphatase 2A protein complex increases with CAG repeat size and stimulates translation of the CAG repeat expansion containing messenger RNA in a MID1-, protein phosphatase 2A- and mammalian target of rapamycin-dependent manner. Our data indicate that pathological CAG repeat expansions upregulate protein translation leading to an overproduction of aberrant protein and suggest that the MID1-complex may serve as a therapeutic target for the treatment of CAG repeat expansion disorders.
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