The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease
By Amy N. Packer, Yi Xing, S. Harper, L. Jones, B. Davidson. Journal of Neuroscience, 2008
656 citations recorded by the source corpus.
The transcription factor REST silences neuronal gene expression in non-neuronal cells. In neurons, the protein is sequestered in the cytoplasm in part through binding to huntingtin. Polyglutamine expansions in huntingtin, which causes Huntington's disease (HD), abrogates REST-huntingtin binding. Consequently, REST translocates to the nucleus, occupies RE1 repressor sequences and decreases neuronal gene expression. In this work, we found that levels of several microRNAs (miRNAs) with upstream RE1 sites are decreased in HD patient cortices relative to healthy controls. Interestingly, one of these, the bifunctional brain enriched miR-9/miR-9*, targets two components of the REST complex: miR-9 targets REST and miR-9* targets CoREST. These data provide evidence for a double negative feedback loop between the REST silencing complex and the miRNAs it regulates.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/8dce8a39398d97423fda523d757cbefbbd3b6468
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Citations in the corpus
- MicroRNAs in development and disease. (2011, background): “miR-9/9* is involved in a double negative feedback loop in which miR-9 targets and suppresses REST, while miR-9* targets and suppresses CoREST (467).”
- Molecular mechanisms and potential therapeutical targets in Huntington's disease. (2010, background): “Particularly, the neural-specific mir-124a that is highly and specifically expressed in the CNS is decreased in human and mouse HD cortex (289, 422).”