PT  - JOURNAL ARTICLE
AU  - Amy N. Packer
AU  - Yi Xing
AU  - Scott Q. Harper
AU  - Lesley Jones
AU  - Beverly L. Davidson
TI  - The Bifunctional microRNA miR-9/miR-9* Regulates REST and CoREST and Is Downregulated in Huntington's Disease
AID  - 10.1523/JNEUROSCI.2390-08.2008
DP  - 2008 Dec 31
TA  - The Journal of Neuroscience
PG  - 14341--14346
VI  - 28
IP  - 53
4099  - http://www.jneurosci.org/content/28/53/14341.short
4100  - http://www.jneurosci.org/content/28/53/14341.full
SO  - J. Neurosci.2008 Dec 31; 28
AB  - 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.