Reciprocal actions of REST and a microRNA promote neuronal identity

By C. Conaco, Stefanie J. Otto, Jong-Jin Han, G. Mandel. Proceedings of the National Academy of Sciences of the United States of America, 2006

749 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/a5011781f1ce55705888f2969227917780af63ed

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Citations in the corpus

MicroRNAs in development and disease. (2011, background): “In particular, it is localized to differentiated neurons (567) and is suppressed in non-neuronal cells by the RE1-silencing transcription factor (REST) (114).”
The MicroRNA miR-124 promotes neuronal differentiation by triggering brain-specific alternative pre-mRNA splicing. (2007, methodology): “5 mouse embryos (Figure 6C) and transfected them with antisense 20-OMeRNAs complementary to miR-124, or with a control 20-OMe-RNA complementary to muscle-specific miRNA miR-1, as described in Conaco et al. (2006).”
The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease (2008, background): “1A), are processed from the same primary transcript from 3 genomic loci (miR-9 –1, 9 –2 and 9 –3); miR-9 –1 and miR-9 –3 both have upstream RE1 sequences that can be occupied by REST (Conaco et al., 2006; Johnson et al., 2008).”
Molecular mechanisms and potential therapeutical targets in Huntington's disease. (2010, background): “In particular, reciprocal actions of REST and a microRNA were found to promote neuronal identity (126).”
MicroRNA-mediated feedback and feedforward loops are recurrent network motifs in mammals. (2007, background): “In addition to potentially targeting NRSF, miR-29 putatively targets a significant number of neuronal genes (T) that are corepressed by NRSF. (B) Illustrates how a miRNA can be embedded simultaneously in both type I and II circuits in relation to a single target.”
Small non-coding RNAs in animal development (2008, background): “REST is a transcription factor that represses the extra-neuronal transcription of several genes, including miR-124 (Ref”
Non-coding RNAs as regulators of embryogenesis (2011, background): “miR-124 itself is transcriptionally repressed by SCP1–REST in non-neuronal cell”
The neuronal microRNA system (2006, background): “Interestingly, miR-124a transcription is under the control of the RE1 silencing transcription factor (REST), which inhibits the expression of neuronal genes in non-neuronal cells, a function reciprocal to that of miR-124a (Ref”
The microRNA miR-124 antagonizes the anti-neural REST/SCP1 pathway during embryonic CNS development. (2007, background): “Interestingly, Drosophila has a functional ortholog of REST, Tramtrack 88 (ttk88) (Dallman et al. 2004), and Drosophila miR-124 promoter contains a consensus ttk88 response element (Conaco et al. 2006).”