Huntingtin interacts with REST/NRSF to modulate the transcription of NRSE-controlled neuronal genes

By C. Zuccato, Marzia Tartari, A. Crotti, Donato Goffredo, M. Valenza, L. Conti, T. Cataudella, B. Leavitt, Michael R. Hayden, T. Timmusk and 2 more. Nature Genetics, 2003

979 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/b95ae58df551192337204b405351661927d4cebe

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Citations in the corpus

Brain-derived neurotrophic factor. (2004, background): “In humans, a valine to methionine polymorphism at the 50 pro-region of the human BDNF protein was found to be associated with poorer episodic memory; in vitro, neurons transfected with met-BDNF-GFP exhib- ited reduced depolarization-induced BDNF secretion (Egan et al., 2003).”
Mouse and rat BDNF gene structure and expression revisited (2006, background): “…also plays an important role in cell-specific and activity-dependent regulation of BDNF gene by recruiting global repressors such as REST/NRSF to promoter II (Palm et al., 1998; Timmusk et al., 1999; Zuccato et al., 2003) and MeCP2 to promoter III (Chen et al., 2003a; Martinowich et al., 2003).”
The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease (2008, background): “However, in patients with HD, mutant Htt fails to bind REST, enabling its nuclear translocation (Zuccato et al., 2003).”
Post-synaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity and Disease (2010, neutral): “Diseases associated with some perturbation of BDNF signaling are diverse: epilepsy (He et al., 2004); mood disorders (Neves-Pereira et al., 2002; Sklar et al., 2002; Schumacher et al., 2005; Strauss et al., 2005), neurodegenerative diseases such Huntington's Disease (Zuccato et al., 2001; Zuccato et”
Molecular mechanisms and potential therapeutical targets in Huntington's disease. (2010, background): “Wild-type huntingtin promotes the expression of brain-derived neurotrophic factor (BDNF) by interacting through REST-interacting LIM domain protein (RILP) and HAP1 with the repressor element-1 transcription factor/neuron-restrictive silencer factor (REST/NRSF) in the cytoplasm, and preventing this c”
The Transcription Repressor REST in Adult Neurons: Physiology, Pathology, and Diseases,, (2015, background): “The attenuation of REST expression in neurons was found to restore BDNF levels, confirming the REST dependence of the aberrant gene transcription in this disease (Zuccato et al., 2007).”
GDNF, NGF and BDNF as therapeutic options for neurodegeneration. (2013, background): “The mechanism by which BDNF is downregulated is at least partly due to the increased binding of the neurone-restrictive silencing factor (NRSF) to the BDNF promoter (Zuccato et al., 2003), thus”
Ageing and neuronal vulnerability (2006, background): “, and lower levels of brain-derived neurotrophic factor ( BDNF ) in ageing, AD and H”
MicroRNAs in development and disease. (2011, background): “The mechanism has been partly attributed to increased activity of the REST as it dissociates from the mutant huntingtin protein (719), which is known to suppress the transcription of neuronal genes.”