Remote control of activity-dependent BDNF gene promoter-I transcription mediated by REST/NRSF.

@article{Hara2009RemoteCO,
  title={Remote control of activity-dependent BDNF gene promoter-I transcription mediated by REST/NRSF.},
  author={Daichi Hara and Mamoru Fukuchi and Toshihide Miyashita and Akiko Tabuchi and Ichiro Takasaki and Yoshihisa Naruse and Nozomu Mori and Takashi Kondo and Masaaki Tsuda},
  journal={Biochemical and biophysical research communications},
  year={2009},
  volume={384 4},
  pages={
          506-11
        }
}
Class I Histone Deacetylase-mediated Repression of the Proximal Promoter of the Activity-regulated Cytoskeleton-associated Protein Gene Regulates Its Response to Brain-derived Neurotrophic Factor*
TLDR
It is found that trichostatin A (TSA), a histone deacetylase (HDAC) inhibitor, significantly enhanced the inductive effects of BDNF or FGF2, but not those of NMDA on Arc expression, contributing to the understanding of the physiological role of Arc expression in neuronal functions such as memory consolidation.
Persistent BDNF exon I-IX mRNA expression following the withdrawal of neuronal activity in neurons.
Pharmacological characterization of BDNF promoters I, II and IV reveals that serotonin and norepinephrine input is sufficient for transcription activation.
TLDR
A rapidly detectable and highly sensitive reporter gene assay was applied to characterize the selective activation profile of BDNF and CRE promoters, through specific and different pharmacological stimuli.
Transcriptional regulation of the neuropeptide VGF by the neuron-restrictive silencer factor/neuron-restrictive silencer element
TLDR
It is shown that the NRSE sequence of the VGF gene critically regulates the repression of VGF expression in NMB cells through a mechanism that is dependent on VGF-NRSE.
Intronic enhancer region governs transcript-specific BDNF expression in neurons
TLDR
A functional E-box element in the enhancer region is uncovered, linking the expression of BDNF and various pro-neural basic helix-loop-helix transcription factors, shed new light on the cell type- and stimulus-specific regulation of the important neurotrophic factor BDNF.
Regulation of neural gene transcription by optogenetic inhibition of the RE1-silencing transcription factor
TLDR
The light-mediated regulation of the repressor element 1 (RE1)-silencing transcription factor (REST), a master regulator of neural genes, is reported, providing a tool for studying neuronal physiology and correcting gene expression changes taking place in brain diseases.
Intronic enhancer region governs transcript-specific Bdnf expression in rodent neurons
TLDR
A functional E-box element in the enhancer region is uncovered, linking the expression of Bdnf and various pro-neural basic helix–loop–helix transcription factors, shed new light on the cell-type- and stimulus-specific regulation of the important neurotrophic factor BDNF.
Brain REST/NRSF Is Not Only a Silent Repressor but Also an Active Protector
TLDR
Findings strongly indicate that REST/NRSF is not only a classical repressor to maintain normal neurogenesis, but it is also a fine fundamental protector against neurodegeneration and other disorders and may be a novel potent therapeutic target for neural disturbances.
The Transcription Repressor REST in Adult Neurons: Physiology, Pathology, and Diseases1,2,3
TLDR
It is suggested that the conflicting results reported for the role of REST in physiology, pathology, and disease depend on its complex, direct, and indirect actions on many gene targets and on the diverse approaches used during the investigations.
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References

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REST4-mediated modulation of REST/NRSF-silencing function during BDNF gene promoter activation.
TLDR
A primary role for REST4 is suggested in preventing the neuron-specific gene from being inactivated by REST/NRSF and allowing gene activation in response to a variety of neuronal stimuli.
Involvement of an Upstream Stimulatory Factor as Well as cAMP-responsive Element-binding Protein in the Activation of Brain-derived Neurotrophic Factor Gene Promoter I*
TLDR
Findings support that not only CREB but also USF1/USF2 contributes to Ca2+ signal-mediated activation of BDNF-PI through the recognition of an overlapping CRE and USF-binding element.
Brain-derived neurotrophic factor expression in vivo is under the control of neuron-restrictive silencer element.
TLDR
The data show that NRSEBDNF is controlling the activity of BDNF promoters I and II in the brain, thymus, and lung, i.e. in the tissues in which the intact reporter gene and endogenous BDNF mRNAs are expressed.
Differential Activation of Brain-derived Neurotrophic Factor Gene Promoters I and III by Ca2+ Signals Evoked vial-type Voltage-dependent andN-Methyl-d-aspartate Receptor Ca2+Channels*
TLDR
The increase in BDNF mRNA expression induced at high K+ was repressed not only by nicardipine, an antagonist for L-VDCC, but also by dl-amino-5-phosphonovalerate, an antagonists for NMDA-R, which was supported by the effects of antagonists on the Ca2+ influx.
Transcriptional repression by REST: recruitment of Sin3A and histone deacetylase to neuronal genes
TLDR
This work provides multiple lines of evidence that the N-terminal domain of REST represses transcription of the GluR2 and type II sodium-channel genes by recruiting the corepressor Sin3A and histone deacetylase to the promoter region in nonneuronal cells.
Huntingtin interacts with REST/NRSF to modulate the transcription of NRSE-controlled neuronal genes
TLDR
It is concluded that wild-type huntingtin acts in the cytoplasm of neurons to regulate the availability of REST/NRSF to its nuclear NRSE-binding site and that this control is lost in the pathology of Huntington disease.
Activation of REST/NRSF Target Genes in Neural Stem Cells Is Sufficient To Cause Neuronal Differentiation
TLDR
It is shown that regulated expression of REST-VP16 in a physiologically relevant NSC line growing under cycling conditions converted the cells rapidly to the mature neuronal phenotype, and the findings suggested that direct activation of genes involved in the terminal stage of differentiation may cause neuronal differentiation of NSCs.
CoREST: a functional corepressor required for regulation of neural-specific gene expression.
TLDR
It is shown that CoREST, a newly identified human protein, functions as a corepressor for REST, a structural feature of the nuclear receptor and silencing mediator for retinoid and thyroid human receptors (SMRT)-extended corepressors that mediate inducible repression by steroid hormone receptors.
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