Derepression of BDNF Transcription Involves Calcium-Dependent Phosphorylation of MeCP2

By Wen G. Chen, Q. Chang, Yingxi Lin, Alexander Meissner, A. West, Eric C. Griffith, R. Jaenisch, Michael E. Greenberg. Science, 2003

1,303 citations recorded by the source corpus.

Subfields: Cognitive Neuroscience, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/b28704c87c06692070fead2a054c29e081acce2f

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Citations in the corpus

Mouse and rat BDNF gene structure and expression revisited (2006, background): “…activity-dependent activation of BDNF gene is mediated by decreased CpG methylation of BDNF promoter IV and release of a repressor complex containing methyl-cytosine binding protein MeCP2, histone deacetylases HDAC1 and HDAC2, and corepressor mSin3A (Chen et al., 2003a; Martinowich et al., 2003).”
Current research trends in early life stress and depression: review of human studies on sensitive periods, gene-environment interactions, and epigenetics. (2012, positive): “to be critical to maintain the DNA methylation status, as the dissociation of this complex and specifically MeCP2 has been associated with site specific demethylation (Chen et al., 2003; Martinowich et al., 2003; Murgatroyd et al., 2009).”
Synaptic dysfunction in neurodevelopmental disorders associated with autism and intellectual disabilities. (2012, background): “Indeed, MeCP2 binds to the promoter regions of several genes that are repressed upon loss of MeCP2 and are activated by its presence, including brain-derived neurotrophic factor (BDNF) and several other neuronal genes (Chen et al. 2003; Martinowich et al. 2003; Yasui et al. 2007; Chahrour et al. 200”
MeCP2 binds to 5hmc enriched within active genes and accessible chromatin in the nervous system (2013, positive): “…the interesting possibility that the posttranslational modifications to MeCP2 that have been shown to occur in response to a variety of stimuli (Chen et al., 2003; Tao et al., 2009; Rutlin et al., 2011; Adkins et al., 2011; Gonzales et al., 2012) could alter its its substrate specificity and…”
REST and its corepressors mediate plasticity of neuronal gene chromatin throughout neurogenesis. (2005, background): “Indeed, the lack of MeCP2 in mouse models causes a 2-fold increase in steady-state levels of BDNF exon III expression in rat cortical neurons ( Chen et al., 2003 ) and subtle transcriptional changes in the brain (Tudor et al., 2002), which could upset the balance of neuronal function, thus resulting”
Post-synaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity and Disease (2010, positive): “In cultured neurons, MeCP2 binds the promoter region of a Bdnf gene and suppresses its transcription (Chen et al., 2003; Martinowich et al., 2003).”
The Angelman Syndrome-associated ubiquitin ligase Ube3A regulates synapse development by ubiquitinating Arc (2010, positive): “Stimulants included Bicuculline (Sigma, 20 μm), Glutamate (Sigma, 10 μm), NMDA (Sigma, 20 μm), recombinant human BDNF (Peprotech, 50 ng/mL), NT3 (Peprotech, 50 ng/mL), NT4 (Peprotech, 50 ng/mL), and 55 mM KCl as previously described (Chen et al., 2003).”
DNA binding selectivity of MeCP2 due to a requirement for A/T sequences adjacent to methyl-CpG. (2005, positive): “MeCP2 has been shown to bind close to an inducible promoter of the rodent Bdnf gene and contribute to maintenance of the silenced state (Chen et al., 2003; Martinowich et al., 2003).”
Neuronal MeCP2 is expressed at near histone-octamer levels and globally alters the chromatin state (2010, background): “MeCP2 Binds Globally across the Genome in the Mouse Brain Previous reports using cultured neurons from embryonic or immature mice have suggested that MeCP2 binds at discrete genomic sites, such as at the brain-derived neurotrophic factor gene locus (Bdnf) (Chen et al., 2003) and at the Dlx5/6 locus ”