MeCP2, a Key Contributor to Neurological Disease, Activates and Represses Transcription

By Maria H. Chahrour, S. Jung, Chad A. Shaw, Xiaobo Zhou, Stephen T. C. Wong, J. Qin, H. Zoghbi. Science, 2008

1,838 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Genetics

View Paper: https://www.semanticscholar.org/paper/5f706f53230a0178d1ab223326aca817f3dd7b9c

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Citations in the corpus

From synapse to nucleus: calcium-dependent gene transcription in the control of synapse development and function. (2008, background): “Recent evidence suggests that MeCP2, in addition to functioning as a repressor of gene expression, may work as an activator in a complex with CREB (Chahrour et al., 2008).”
Autism risk factors: genes, environment, and gene-environment interactions (2012, background): “Indeed, MeCP2 binds to methylated DNA and represses the transcription of target genes.(70) Second, several chromosomal regions subject to parental imprinting (transcriptional regulation of either the maternal allele or the paternal allele inducing monoallelic expression) were associated with autism.”
A model for neural development and treatment of Rett Syndrome using human induced pluripotent stem cells (2010, background): “MeCP2 may be involved in the epigenetic regulation of target genes, by binding to methylated CpG dinucleotides within promoters, andmay function as a transcriptional repressor, although this view has been challenged recently (Chahrour et al., 2008; Yasui et al., 2007).”
Brain-Derived Neurotrophic Factor and Neuropsychiatric Disorders (2012, background): “, 2009) although more recent evidence suggests it may also activate transcription (Yasui et al., 2007; Chahrour et al., 2008).”
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”
Post-synaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity and Disease (2010, positive): “Recent studies show that the Bdnf gene can be regulated by MeCP2 and that MeCP2 associates with CREB1 at the promoter of an activated target, but not at the promoter of a repressed target (Chahrour et al., 2008).”
How can memories last for days, years, or a lifetime? Proposed mechanisms for maintaining synaptic potentiation and memory (2019, background): “Two, not mutually exclusive, possibilities are: (1) Less commonly, DNA methylation correlates paradoxically with activation of gene transcription (Chahrour et al. 2008; Kotini et al. 2011).”
Neuronal MeCP2 is expressed at near histone-octamer levels and globally alters the chromatin state (2010, background): “, 2007) but more recently have reported large numbers of subtle alterations comprising both increases and decreases in gene expression (Chahrour et al., 2008).”
The autistic neuron: troubled translation? (2008, background): “Rett’s syndrome is caused by loss-offunction mutations in the methyl-CpG binding protein 2 (MeCP2), which can function as both a transcriptional activator and repressor (Chahrour et al., 2008).”