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Times Cited: 224
Times Cited: 224
Times Cited
Times Co-cited
Similarity
Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl-CpG-binding protein 2.
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Transcriptional repression by the methyl-CpG-binding protein MeCP2 involves a histone deacetylase complex.
X Nan, H H Ng, C A Johnson, C D Laherty, B M Turner, R N Eisenman, A Bird. Nature 1998
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A mouse Mecp2-null mutation causes neurological symptoms that mimic Rett syndrome.
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MeCP2, a key contributor to neurological disease, activates and represses transcription.
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Neuronal MeCP2 is expressed at near histone-octamer levels and globally alters the chromatin state.
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Disruption of DNA-methylation-dependent long gene repression in Rett syndrome.
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Purification, sequence, and cellular localization of a novel chromosomal protein that binds to methylated DNA.
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MeCP2 is a transcriptional repressor with abundant binding sites in genomic chromatin.
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An AT-hook domain in MeCP2 determines the clinical course of Rett syndrome and related disorders.
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Radically truncated MeCP2 rescues Rett syndrome-like neurological defects.
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Activity-dependent phosphorylation of MeCP2 threonine 308 regulates interaction with NCoR.
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MeCP2 binds to non-CG methylated DNA as neurons mature, influencing transcription and the timing of onset for Rett syndrome.
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Structure of the MeCP2-TBLR1 complex reveals a molecular basis for Rett syndrome and related disorders.
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Duplication of the MECP2 region is a frequent cause of severe mental retardation and progressive neurological symptoms in males.
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Biotin tagging of MeCP2 in mice reveals contextual insights into the Rett syndrome transcriptome.
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MeCP2 binds to 5hmC enriched within active genes and accessible chromatin in the nervous system.
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Global transcriptional and translational repression in human-embryonic-stem-cell-derived Rett syndrome neurons.
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Mild overexpression of MeCP2 causes a progressive neurological disorder in mice.
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Methylated DNA and MeCP2 recruit histone deacetylase to repress transcription.
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The disease progression of Mecp2 mutant mice is affected by the level of BDNF expression.
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Derepression of BDNF transcription involves calcium-dependent phosphorylation of MeCP2.
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Rett syndrome mutation MeCP2 T158A disrupts DNA binding, protein stability and ERP responses.
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Mice with truncated MeCP2 recapitulate many Rett syndrome features and display hyperacetylation of histone H3.
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Specific mutations in methyl-CpG-binding protein 2 confer different severity in Rett syndrome.
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Dissection of the methyl-CpG binding domain from the chromosomal protein MeCP2.
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MeCP2 Rett mutations affect large scale chromatin organization.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.