Abstract
An epigenetic key protein MeCP2 is thought to be expressed exclusively in mature neurons. Here, we show that MeCP2 is expressed in embryonic non-neuronal cells by immunocytochemistry and Western blotting, and that knockdown of MeCP2 levels using RNA interference reduces their proliferation. These findings suggest that MeCP2 is essential to non-neuronal cell growth during brain development, which may be associated with microcephaly of Rett syndrome patients with MeCP2 mutations.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Blotting, Western / methods
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Bromodeoxyuridine / metabolism
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Cell Count / methods
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Cell Fractionation / methods
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Cell Proliferation / drug effects
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Cells, Cultured
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Cerebral Cortex / cytology*
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Chromosomal Proteins, Non-Histone / chemistry
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Chromosomal Proteins, Non-Histone / deficiency
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Chromosomal Proteins, Non-Histone / metabolism*
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DNA-Binding Proteins / chemistry
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DNA-Binding Proteins / deficiency
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DNA-Binding Proteins / metabolism*
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Embryo, Mammalian
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Gene Expression Regulation, Developmental / physiology*
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Glial Fibrillary Acidic Protein / metabolism
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Immunohistochemistry / methods
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Methyl-CpG-Binding Protein 2
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Mice
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Mice, Knockout
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Microtubule-Associated Proteins / metabolism
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Neuroglia / drug effects
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Neuroglia / metabolism*
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RNA, Small Interfering / pharmacology
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Repressor Proteins / chemistry
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Repressor Proteins / metabolism*
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Rett Syndrome / genetics
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Rett Syndrome / metabolism*
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Time Factors
Substances
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Chromosomal Proteins, Non-Histone
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DNA-Binding Proteins
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Glial Fibrillary Acidic Protein
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Mecp2 protein, mouse
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Methyl-CpG-Binding Protein 2
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Microtubule-Associated Proteins
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Mtap2 protein, mouse
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RNA, Small Interfering
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Repressor Proteins
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Bromodeoxyuridine