ArticleNeuroscience bulletin2017
Expression of Phospho-MeCP2s in the Developing Rat Brain and Function of Postnatal MeCP2 in Cerebellar Neural Cell Development.
Article in Neuroscience bulletin, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- The Cell Adhesion Molecule L1 Interacts with Methyl CpG Binding Protein 2 via Its Intracellular Domain.International journal of molecular sciences · 2022Article
- Role of miR-132/methyl-CpG-binding protein 2 in the regulation of neural stem cell differentiation.Neural regeneration research · 2021Article
- Surface- and voxel-based brain morphologic study in Rett and Rett-like syndrome with MECP2 mutation.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2019Article
- SUMOylation of Fragile X Mental Retardation Protein: A Critical Mechanism of FMRP-Mediated Neuronal Function.Neuroscience bulletin · 2018Review
- Article
- Differential Regulation of MeCP2 Phosphorylation by Laminin in Oligodendrocytes.Journal of molecular neuroscience : MN · 2017Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal expression and dysfunction of methyl-CpG binding protein 2 (MeCP2) cause Rett syndrome (RTT). The diverse phosphorylation modifications modulate MeCP2 function in neural cells. Using western blot and immunohistochemistry, we examined the expression patterns of MeCP2 and three phospho-MeCP2s (pMeCP2s) in the developing rat brain. The expression of MeCP2 and phospho-S80 (pS80) MeCP2 increased while pS421 MeCP2 and pS292 MeCP2 decreased with brain maturation. In contrast to the nuclear localization of MeCP2 and pS80 MeCP2, pS421 MeCP2 and pS292 MeCP2 were mainly expressed in the cytoplasmic compartment. Apart from their distribution in neurons, they were also detected at a low level in astrocytes. Postnatally-initiated MeCP2 deficiency affected cerebellar neural cell development, as determined by the abnormal expression of GFAP, DCX, Tuj1, MAP-2, and calbindin-D28k. Together, these results demonstrate that MeCP2 and diverse pMeCP2s have distinct features of spatio-temporal expression in the rat brain, and that the precise levels of MeCP2 in the postnatal period are vital to cerebellar neural cell development.
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Registered trials
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