ArticleJournal of molecular neuroscience : MN2017
Differential Regulation of MeCP2 Phosphorylation by Laminin in Oligodendrocytes.
Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- MeCP2 Lactylation Protects against Ischemic Brain Injury by Transcriptionally Regulating Neuronal Apoptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Glial Dysfunction in MeCP2 Deficiency Models: Implications for Rett Syndrome.International journal of molecular sciences · 2019Review
- Mitochondrial Electron Transport Chain Complex Dysfunction in MeCP2 Knock-Down Astrocytes: Protective Effects of Quercetin Hydrate.Journal of molecular neuroscience : MN · 2019Article
- MeCP2 Differentially Regulate the Myelin MBP and PLP Protein Expression in Oligodendrocytes and C6 Glioma.Journal of molecular neuroscience : MN · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oligodendrocytes (OLGs) are the myelinating cells of the central nervous system (CNS), and its proper differentiation is crucial for normal functioning of neurons. Methyl-CpG-binding protein 2 (MeCP2) is a multifunctional methylated DNA binding protein; mutation of which causes Rett syndrome, a severe neurodevelopmental disorder. Previously, we reported that MeCP2 is expressed in all the stages of oligodendrocyte development, and also shown the role of MeCP2 as a transcription regulator of myelin genes in OLGs. The expression and function of MeCP2 phosphorylation at S80 (pS80MeCP2) has been well studied in neurons and astrocytes; however, there is no data so far available in OLGs regarding pS80MeCP2. Certain developmental stimuli such as growth factors and extracellular matrix (ECM) protein play important role in OLG development. In the present study, we have examined the effects of external stimuli (growth factors (GFs) and extracellular matrix (ECMs)) on S80 phosphorylation of MeCP2 in N19 oligodendroglial cells (N19 OLGs). This study provides the first evidence that laminin (LN) differentially regulates the expression of pS80MeCP2 in immature and mature N19 OLGs. Thus, MeCP2 is phosphorylated in a stimulus-dependent manner during oligodendrocyte development, and thereby, it may regulate the oligodendrocyte behavior.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.