ArticleEpigenetics & chromatin2019
MeCP2-E1 isoform is a dynamically expressed, weakly DNA-bound protein with different protein and DNA interactions compared to MeCP2-E2.
Article in Epigenetics & chromatin, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 71 citations in OpenAlex.
- MeCP2 MBD-ID module: a unified DNA/RNA binding interface disrupted in Rett syndrome.Nucleic acids research · 2026Article
- Single-dose administration of therapeutic divalent siRNA targeting MECP2 prevents lethality in an MECP2 duplication mouse model.Nature communications · 2026Article
- Article
- MeCP2 NID interaction with RNA: implications for Rett syndrome-relevant protein regulation.Human molecular genetics · 2026Article
- Modulating alternative splicing ofScience translational medicine · 2026Article
- Structural Plasticity and Functional Dynamics of Pigeon Cryptochrome 4 as Avian Magnetoreceptor.Journal of molecular biology · 2025Article
- Human MeCP2 binds to promoters and inhibits transcription in an unmethylated yeast genome.Genetics · 2025Article
- Exploring the complexity of MECP2 function in Rett syndrome.Nature reviews. Neuroscience · 2025Review
- SRSF9-Mediated Exon Recognition Promotes Exon 2 Inclusion inInternational journal of molecular sciences · 2025Article
- Testing the PEST hypothesis using relevant Rett mutations in MeCP2 E1 and E2 isoforms.Human molecular genetics · 2024Article
- An Irak1-Mecp2 tandem duplication mouse model for the study of MECP2 duplication syndrome.Disease models & mechanisms · 2024Article
- Reciprocal crosslink among MeCP2/BDNF /CREB signaling pinpointed in autism spectrum disorder.Toxicology reports · 2024Article
- Systematic and quantitative analysis of stop codon readthrough in Rett syndrome nonsense mutations.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Extending MeCP2 interactome: canonical nucleosomal histones interact with MeCP2.Nucleic acids research · 2024Article
- A-Z of Epigenetic Readers: Targeting Alternative Splicing and Histone Modification Variants in Cancer.Cancers · 2024Review
- Rett Syndrome and the Role of MECP2: Signaling to Clinical Trials.Brain sciences · 2024Review
- Nuclease-free precise genome editing corrects MECP2 mutations associated with Rett syndrome.Frontiers in genome editing · 2024Article
- Analysis of the interplay between MeCP2 and histone H1 duringEpigenetics · 2023Article
- A Severity Comparison between Italian and Israeli Rett Syndrome Cohorts.Diagnostics (Basel, Switzerland) · 2023Article
- Wild-type MECP2 expression coincides with age-dependent sensory phenotypes in a female mouse model for Rett syndrome.Journal of neuroscience research · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 10 institutions in 6 countries.
Funding
Abstract
backgroundMeCP2-a chromatin-binding protein associated with Rett syndrome-has two main isoforms, MeCP2-E1 and MeCP2-E2, differing in a few N-terminal amino acid residues. Previous studies have shown brain region-specific expression of these isoforms which, in addition to their different cellular localization and differential expression during brain development, suggest that they may also have non-overlapping molecular mechanisms. However, differential functions of MeCP2-E1 and E2 remain largely unexplored.
resultsHere, we show that the N-terminal domains (NTD) of MeCP2-E1 and E2 modulate the ability of the methyl-binding domain (MBD) to interact with DNA as well as influencing the turn-over rates, binding dynamics, response to neuronal depolarization, and circadian oscillations of the two isoforms. Our proteomics data indicate that both isoforms exhibit unique interacting protein partners. Moreover, genome-wide analysis using ChIP-seq provide evidence for a shared as well as a specific regulation of different sets of genes.
conclusionsOur study supports the idea that Rett syndrome might arise from simultaneous impairment of cellular processes involving non-overlapping functions of MECP2 isoforms. For instance, MeCP2-E1 mutations might impact stimuli-dependent chromatin regulation, while MeCP2-E2 mutations could result in aberrant ribosomal expression. Overall, our findings provide insight into the functional complexity of MeCP2 by dissecting differential aspects of its two isoforms.
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.