ArticleNature communications2018
Apparent bias toward long gene misregulation in MeCP2 syndromes disappears after controlling for baseline variations.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 44 citations in OpenAlex.
- DNA methylation, nucleic acid structure, and rett mutations tune MeCP2 binding affinity and cooperativity.The Journal of biological chemistry · 2026Article
- Exploring the complexity of MECP2 function in Rett syndrome.Nature reviews. Neuroscience · 2025Review
- A transcriptome-based human universal senescence index (hUSI) robustly predicts cellular senescence under various conditions.Nature aging · 2025Article
- Article
- Repeated birth injuries lead to long-term pelvic floor muscle dysfunction in the preclinical rat model.American journal of obstetrics and gynecology · 2025Article
- Integrated gene expression and alternative splicing analysis in human and mouse models of Rett syndrome.Scientific reports · 2025Article
- Modeling antisense oligonucleotide therapy in MECP2 duplication syndrome human iPSC-derived neurons reveals gene expression programs responsive to MeCP2 levels.Human molecular genetics · 2024Article
- Proregenerative extracellular matrix hydrogel mitigates pathological alterations of pelvic skeletal muscles after birth injury.Science translational medicine · 2023Article
- MeCP2 regulateseLife · 2023Article
- Convergent cerebrospinal fluid proteomes and metabolic ontologies in humans and animal models of Rett syndrome.iScience · 2022Article
- MeCP2 loss-of-function dysregulates microRNAs regionally and disrupts excitatory/inhibitory synaptic transmission balance.Hippocampus · 2022Article
- The Cell Adhesion Molecule L1 Interacts with Methyl CpG Binding Protein 2 via Its Intracellular Domain.International journal of molecular sciences · 2022Article
- Angelman Syndrome and Angelman-like Syndromes Share the Same Calcium-Related Gene Signatures.International journal of molecular sciences · 2021Article
- Transcriptomic and Epigenomic Landscape in Rett Syndrome.Biomolecules · 2021Review
- A research parasite's perspective on establishing a baseline to avoid errors in secondary analyses.GigaScience · 2021Article
- RAD51AP1 promotes progression of ovarian cancer via TGF-β/Smad signalling pathway.Journal of cellular and molecular medicine · 2021Article
- Developmental Accumulation of Gene Body and Transposon Non-CpG Methylation in the Zebrafish Brain.Frontiers in cell and developmental biology · 2021Article
- The Molecular Functions of MeCP2 in Rett Syndrome Pathology.Frontiers in genetics · 2021Review
- Rett Syndrome and Fragile X Syndrome: Different Etiology With Common Molecular Dysfunctions.Frontiers in cellular neuroscience · 2021Review
- Emerging Insights into the Distinctive Neuronal Methylome.Trends in genetics : TIG · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Recent studies have suggested that genes longer than 100 kb are more likely to be misregulated in neurological diseases associated with synaptic dysfunction, such as autism and Rett syndrome. These length-dependent transcriptional changes are modest in MeCP2-mutant samples, but, given the low sensitivity of high-throughput transcriptome profiling technology, here we re-evaluate the statistical significance of these results. We find that the apparent length-dependent trends previously observed in MeCP2 microarray and RNA-sequencing datasets disappear after estimating baseline variability from randomized control samples. This is particularly true for genes with low fold changes. We find no bias with NanoString technology, so this long gene bias seems to be particular to polymerase chain reaction amplification-based platforms. In contrast, authentic long gene effects, such as those caused by topoisomerase inhibition, can be detected even after adjustment for baseline variability. We conclude that accurate characterization of length-dependent (or other) trends requires establishing a baseline from randomized control samples.
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.