ArticleBMC neuroscience2010
Downstream targets of methyl CpG binding protein 2 and their abnormal expression in the frontal cortex of the human Rett syndrome brain.
Article in BMC neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 7 citations in OpenAlex.
- Oxidative stress in Rett syndrome: natural history, genotype, and variants.Redox report : communications in free radical research · 2011Trial
- Metabolites with a message: impacts on epigenetics and implications for epimetabopathies.EMBO reports · 2026Review
- MeCP2 at the crossroads of hypoxia, oxidative stress, and gene regulation in Rett syndrome.Epigenomics · 2025Review
- Evaluating the utility of growth differentiation factor 15 and fibroblast growth factor 21 as blood biomarkers for Rett syndrome.Scientific reports · 2025Article
- Neurodegeneration in Autism: A Study of Clusterin, Very Long-Chain Fatty Acids, and Carnitine.Journal of molecular neuroscience : MN · 2025Article
- Rett Syndrome: Thinking Beyond Brain Borders.Advances in experimental medicine and biology · 2025Review
- Protective effects of pyrroloquinoline quinone in brain folate deficiency.Fluids and barriers of the CNS · 2023Article
- Mitochondrial Proteome Changes in Rett Syndrome.Biology · 2023Article
- Multilevel evidence of MECP2-associated mitochondrial dysfunction and its therapeutic implications.Frontiers in psychiatry · 2023Article
- Transcriptomic and Epigenomic Landscape in Rett Syndrome.Biomolecules · 2021Review
- Article
- Mitochondria May Mediate Prenatal Environmental Influences in Autism Spectrum Disorder.Journal of personalized medicine · 2021Review
- Overshooting Subcellular Redox-Responses in Rett-Mouse Hippocampus during Neurotransmitter Stimulation.Cells · 2020Article
- Expansion of the phenotypic spectrum of de novo missense variants in kinesin family member 1A (KIF1A).Human mutation · 2020Article
- Drug Studies on Rett Syndrome: From Bench to Bedside.Journal of autism and developmental disorders · 2020Review
- Transcriptome data of temporal and cingulate cortex in the Rett syndrome brain.Scientific data · 2020Article
- Tau overexpression impairs neuronal endocytosis by decreasing the GTPase dynamin 1 through the miR-132/MeCP2 pathway.Aging cell · 2019Article
- Mitochondrial Dysfunction Is Inducible in Lymphoblastoid Cell Lines From Children With Autism and May Involve the TORC1 Pathway.Frontiers in psychiatry · 2019Article
- Neuronal Redox-Imbalance in Rett Syndrome Affects Mitochondria as Well as Cytosol, and Is Accompanied by Intensified Mitochondrial OFrontiers in physiology · 2019Article
- Clusterin in Alzheimer's Disease: Mechanisms, Genetics, and Lessons From Other Pathologies.Frontiers in neuroscience · 2019Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundThe Rett Syndrome (RTT) brain displays regional histopathology and volumetric reduction, with frontal cortex showing such abnormalities, whereas the occipital cortex is relatively less affected.
resultsUsing microarrays and quantitative PCR, the mRNA expression profiles of these two neuroanatomical regions were compared in postmortem brain tissue from RTT patients and normal controls. A subset of genes was differentially expressed in the frontal cortex of RTT brains, some of which are known to be associated with neurological disorders (clusterin and cytochrome c oxidase subunit 1) or are involved in synaptic vesicle cycling (dynamin 1). RNAi-mediated knockdown of MeCP2 in vitro, followed by further expression analysis demonstrated that the same direction of abnormal expression was recapitulated with MeCP2 knockdown, which for cytochrome c oxidase subunit 1 was associated with a functional respiratory chain defect. Chromatin immunoprecipitation (ChIP) analysis showed that MeCP2 associated with the promoter regions of some of these genes suggesting that loss of MeCP2 function may be responsible for their overexpression.
conclusionsThis study has shed more light on the subset of aberrantly expressed genes that result from MECP2 mutations. The mitochondrion has long been implicated in the pathogenesis of RTT, however it has not been at the forefront of RTT research interest since the discovery of MECP2 mutations. The functional consequence of the underexpression of cytochrome c oxidase subunit 1 indicates that this is an area that should be revisited.
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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.