ArticleMediators of inflammation2013
Genes related to mitochondrial functions, protein degradation, and chromatin folding are differentially expressed in lymphomonocytes of Rett syndrome patients.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 78 citations in OpenAlex.
- MECP2 Duplication Uncouples Mitochondrial and Purine Metabolism During neuronal maturation.bioRxiv : the preprint server for biology · 2025Article
- MeCP2 at the crossroads of hypoxia, oxidative stress, and gene regulation in Rett syndrome.Epigenomics · 2025Review
- Identifying a novel Mecp2-mediated epigenetic mechanism controlling Lonp1 in the hippocampus and its disruption by aging.Scientific reports · 2025Article
- Probing DNA damage in Rett syndrome neurons uncovers a role for MECP2 regulation of PARP1.Stem cell reports · 2025Article
- Optimized clonal isolation and immortalization of Rett syndrome patient fibroblasts for in vitro modeling of MECP2 mutations.Scientific reports · 2025Article
- Deregulated Nrf2-Keap1-BACH1 axis in autism spectrum disorder.Redox biology · 2025Article
- Review
- Growth Performance, Dietary Energetics, Blood Metabolites, Carcass Traits, Meat Quality, and Gene Expression of Lambs Supplemented with a Polyherbal Phytogenic Additive.Veterinary sciences · 2024Article
- Systemic proteome phenotypes reveal defective metabolic flexibility in Mecp2 mutants.Human molecular genetics · 2023Article
- Systemic Proteome Phenotypes Reveal Defective Metabolic Flexibility in Mecp2 Mutants.bioRxiv : the preprint server for biology · 2023Article
- Mitochondrial Proteome Changes in Rett Syndrome.Biology · 2023Article
- Multilevel evidence of MECP2-associated mitochondrial dysfunction and its therapeutic implications.Frontiers in psychiatry · 2023Article
- Identification of key genes and miRNAs related to polycystic ovary syndrome by comprehensive analysis of microarray.BMC medical genomics · 2022Article
- Oral Feeding of an Antioxidant Cocktail as a Therapeutic Strategy in a Mouse Model of Rett Syndrome: Merits and Limitations of Long-Term Treatment.Antioxidants (Basel, Switzerland) · 2022Article
- Molecular Signatures of Response to Mecasermin in Children With Rett Syndrome.Frontiers in neuroscience · 2022Article
- Transcriptome comparative analysis of ovarian follicles reveals the key genes and signaling pathways implicated in hen egg production.BMC genomics · 2021Article
- Aberrant lung lipids cause respiratory impairment in a Mecp2-deficient mouse model of Rett syndrome.Human molecular genetics · 2021Article
- Transcriptomic and Epigenomic Landscape in Rett Syndrome.Biomolecules · 2021Review
- MeCP2 deficiency exacerbates the neuroinflammatory setting and autoreactive response during an autoimmune challenge.Scientific reports · 2021Article
- Gulf War Illness: Mechanisms Underlying Brain Dysfunction and Promising Therapeutic Strategies.Pharmacology & therapeutics · 2021Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rett syndrome (RTT) is mainly caused by mutations in the X-linked methyl-CpG binding protein (MeCP2) gene. By binding to methylated promoters on CpG islands, MeCP2 protein is able to modulate several genes and important cellular pathways. Therefore, mutations in MeCP2 can seriously affect the cellular phenotype. Today, the pathways that MeCP2 mutations are able to affect in RTT are not clear yet. The aim of our study was to investigate the gene expression profiles in peripheral blood lymphomonocytes (PBMC) isolated from RTT patients to try to evidence new genes and new pathways that are involved in RTT pathophysiology. LIMMA (Linear Models for MicroArray) and SAM (Significance Analysis of Microarrays) analyses on microarray data from 12 RTT patients and 7 control subjects identified 482 genes modulated in RTT, of which 430 were upregulated and 52 were downregulated. Functional clustering of a total of 146 genes in RTT identified key biological pathways related to mitochondrial function and organization, cellular ubiquitination and proteosome degradation, RNA processing, and chromatin folding. Our microarray data reveal an overexpression of genes involved in ATP synthesis suggesting altered energy requirement that parallels with increased activities of protein degradation. In conclusion, these findings suggest that mitochondrial-ATP-proteasome functions are likely to be involved in RTT clinical features.
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