ArticleHuman molecular genetics2008
The loss of methyl-CpG binding protein 1 leads to autism-like behavioral deficits.
Article in Human molecular genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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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.
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Who cites it
54 citing papers in PubMed, 98 citations in OpenAlex.
- Extracellular vesicle profiling reveals novel autism signatures in patient-derived forebrain organoids.Translational psychiatry · 2025Article
- Genome-wide DNA methylation profiles in the raphe nuclei of patients with autism spectrum disorder.Psychiatry and clinical neurosciences · 2025Article
- Versatile functions of methyl-CpG-binding domain 2 (MBD2) in cellular characteristics and differentiation.Molecular biology reports · 2025Review
- MBD1 protects replication fork stability by recruiting PARP1 and controlling transcription-replication conflicts.Cancer gene therapy · 2024Article
- Implication of Hippocampal Neurogenesis in Autism Spectrum Disorder: Pathogenesis and Therapeutic Implications.Current neuropharmacology · 2023Review
- FXR1 regulation of parvalbumin interneurons in the prefrontal cortex is critical for schizophrenia-like behaviors.Molecular psychiatry · 2021Article
- The Epigenome in Neurodevelopmental Disorders.Frontiers in neuroscience · 2021Review
- Epigenetic Regulation of the Hippocampus, with Special Reference to Radiation Exposure.International journal of molecular sciences · 2020Review
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- Diverse and dynamic DNA modifications in brain and diseases.Human molecular genetics · 2019Review
- Brain changes in a maternal immune activation model of neurodevelopmental brain disorders.Progress in neurobiology · 2019Review
- DNA Methylation and Adult Neurogenesis.Brain plasticity (Amsterdam, Netherlands) · 2017Review
- High Resolution Imaging of DNA Methylation Dynamics using a Zebrafish Reporter.Scientific reports · 2017Article
- Adult Neural Stem Cell Multipotency and Differentiation Are Directed by the Methyl-CpG-Binding Protein MBD1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Methyl-CpG-Binding Protein MBD1 Regulates Neuronal Lineage Commitment through Maintaining Adult Neural Stem Cell Identity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Genetics and Epigenetics in Adult Neurogenesis.Cold Spring Harbor perspectives in biology · 2016Review
- Tagging methyl-CpG-binding domain proteins reveals different spatiotemporal expression and supports distinct functions.Epigenomics · 2016Article
- Emerging Molecular and Biological Functions of MBD2, a Reader of DNA Methylation.Frontiers in genetics · 2016Review
- An epigenetic regulator: methyl-CpG-binding domain protein 1 (MBD1).International journal of molecular sciences · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Methyl-CpG binding proteins (MBDs) are central components of DNA methylation-mediated epigenetic gene regulation. Alterations of epigenetic pathways are known to be associated with several neurodevelopmental disorders, particularly autism. Our previous studies showed that the loss of Mbd1 led to reduced hippocampal neurogenesis and impaired learning in mice. However, whether MBD1 regulates the autism-related cognitive functions remains unknown. Here we show that Mbd1 mutant (Mbd1(-/-)) mice exhibit several core deficits frequently associated with autism, including reduced social interaction, learning deficits, anxiety, defective sensory motor gating, depression and abnormal brain serotonin activity. Furthermore, we find that Mbd1 can directly regulate the expression of Htr2c, one of the serotonin receptors, by binding to its promoter, and the loss of Mbd1 led to elevated expression of Htr2c. Our results, therefore, demonstrate the importance of epigenetic regulation in mammalian brain development and cognitive functions. Understanding how the loss of Mbd1 could lead to autism-like behavioral phenotypes would reveal much-needed information about the molecular pathogenesis of autism.
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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.