ArticleJCI insight2018
Epigenetic dysregulation of Oxtr in Tet1-deficient mice has implications for neuropsychiatric disorders.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 34 citations in OpenAlex.
- The novel role of GADD45A in the etiology of autism: modulating neuronal excitability via TET1/R-loop dependent regulation of KCNQ5.Molecular psychiatry · 2026Article
- MidbrainbioRxiv : the preprint server for biology · 2026Article
- Autophagy Modulation by Antidepressants: Mechanisms and Implications.Neurochemical research · 2025Review
- Oxytocin treatment at birth accelerates an epigenetic shift in the oxytocin receptor gene in the maternal brain.BMC pregnancy and childbirth · 2025Article
- DNA Methylation in Long-Term Memory.Physiology (Bethesda, Md.) · 2025Review
- Maternal Vitamin C Deficiency and Genetic Risk Factors Contribute to Congenital Defects through Dysregulation of DNA Methylation.bioRxiv : the preprint server for biology · 2025Article
- Prenatal 1-Nitropyrene Exposure Causes Autism-Like Behavior Partially by Altering DNA Hydroxymethylation in Developing Brain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Intertwined associations between oxytocin, immune system and major depressive disorder.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Review
- Dual functions of TET1 in germ layer lineage bifurcation distinguished by genomic context and dependence on 5-methylcytosine oxidation.Nucleic acids research · 2023Article
- Is oxytocin receptor signaling really dispensable for social attachment?Comprehensive psychoneuroendocrinology · 2023Article
- Transcriptional diversity of the oxytocin receptor in prairie voles: mechanistic implications for behavioral neuroscience and maternal physiology.Frontiers in genetics · 2023Article
- Mutations of the histone linker H1-4 in neurodevelopmental disorders and functional characterization of neurons expressing C-terminus frameshift mutant H1.4.Human molecular genetics · 2022Article
- An epigenetic rheostat of experience: DNA methylation ofComprehensive psychoneuroendocrinology · 2021Review
- The role of TET proteins in stress-induced neuroepigenetic and behavioural adaptations.Neurobiology of stress · 2021Review
- Ten-eleven translocation 1 mediated-DNA hydroxymethylation is required for myelination and remyelination in the mouse brain.Nature communications · 2021Article
- TET1-mediated DNA hydroxymethylation regulates adult remyelination in mice.Nature communications · 2021Article
- Genetic, epigenetic, and environmental factors controlling oxytocin receptor gene expression.Clinical epigenetics · 2021Article
- Article
- Oxytocin Receptor Exon III Methylation in the Umbilical Cord Blood of Newborns With Prenatal Exposure to Crack Cocaine.Frontiers in cell and developmental biology · 2021Article
- Is Oxytocin "Nature's Medicine"?Pharmacological reviews · 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
17 authors at 4 institutions in 3 countries.
Funding
Abstract
OXTR modulates a variety of behaviors in mammals, including social memory and recognition. Genetic and epigenetic dysregulation of OXTR has been suggested to be implicated in neuropsychiatric disorders, including autism spectrum disorder (ASD). While the involvement of DNA methylation is suggested, the mechanism underlying epigenetic regulation of OXTR is largely unknown. This has hampered the experimental design and interpretation of the results of epigenetic studies of OXTR in neuropsychiatric disorders. From the generation and characterization of a new line of Tet1 mutant mice - by deleting the largest coding exon 4 (Tet1Δe4) - we discovered for the first time to our knowledge that Oxtr has an array of mRNA isoforms and a complex transcriptional regulation. Select isoforms of Oxtr are significantly reduced in the brain of Tet1Δe4-/- mice. Accordingly, CpG islands of Oxtr are hypermethylated during early development and persist into adulthood. Consistent with the reduced express of OXTR, Tet1Δe4-/- mice display impaired maternal care, social behavior, and synaptic responses to oxytocin stimulation. Our findings elucidate a mechanism mediated by TET1 protein in regulating Oxtr expression by preventing DNA hypermethylation of Oxtr. The discovery of epigenetic dysregulation of Oxtr in TET1-deficient mouse brain supports the necessity of a reassessment of existing findings and a value of future studies of OXTR in neuropsychiatric disorders.
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.