ArticleCell2009
Abnormal behavior in a chromosome-engineered mouse model for human 15q11-13 duplication seen in autism.
Article in Cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 264 papers, 1 of them a synthesis that pooled it.
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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
264 citing papers in PubMed, 1 synthesis or guideline pooled it, 486 citations in OpenAlex.
- Comparing the Gut Microbiome in Autism and Preclinical Models: A Systematic Review.Frontiers in cellular and infection microbiology · 2022Pooled it
- Copy number variations independently induce autism spectrum disorder.Bioscience reports · 2017Trial
- Article
- Dup15q model mice exhibit impaired gastrointestinal motility and a constipation-like phenotype, alleviated by prucalopride.Translational psychiatry · 2026Article
- Review
- Restoration of axon initial segment plasticity via chemogenetic activation rescues autism-related behaviors.Cell death & disease · 2026Article
- Sex differences in autism spectrum disorder: behavioral and sensory phenotypes in humans and mouse models.Translational psychiatry · 2026Article
- RO4938581, a GABAMolecular psychiatry · 2026Article
- Neonatal social communication and single genes predict the variability of post-pubertal social behavior in a mouse model of paternal 15q11-13 duplication.Research square · 2026Article
- Occludin deficiency is associated with developmental impairment, locomotor dysfunction, and social deficiencies.Tissue barriers · 2026Article
- Species-Specific Parent-Of-Origin Expression of Adam23 in the Mammalian Brain.Genes to cells : devoted to molecular & cellular mechanisms · 2026Article
- A simple method that doubles learning speed for mice in touchscreen-based visual discrimination.Scientific reports · 2025Article
- Placental Igf1 overexpression sex-specifically impacts mouse placenta structure, altering offspring striatal development and behavior.Experimental neurology · 2025Article
- The Aryl Hydrocarbon Receptor in Neurotoxicity: An Intermediator Between Dioxins and Neurons in the Brain.Toxics · 2025Review
- Mutation of the histone demethylase Gasc1 causes ASD-like symptoms in mice.Inflammation and regeneration · 2025Article
- Developmental Disturbances in Animal Models of Autism Spectrum Disorder.Developmental neurobiology · 2025Review
- ESC models of autism with copy-number variations reveal cell-type-specific translational vulnerability.Cell genomics · 2025Article
- Genome-wide identification and analysis of recurring patterns of epigenetic variation across individuals.Communications biology · 2025Article
- Mom genes and dad genes: genomic imprinting in the regulation of social behaviors.Epigenomics · 2025Review
- Article
204 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Substantial evidence suggests that chromosomal abnormalities contribute to the risk of autism. The duplication of human chromosome 15q11-13 is known to be the most frequent cytogenetic abnormality in autism. We have modeled this genetic change in mice by using chromosome engineering to generate a 6.3 Mb duplication of the conserved linkage group on mouse chromosome 7. Mice with a paternal duplication display poor social interaction, behavioral inflexibility, abnormal ultrasonic vocalizations, and correlates of anxiety. An increased MBII52 snoRNA within the duplicated region, affecting the serotonin 2c receptor (5-HT2cR), correlates with altered intracellular Ca(2+) responses elicited by a 5-HT2cR agonist in neurons of mice with a paternal duplication. This chromosome-engineered mouse model for autism seems to replicate various aspects of human autistic phenotypes and validates the relevance of the human chromosome abnormality. This model will facilitate forward genetics of developmental brain disorders and serve as an invaluable tool for therapeutic development.
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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.