ArticleJournal of neurodevelopmental disorders2011
The neurobiology of mouse models syntenic to human chromosome 15q.
Article in Journal of neurodevelopmental disorders, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 25 citations in OpenAlex.
- Glial expression of Drosophila UBE3A causes spontaneous seizures that can be modulated by 5-HT signaling.Neurobiology of disease · 2024Article
- Are sleep disturbances a cause or consequence of autism spectrum disorder?Psychiatry and clinical neurosciences · 2023Article
- Translational Magnetic Resonance Imaging in Autism Spectrum Disorder From the Mouse Model to Human.Frontiers in neuroscience · 2022Review
- Understanding autism spectrum disorders with animal models: applications, insights, and perspectives.Zoological research · 2021Review
- UBE3A regulates the transcription of IRF, an antiviral immunity.Human molecular genetics · 2019Article
- Distinct Defects in Spine Formation or Pruning in Two Gene Duplication Mouse Models of Autism.Neuroscience bulletin · 2017Article
- Transcriptome profiling of white adipose tissue in a mouse model for 15q duplication syndrome.Genomics data · 2015Article
- Imprinted Zac1 in neural stem cells.World journal of stem cells · 2015Review
- Ube3a imprinting impairs circadian robustness in Angelman syndrome models.Current biology : CB · 2015Article
- Assessing behavioural and cognitive domains of autism spectrum disorders in rodents: current status and future perspectives.Psychopharmacology · 2014Review
- Animal models of psychiatric disorders that reflect human copy number variation.Neural plasticity · 2012Review
- Using mouse models of autism spectrum disorders to study the neurotoxicology of gene-environment interactions.Neurotoxicology and teratologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism is a neurodevelopmental disorder that manifests in childhood as social behavioral abnormalities, such as abnormal social interaction, impaired communication, and restricted interest or behavior. Of the known causes of autism, duplication of human chromosome 15q11-q13 is the most frequently associated cytogenetic abnormality. Chromosome 15q11-q13 is also known to include imprinting genes. In terms of neuroscience, it contains interesting genes such as Necdin, Ube3a, and a cluster of GABA(A) subunits as well as huge clusters of non-coding RNAs (small nucleolar RNAs, snoRNAs). Phenotypic analyses of mice genetically or chromosomally engineered for each gene or their clusters on a region of mouse chromosome seven syntenic to human 15q11-q13 indicate that this region may be involved in social behavior, serotonin metabolism, and weight control. Further studies using these models will provide important clues to the pathophysiology of autism. This review overviews phenotypes of mouse models of genes in 15q11-q13 and their relationships to autism.
Identifiers
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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.