ArticleMolecular brain2021
Mice with mutations in Trpm1, a gene in the locus of 15q13.3 microdeletion syndrome, display pronounced hyperactivity and decreased anxiety-like behavior.
Article in Molecular brain, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Non-canonical pore architecture underlies constitutive gating of human retinal TRPM1.Nature communications · 2026Article
- Genetic mutations and synaptic dysfunctions in social interaction disorders: insights from invertebrate models to humans.Metabolic brain disease · 2026Review
- Maternal immune activation in mice recapitulates features of attention-deficit/hyperactivity disorder (ADHD) in susceptible offspring.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Progress towards understanding risk factor mechanisms in the development of autism spectrum disorders.Biochemical Society transactions · 2024Review
- Impaired OTUD7A-dependent Ankyrin regulation mediates neuronal dysfunction in mouse and human models of the 15q13.3 microdeletion syndrome.Molecular psychiatry · 2023Article
- Article
- Altered gene expression profiles impair the nervous system development in individuals with 15q13.3 microdeletion.Scientific reports · 2022Article
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Authors and funding
6 authors at 3 institutions in 1 country.
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Abstract
The 15q13.3 microdeletion syndrome is a genetic disorder characterized by a wide spectrum of psychiatric disorders that is caused by the deletion of a region containing 7 genes on chromosome 15 (MTMR10, FAN1, TRPM1, MIR211, KLF13, OTUD7A, and CHRNA7). The contribution of each gene in this syndrome has been studied using mutant mouse models, but no single mouse model recapitulates the whole spectrum of human 15q13.3 microdeletion syndrome. The behavior of Trpm1
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