ArticleMolecular and cellular biology2002
Dyrk1A haploinsufficiency affects viability and causes developmental delay and abnormal brain morphology in mice.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 papers.
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Who cites it
167 citing papers in PubMed, 339 citations in OpenAlex.
- Phosphoproteomics identifies the DYRK1B protein kinase as a regulator of processing bodies.Journal of cell science · 2026Article
- A Researcher's guide to rodent models of Down syndrome: Recent insights and translational perspectives.STAR protocols · 2026Review
- Sex-specific developmental phenotypes and their response to neonatalbioRxiv : the preprint server for biology · 2026Article
- Epigenetic treatment of synaptic and behavioral deficits in Dyrk1a-mutant mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Genetic analysis of triplicated genes affecting sex-specific skeletal deficits in Down syndrome model mice.G3 (Bethesda, Md.) · 2026Article
- Up-regulation of Minibrain/DYRK1A contributes to macrocephaly and brain overgrowth in aProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Genetic analysis of triplicated genes affecting sex-specific skeletal deficits in Down syndrome model mice.bioRxiv : the preprint server for biology · 2025Article
- Interneuron migration defects during corticogenesis contribute to Dyrk1a haploinsufficiency syndrome pathogenesis.Molecular psychiatry · 2025Article
- Myocardial phosphoproteomics unveils a key role of DYRK1A in aortic valve replacement-induced reverse remodelling.Basic research in cardiology · 2025Article
- Structural Dynamics and Network Pharmacology for the Discovery of Inhibitors Targeting DYRK1 A in Neurological Disorders.Molecular neurobiology · 2025Article
- The role of Goldilocks protein kinase DYRK1A in embryonic development.Developmental biology · 2025Review
- Unlocking the Therapeutic Potential of the Dual-Specificity Tyrosine Phosphorylation-Regulated Kinase 1A Inhibitors in Alzheimer's Diseases.Molecular neurobiology · 2025Review
- Lithium normalizes ASD-related neuronal, synaptic, and behavioral phenotypes in DYRK1A-knockin mice.Molecular psychiatry · 2025Article
- Visual and auditory attention in individuals with DYRK1A and SCN2A disruptive variants.Autism research : official journal of the International Society for Autism Research · 2025Article
- DYRK1A roles in human neural progenitors.Frontiers in neuroscience · 2025Article
- Article
- Sex-specific trisomic Dyrk1a-related skeletal phenotypes during development in a Down syndrome model.Disease models & mechanisms · 2024Article
- Dyrk1a is required for craniofacial development in Xenopus laevis.Developmental biology · 2024Article
- Characterizing Sensory Phenotypes of Subgroups with a Known Genetic Etiology Pertaining to Diagnoses of Autism Spectrum Disorder and Intellectual Disability.Journal of autism and developmental disorders · 2024Article
- Sex specific emergence of trisomicbioRxiv : the preprint server for biology · 2024Article
107 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DYRK1A is the human orthologue of the Drosophila minibrain (mnb) gene, which is involved in postembryonic neurogenesis in flies. Because of its mapping position on chromosome 21 and the neurobehavioral alterations shown by mice overexpressing this gene, involvement of DYRK1A in some of the neurological defects of Down syndrome patients has been suggested. To gain insight into its physiological role, we have generated mice deficient in Dyrk1A function by gene targeting. Dyrk1A(-/-) null mutants presented a general growth delay and died during midgestation. Mice heterozygous for the mutation (Dyrk1A(+/-)) showed decreased neonatal viability and a significant body size reduction from birth to adulthood. General neurobehavioral analysis revealed preweaning developmental delay of Dyrk1A(+/-) mice and specific alterations in adults. Brains of Dyrk1A(+/-) mice were decreased in size in a region-specific manner, although the cytoarchitecture and neuronal components in most areas were not altered. Cell counts showed increased neuronal densities in some brain regions and a specific decrease in the number of neurons in the superior colliculus, which exhibited a significant size reduction. These data provide evidence about the nonredundant, vital role of Dyrk1A and suggest a conserved mode of action that determines normal growth and brain size in both mice and flies.
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