ReviewExperimental neurobiology2013
New Perspectives of Dyrk1A Role in Neurogenesis and Neuropathologic Features of Down Syndrome.
Review in Experimental neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 103 citations in OpenAlex.
- Sex-specific developmental phenotypes and their response to neonatalbioRxiv : the preprint server for biology · 2026Article
- Cholinergic System Structure and Function Changes in Individuals with Down Syndrome During the Development of Alzheimer's Disease.Current topics in behavioral neurosciences · 2025Review
- DYRK1A in blood and immune function: implications in leukemia, inflammatory disorders, infection and Down syndrome.Frontiers in cell and developmental biology · 2025Review
- Article
- Sex-specific developmental alterations in DYRK1A expression in the brain of a Down syndrome mouse model.Neurobiology of disease · 2024Article
- Characterizing executive functioning and associated behaviors in individuals with dual-specificity tyrosine phosphorylation-regulated kinase 1A (Frontiers in neuroscience · 2024Article
- Skeletal health inFrontiers in neuroscience · 2024Review
- Over-expression of Dyrk1A affects bleeding by modulating plasma fibronectin and fibrinogen level in mice.Journal of cellular and molecular medicine · 2023Article
- DYRK1A promotes viral entry of highly pathogenic human coronaviruses in a kinase-independent manner.PLoS biology · 2023Article
- Insights from the protein interaction Universe of the multifunctional "Goldilocks" kinase DYRK1A.Frontiers in cell and developmental biology · 2023Review
- DYRK3 phosphorylates SNAPIN to regulate axonal retrograde transport and neurotransmitter release.Cell death discovery · 2022Article
- TTC3-Mediated Protein Quality Control, A Potential Mechanism for Cognitive Impairment.Cellular and molecular neurobiology · 2022Review
- Article
- Sexually dimorphic DYRK1A overexpression on postnatal day 15 in the Ts65Dn mouse model of Down syndrome: Effects of pharmacological targeting on behavioral phenotypes.Pharmacology, biochemistry, and behavior · 2022Article
- Developmental Neuropathology and Neurodegeneration of Down Syndrome: Current Knowledge in Humans.Frontiers in cell and developmental biology · 2022Review
- Review
- Diabetic Kinome Inhibitors-A New Opportunity for β-Cells Restoration.International journal of molecular sciences · 2021Review
- Importance of determining variations in the number of copies in newborns with autosomal aneuploidiesBiomedica : revista del Instituto Nacional de Salud · 2021Article
- DYRK1A pathogenic variants in two patients with syndromic intellectual disability and a review of the literature.Molecular genetics & genomic medicine · 2020Review
- Abnormalities of DYRK1A-Cytoskeleton Complexes in the Blood Cells as Potential Biomarkers of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Down syndrome (DS) is one of the most common genetic disorders accompanying with mental retardation, cognitive impairment, and deficits in learning and memory. The brains with DS also display many neuropathological features including alteration in neurogenesis and synaptogenesis and early onset of Alzheimer's disease (AD)-like symptoms. Triplication of all or a part of human chromosome 21, especially the 21q22.1~21q22.3 region called 'Down syndrome critical region (DSCR)', has been considered as the main cause of DS. One gene product of DSCR, dual-specificity tyrosine-phosphorylation-regulated kinase 1A (Dyrk1A), has been highlighted as a key contributor to the neural consequences of DS. This minireview summarizes accumulating recent reports about Dyrk1A involvement in the neuritogenesis, synaptogenesis, and AD-like neurofibrillary tangle formation, which is mainly focusing on Dyrk1A-mediated regulation of cytoskeletal proteins, such as tubulin, actin, and microtubule-associated protein tau. Understanding the molecular mechanisms of these phenomena may provide us a rational for new preventive and therapeutic treatment of DS.
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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.