Cited by 220Down syndrome and intellectual disability researchGenetics and Neurodevelopmental DisordersAlzheimer's disease research and treatments

DYRK1A BAC transgenic mice show altered synaptic plasticity with learning and memory defects

Open access
Ahn, Kyoung-Jin, Jeong, Hey Kyeong, Choi, Han-Saem, Ryoo, Soo-Ryoon, Kim, Yeon Ju, Goo, Jun-Seo, Choi, Se-Young, Han, Jung-Soo +2 more·2006·Neurobiology of Disease

Abstract

Among the various phenotypes seen in Down syndrome (DS), mental retardation is the most common and most debilitating condition suffered by individuals with DS. The DYRK1A gene on human chromosome 21q22.2 encodes a subfamily of protein kinases that displays dual substrate specificities and is known to play a critical role in neurodevelopment. To study DS mental retardation, we have generated transgenic mice that contain only one copy of the complete human DYRK1A gene in a bacterial artificial chromosome. The transgenic mice showed significant impairment in hippocampal-dependent memory tasks in a Morris water maze. Interestingly, we observed shifts in both long-term potentiation and long-term depression, which suggests a role for DYRK1A in bidirectional synaptic plasticity. These mice represent the most clinically relevant DYRK1A mouse model to date and provide us a valuable tool for the in vivo study of mechanisms that underlie the learning and memory deficit in DS.

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Crossref · 10.1016/j.nbd.2005.12.006

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  • DYRK1A is a serine-threonine kinase that utilizes autophosphorylation to enhance activity and stabilize itself, regulates many downstream proteins and transcription factors, and has a crucial role during brain development.

    “DYRK1A is a serine-threonine kinase that utilizes autophosphorylation to enhance activity and stabilize itself, regulates many downstream proteins and transcription factors, and has a crucial role during brain development (Ahn et al., 2006; Arron et al., 2006; Atas-Ozcan et al., 2021; Branchi et al., 2004; Canzonetta et al., 2008; Hammerle et al., 2011; Martinez de Lagran et al., 2004; Park and Ch”

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Authors
Ahn, K.-J., Jeong, H. K., Choi, H.-S., Ryoo, S.-R., Kim, Y. J., Goo, J.-S., Choi, S.-Y., Han, J.-S., Ha, I., & Song, W.-J.
Affiliations
  • Inje University (KR)
  • Seoul National University (KR)
Corresponding author
  • Ha, Ilho
  • Song, Woo-Joo
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2006-06
Volume
22
Issue
3
Pages
463-472
ISSN
0969-9961 (ISSN-L)
OpenAlex
W2110646442
Cited by
220
References
54
Citations by year
2026: 1 · 2025: 4 · 2024: 5 · 2023: 7 · 2022: 11 · 2021: 6 · 2020: 7 · 2019: 10 · 2018: 8 · 2017: 17 · 2016: 9 · 2015: 6 · 2014: 15 · 2013: 15 · 2012: 27
FWCI
14.00
Type
journal article
Language
en
Open access
Locations
  • Neurobiology of Disease (publishedVersion)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Seoul National University Open Repository (Seoul National University) (submittedVersion)
Topics
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Keywords
DYRK1A, Down syndrome, intellectual disability, transgenic mouse model, bacterial artificial chromosome, synaptic plasticity, long-term potentiation, long-term depression, hippocampal-dependent memory, learning and memory impairment, protein kinases
MeSH terms
Dyrk Kinases, Animals, Disease Models, Animal, Down Syndrome, Humans, Immunohistochemistry, Learning Disabilities, Memory Disorders, Mice, Transgenic, Neuronal Plasticity, Protein-Tyrosine Kinases, Polymerase Chain Reaction, Protein Serine-Threonine Kinases, In Situ Hybridization, Fluorescence, Chromosomes, Artificial, Bacterial, Mice

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