ArticleNature communications2023
B cell class switch recombination is regulated by DYRK1A through MSH6 phosphorylation.
Article in Nature communications, 2023. 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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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- Enterovirus infections in children.Pediatric investigation · 2026Review
- DYRK1A enhances antitumor immunity in type 1 conventional dendritic cells via mTORC1 activation.The Journal of clinical investigation · 2026Article
- Mapping the Brain Interaction Network of the Dual-Specificity, Tyrosine Phosphorylation-Regulated Kinase 1A (DYRK1A) Targeted by Leucettinib-21 Using Affinity Chromatography.ACS pharmacology & translational science · 2026Article
- Live long and persist: polyomavirus immune evasion in the brain and kidney.Future virology · 2025Article
- Enteroviruses Activate Cellular Innate Immune Responses Prior to Adaptive Immunity and Tropism Contributes to Severe Viral Pathogenesis.Microorganisms · 2025Review
- Estrogen influences class-switched memory B cell frequency only in humans with two X chromosomes.The Journal of experimental medicine · 2025Article
- DYRK1A in blood and immune function: implications in leukemia, inflammatory disorders, infection and Down syndrome.Frontiers in cell and developmental biology · 2025Review
- SMARCA5-mediated chromatin remodeling is required for germinal center formation.The Journal of experimental medicine · 2024Article
- Nuclear F-actin assembly on damaged chromatin is regulated by DYRK1A and Spir1 phosphorylation.Nucleic acids research · 2024Article
- Article
- B-cell dynamics underlying poor response upon split-inactivated influenza virus vaccination.Frontiers in immunology · 2024Article
- Insights from the protein interaction Universe of the multifunctional "Goldilocks" kinase DYRK1A.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protection from viral infections depends on immunoglobulin isotype switching, which endows antibodies with effector functions. Here, we find that the protein kinase DYRK1A is essential for B cell-mediated protection from viral infection and effective vaccination through regulation of class switch recombination (CSR). Dyrk1a-deficient B cells are impaired in CSR activity in vivo and in vitro. Phosphoproteomic screens and kinase-activity assays identify MSH6, a DNA mismatch repair protein, as a direct substrate for DYRK1A, and deletion of a single phosphorylation site impaired CSR. After CSR and germinal center (GC) seeding, DYRK1A is required for attenuation of B cell proliferation. These findings demonstrate DYRK1A-mediated biological mechanisms of B cell immune responses that may be used for therapeutic manipulation in antibody-mediated autoimmunity.
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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 Socratic graph.