Evidence map›Paper›PMID 40390093›Full record

ArticleMolecular brain2025

DYRK1A modulates fear memory formation via epigenetic modification.

Dae-Si Kang, Ja Wook Koo

Abstract read
In one paragraph

Article in Molecular brain, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Dae-Si KangEmotion, Cognition and Behavior Research Group, Korea Brain Research Institute, Daegu, 41062, Republic of Korea.
Ja Wook KooEmotion, Cognition and Behavior Research Group, Korea Brain Research Institute, Daegu, 41062, Republic of Korea. jawook.koo@kbri.re.kr.

Funding

Ministry of Science and ICT, South Korea NRF-2022M3E5E8081182
6 · The paper itself

Abstract

Fear memory formation is crucial for survival, with the hippocampus playing a central role. This study investigates the behavioral and molecular aspects of fear memory formation, focusing on Dual-specificity tyrosine phosphorylation-regulated kinase 1 A (DYRK1A), a protein known to be critical for cognitive functions. Our results demonstrate that DYRK1A expression in hippocampal CA1 pyramidal neurons is downregulated after contextual fear conditioning (CFC). We also observed a decrease in DYRK1A binding to the Maoa promoter, suggesting its involvement in transcriptional regulation during fear memory formation. In subsequent experiments, we modulated DYRK1A expression using viral vectors. DYRK1A overexpression reduced freezing behavior, while knockdown enhanced it. At the molecular level, DYRK1A overexpression resulted in elevated H3K4me3 levels, while knockdown decreased it. These findings indicate that DYRK1A regulates fear memory formation via epigenetic modifications, altering H3K4me3 levels and influencing Maoa transcription in the hippocampus. This research highlights the nuclear role of DYRK1A and suggests its potential as a therapeutic target for neuropsychiatric disorders related to fear and memory.

Indexed as

Epigenesis, GeneticFearMemoryProtein Serine-Threonine KinasesProtein-Tyrosine KinasesAnimalsBehavior, AnimalDyrk KinasesHistonesMaleMethylationMiceMice, Inbred C57BLMonoamine OxidasePromoter Regions, GeneticProtein BindingDyrk Kinaseshistone H3 trimethyl Lys4HistonesMonoamine OxidaseProtein Serine-Threonine KinasesProtein-Tyrosine KinasesContextual fear conditioningDYRK1AHistone modification

Identifiers

PMID40390093
PMCPMC12090515

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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.