ArticleFrontiers in molecular neuroscience2020
Loss of DEK Expression Induces Alzheimer's Disease Phenotypes in Differentiated SH-SY5Y Cells.
Article in Frontiers in molecular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- DEK Loss Induces Task-specific Deficits in Learning and Memory and Reprograms the Hippocampal Transcriptome in Mice.Molecular neurobiology · 2026Article
- All hands on DEK: structural insights into a unique histone modifier and chromatin remodeler.Epigenetics & chromatin · 2026Review
- Cell death-associated genes as novel diagnostic biomarkers for autism spectrum disorder.Apoptosis : an international journal on programmed cell death · 2026Article
- Dek Loss Induces Sex-Dependent, Task-Specific Cognitive Deficits and Reprograms the Hippocampal Transcriptome in Mice.Research square · 2025Article
- The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia.Experimental hematology · 2023Review
- Dysregulated miRNAs in Progression and Pathogenesis of Alzheimer's Disease.Molecular neurobiology · 2022Review
- Lead-exposure associated miRNAs in humans and Alzheimer's disease as potential biomarkers of the disease and disease processes.Scientific reports · 2022Article
- In silico gene expression and pathway analysis of DEK in the human brain across the lifespan.The European journal of neuroscience · 2022Article
- Article
- Novel molecular mechanisms in Alzheimer's disease: The potential role of DEK in disease pathogenesis.Frontiers in aging neuroscience · 2022Review
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Authors and funding
4 authors at 3 institutions in 1 country.
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Abstract
Alzheimer's disease (AD) is the most common cause of dementia and is characterized by the buildup of β-amyloid plaques and neurofibrillary Tau tangles. This leads to decreased synaptic efficacy, cell death, and, consequently, brain atrophy in patients. Behaviorally, this manifests as memory loss and confusion. Using a gene ontology analysis, we recently identified AD and other age-related dementias as candidate diseases associated with the loss of DEK expression. DEK is a nuclear phosphoprotein with roles in DNA repair, cellular proliferation, and inhibiting apoptosis. Work from our laboratory determined that DEK is highly expressed in the brain, particularly in regions relevant to learning and memory, including the hippocampus. Moreover, we have also determined that DEK is highly expressed in neurons. Consistent with our gene ontology analysis, we recently reported that cortical DEK protein levels are inversely proportional to dementia severity scores in elderly female patients. However, the functional role of DEK in neurons is unknown. Thus, we knocked down DEK in an
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