ArticleMolecular neurobiology2017
Regulation of SET Gene Expression by NFkB.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Common Signaling Pathways in Cancer and Alzheimer's Disease May Point to New Treatments.Current topics in medicinal chemistry · 2025Review
- Exploring the Therapeutic Potential of Glycyrrhiza Compounds in Alzheimer's Disease: A Comprehensive Review.Current topics in medicinal chemistry · 2025Review
- Unveiling the Therapeutic Potential of Kelulut (Stingless Bee) Honey in Alzheimer's Disease: Findings from a Rat Model Study.Antioxidants (Basel, Switzerland) · 2024Article
- The next decade of SET: from an oncoprotein to beyond.Journal of molecular cell biology · 2024Review
- The neuroprotective effects of targeting key factors of neuronal cell death in neurodegenerative diseases: The role of ER stress, oxidative stress, and neuroinflammation.Frontiers in cellular neuroscience · 2023Review
- Potential of hsa-miR200a-3p and hsa-miR502-3p as blood-based biomarker for Alzheimer's disease.Molecular biology reports · 2022Article
- The Pivotal Role of NF-kB in the Pathogenesis and Therapeutics of Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Deep Neural Network Classifier for Alzheimer's Disease.Journal of student research · 2022Article
- Paraquat Induces Lung InjuryFrontiers in pharmacology · 2022Article
- Effect ofBiomedical reports · 2021Article
- Endoplasmic Reticulum Stress and Unfolded Protein Response in Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Transcriptional activation of USP16 gene expression by NFκB signaling.Molecular brain · 2019Article
- Cyclin-dependent kinase 1-mediated phosphorylation of SET at serine 7 is essential for its oncogenic activity.Cell death & disease · 2019Article
- Fluoride Exposure Induces Inhibition of Sodium-and Potassium-Activated Adenosine Triphosphatase (NaInternational journal of environmental research and public health · 2019Review
- The Contribution of Fluoride to the Pathogenesis of Eye Diseases: Molecular Mechanisms and Implications for Public Health.International journal of environmental research and public health · 2019Review
- Nuclear Factor-Kappa B and Alzheimer Disease, Unifying Genetic and Environmental Risk Factors from Cell to Humans.Frontiers in immunology · 2017Review
- Zinc Finger and X-Linked Factor (ZFX) Binds to Human SET Transcript 2 Promoter and Transactivates SET Expression.International journal of molecular sciences · 2016Article
- The multifaceted roles of the transcription factorAlzheimer's & dementia (New York, N. Y.)Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
SET is elevated and mislocalized in the neuronal cytoplasm in brains of Alzheimer's disease (AD) and Down syndrome (DS) patients. Cytoplasm SET leads to inhibition of protein phosphatase 2A and is involved in the tau pathology. However, the regulation of SET gene expression remains elusive. In the present study, we cloned a 1399-bp segment of the 5' flanking region of the human SET gene and identified that the transcription start site (TSS) of SET transcript 1 is located at 123 bp upstream of the translation start site ATG in exon 1. Sequence analysis reveals several putative regulatory elements including NFkB, Sp1, and HSE. Luciferase assay and electrophoretic mobility shift assay (EMSA) identified a functional cis-acting NFkB-responsive element in the SET gene promoter. Overexpression and activation of NFkB upregulate transcription of SET isoform 1 but not isoform 2, indicating that the expression of these two isoforms is differentially regulated. The results demonstrate that NFkB plays an important role in regulation of the human SET gene expression. Our findings suggest that oxidative stress and inflammatory responses could result in abnormal SET gene expression, contributing to the tauopathy in AD pathogenesis.
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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 OpenQuestion graph.