ArticleInternational journal of molecular sciences2016
Zinc Finger and X-Linked Factor (ZFX) Binds to Human SET Transcript 2 Promoter and Transactivates SET Expression.
Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Potential links between PCOS/PMOS and Alzheimer disease and related dementias.Journal of the Endocrine Society · 2026Review
- Detecting Biomarkers of Alzheimer's Disease Based on Multi-constrained Uncertainty-Aware Adaptive Sparse Multi-view Canonical Correlation Analysis.Journal of molecular neuroscience : MN · 2022Article
- ExonSkipAD provides the functional genomic landscape of exon skipping events in Alzheimer's disease.Briefings in bioinformatics · 2021Article
- Network Analysis Identifies Sex-Specific Gene Expression Changes in Blood of Amyotrophic Lateral Sclerosis Patients.International journal of molecular sciences · 2021Article
- Zinc Finger Proteins in Neuro-Related Diseases Progression.Frontiers in neuroscience · 2021Review
- HOXA-AS2 promotes type I endometrial carcinoma via miRNA-302c-3p-mediated regulation of ZFX.Cancer cell international · 2020Article
- SE translocation gene but not zinc finger or X-linked factor is down-regulated in gastric cancer.Gastroenterology and hepatology from bed to bench · 2020Article
- Development and identification of Set transgenic mice.Experimental and therapeutic medicine · 2018Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SET (SE Translocation) protein carries out multiple functions including those for protein phosphatase 2A (PP2A) inhibition, histone modification, DNA repair, and gene regulation. SET overexpression has been detected in brain neurons of patients suffering Alzheimer's disease, follicle theca cells of Polycystic Ovary Syndrome (PCOS) patients, and ovarian cancer cells, indicating that SET may play a pathological role for these disorders. SET transcript 2, produced by a specific promoter, represents a major transcript variant in different cell types. In this study, we characterized the transcriptional activation of human SET transcript 2 promoter in HeLa cells. Promoter deletion experiments and co-transfection assays indicated that ZFX, the Zinc finger and X-linked transcription factor, was able to transactivate the SET promoter. A proximal promoter region containing four ZFX-binding sites was found to be critical for the ZFX-mediated transactivation. Mutagenesis study indicated that the ZFX-binding site located the closest to the transcription start site accounted for most of the ZFX-mediated transactivity. Manipulation of ZFX levels by overexpression or siRNA knockdown confirmed the significance and specificity of the ZFX-mediated SET promoter activation. Chromatin immunoprecipitation results verified the binding of ZFX to its cognate sites in the SET promoter. These findings have led to identification of ZFX as an upstream factor regulating
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