ArticleThe EMBO journal2000
Loss of FBP function arrests cellular proliferation and extinguishes c-myc expression.
Article in The EMBO journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 150 citations in OpenAlex.
- PRMT5-mediated FUBP1 methylation accelerates prostate cancer progression.The Journal of clinical investigation · 2024Article
- DNA superhelicity.Nucleic acids research · 2024Article
- Article
- Musashi-2 (MSI2) promotes neuroblastoma tumorigenesis through targeting MYC-mediated glucose-6-phosphate dehydrogenase (G6PD) transcriptional activation.Medical oncology (Northwood, London, England) · 2023Article
- Psi promotes Drosophila wing growth via direct transcriptional activation of cell cycle targets and repression of growth inhibitors.Development (Cambridge, England) · 2023Article
- Lnc-EST12, which is negatively regulated by mycobacterial EST12, suppresses antimycobacterial innate immunity through its interaction with FUBP3.Cellular & molecular immunology · 2022Article
- Far upstream element -binding protein 1 (FUBP1) participates in the malignant process and glycolysis of colon cancer cells by combining with c-Myc.Bioengineered · 2022Article
- LCAT3, a novel m6A-regulated long non-coding RNA, plays an oncogenic role in lung cancer via binding with FUBP1 to activate c-MYC.Journal of hematology & oncology · 2021Article
- Fangchinoline suppresses conjunctival melanoma by directly binding FUBP2 and inhibiting the homologous recombination pathway.Cell death & disease · 2021Article
- Developmental Roles of FUSE Binding Protein 1 (International journal of molecular sciences · 2020Article
- FUBP1 and FUBP2 enforce distinct epigenetic setpoints for MYC expression in primary single murine cells.Communications biology · 2020Article
- Transcriptional repression of Myc underlies the tumour suppressor function of AGO1 inDevelopment (Cambridge, England) · 2020Article
- Causal network perturbations for instance-specific analysis of single cell and disease samples.Bioinformatics (Oxford, England) · 2020Article
- Identification of FUBP1 as a Long Tail Cancer Driver and Widespread Regulator of Tumor Suppressor and Oncogene Alternative Splicing.Cell reports · 2019Article
- The transcriptional regulator FUBP1 influences disease outcome in murine and human myeloid leukemia.Leukemia · 2019Article
- Molecular Pathogenesis of Low-Grade Glioma.Neurosurgery clinics of North America · 2019Review
- The master regulator FUBP1: its emerging role in normal cell function and malignant development.Cellular and molecular life sciences : CMLS · 2019Review
- Interplay between transcription regulators RUNX1 and FUBP1 activates an enhancer of the oncogene c-KIT and amplifies cell proliferation.Nucleic acids research · 2018Article
- Somatic Mutational Landscape of Splicing Factor Genes and Their Functional Consequences across 33 Cancer Types.Cell reports · 2018Article
- Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas.Cell systems · 2018Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The c-myc regulatory region includes binding sites for a large set of transcription factors. The present studies demonstrate that in the absence of FBP [far upstream element (FUSE)-binding protein], which binds to the single-stranded FUSE, the remainder of the set fails to sustain endogenous c-myc expression. A dominant-negative FBP DNA-binding domain lacking effector activity or an antisense FBP RNA, expressed via replication-defective adenovirus vectors, arrested cellular proliferation and extinguished native c-myc transcription from the P1 and P2 promoters. The dominant-negative FBP initially augmented the single-stranded character of FUSE; however, once c-myc expression was abolished, melting at FUSE could no longer be supported. In contrast, with antisense FBP RNA, the single-stranded character of FUSE decreased monotonically as the transcription of endogenous c-myc declined. Because transcription is the major source of super-coiling in vivo, we propose that by binding torsionally strained DNA, FBP measures promoter activity directly. We also show that FUSE is predicted to behave as a torsion-regulated switch poised to regulate c-myc and to confer a higher order regulation on a large repertoire of factors.
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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.