The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
HIF-1-mediated activation of transferrin receptor gene transcription by iron chelation
Open accessAbstract
Treatment with iron chelators mimics hypoxic induction of the hypoxia inducible factor (HIF-1) which activates transcription by binding to hypoxia responsive elements (HRE). We investigated whether HIF-1 is involved in transcriptional activation of the transferrin receptor (TfR), a membrane protein which mediates cellular iron uptake, in response to iron deprivation. The transcription rate of the TfR gene in isolated nuclei was up-regulated by treatment of Hep3B human hepatoma cells with the iron chelator desferrioxamine (DFO). The role of HIF-1 in the activation of TfR was indicated by the following observations: (i) DFO-dependent activation of a luciferase reporter gene in transfected Hep3B cells was mediated by a fragment of the human TfR promoter containing a putative HRE sequence; (ii) mutation of this sequence prevented stimulation of luciferase activity; (iii) binding to this sequence of HIF-1alpha, identified by competition experiments and supershift assays, was induced by DFO. Furthermore, in mouse hepatoma cells unable to assemble functional HIF-1, inducibility of TfR transcription by DFO was lost and TfR mRNA up-regulation was reduced. These results, which show the role of HIF-1 in the control of TfR gene expression in conditions of iron depletion, give insights into the mechanisms of transcriptional regulation which concur with the well-characterized post-transcriptional control of TfR expression to expand the extent of response to iron deficiency.
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“The GAA triplet-repeat expansion in the frataxin gene was shown to interfere with frataxin gene transcription (223) because of a self-associated triplex formation at long GAA:TTC repeats (sticky DNA) (22, 193, 267, 268).”
From Intracellular iron transport and storage: from molecular mechanisms to health implications (2008) · cites this paper as [22]
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Hypoxia-Inducible Factor-1 (HIF-1)
Ke, Q., & Costa, M. (2006) · Molecular Pharmacology · doi:10.1124/mol.106.027029 · Cited by 1,690
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Intracellular iron transport and storage: from molecular mechanisms to health implications
Mackenzie, E. L., Iwasaki, K., & Tsuji, Y. (2008) · Antioxidants & Redox Signaling · doi:10.1089/ars.2007.1893 · Cited by 526
Gupta, N., & Wish, J. B. (2017) · American Journal of Kidney Diseases · doi:10.1053/j.ajkd.2016.12.011 · Cited by 460
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Metadata
- Authors
- Bianchi, L., Tacchini, L., & Cairo, G.
- Affiliations
- University of Milan (IT)
- Corresponding author
- Cairo, G.
- Venue
- Nucleic Acids Research
- Publisher
- Oxford University Press (OUP)
- Published
- 1999-11-01
- Volume
- 27
- Issue
- 21
- Pages
- 4223-4227
- ISSN
- 0305-1048 (ISSN-L)
- 1362-4962
- PMC
- PMC148697
- OpenAlex
- W2130304025
- Cited by
- 189
- References
- 33
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 7 · 2023: 12 · 2022: 9 · 2021: 12 · 2020: 8 · 2019: 5 · 2018: 2 · 2017: 3 · 2016: 4 · 2015: 4 · 2014: 4 · 2013: 7 · 2012: 6
- FWCI
- 2.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Nucleic Acids Research (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Consiglio Nazionale delle Ricerche
- Ministero dell'Università e della Ricerca
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
- Keywords
- HIF-1, transferrin receptor, iron chelation, deferoxamine, iron deficiency, hypoxia response element, transcriptional regulation, HIF-1α, hepatoma cells, iron absorption, gene expression
- MeSH terms
- Iron Deficiencies, Animals, Base Sequence, Cobalt, Deferoxamine, DNA, DNA-Binding Proteins, Carcinoma, Hepatocellular, Humans, Iron, Iron Chelating Agents, Mutation, Nuclear Proteins, Promoter Regions, Genetic, Receptors, Transferrin, Transcription Factors, Transcription, Genetic, Transfection, Tumor Cells, Cultured, Transcriptional Activation, Cell Hypoxia, Response Elements, Mice, Hypoxia-Inducible Factor 1, Hypoxia-Inducible Factor 1, alpha Subunit
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