ArticlePloS one2011
Direct inhibition of TNF-α promoter activity by Fanconi anemia protein FANCD2.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
20 citing papers in PubMed, 32 citations in OpenAlex.
- The FANCD2-FANCI heterodimer coordinates chromatin openness and cell cycle progression throughout DNA double-strand break repair.Cell reports · 2026Article
- The tight bond between Fanconi anemia and aging.Frontiers in aging · 2026Review
- Beyond DNA repair and chromosome instability-Fanconi anaemia as a cellular senescence-associated syndrome.Cell death and differentiation · 2021Review
- Fanconi anemia A protein participates in nucleolar homeostasis maintenance and ribosome biogenesis.Science advances · 2021Article
- Microphthalmia transcription factor expression contributes to bone marrow failure in Fanconi anemia.The Journal of clinical investigation · 2020Article
- FANCI Cooperates with IMPDH2 to Promote Lung Adenocarcinoma Tumor Growth via a MEK/ERK/MMPs Pathway.OncoTargets and therapy · 2020Article
- Fanconi anemia proteins counteract the implementation of the oncogene-induced senescence program.Scientific reports · 2019Article
- Fanconi Anemia: A DNA repair disorder characterized by accelerated decline of the hematopoietic stem cell compartment and other features of aging.Ageing research reviews · 2017Review
- Maintenance of genome stability by Fanconi anemia proteins.Cell & bioscience · 2017Review
- V(D)J recombination process and the Pre-B to immature B-cells transition are altered in FancaScientific reports · 2016Article
- TGF-β Inhibition Rescues Hematopoietic Stem Cell Defects and Bone Marrow Failure in Fanconi Anemia.Cell stem cell · 2016Article
- Understanding complexity of Fanconi anaemia.The Indian journal of medical research · 2016Article
- Targeting downstream transcription factors and epigenetic modifications following Toll-like receptor 7/8 ligation to forestall tissue injury in anti-Ro60 associated heart block.Journal of autoimmunity · 2016Article
- Review
- The Fanconi anemia pathway has a dual function in Dickkopf-1 transcriptional repression.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The Fanconi anemia ID2 complex: dueling saxes at the crossroads.Cell cycle (Georgetown, Tex.) · 2014Review
- TNF-α signaling in Fanconi anemia.Blood cells, molecules & diseases · 2014Review
- Article
- FANCD2 activates transcription of TAp63 and suppresses tumorigenesis.Molecular cell · 2013Article
- The many faces of C/EBPδ and their relevance for inflammation and cancer.International journal of biological sciences · 2013Review
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 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fanconi anemia (FA), an inherited disease, is associated with progressive bone marrow failure, predisposition to cancer, and genomic instability. Genes corresponding to 15 identified FA complementation groups have been cloned, and each gene product functions in the response to DNA damage induced by cross-linking agents and/or in protection against genome instability. Interestingly, overproduction of inflammatory cytokines such as tumor necrosis factor alpha (TNF-α) and aberrant activation of NF-κB-dependent transcriptional activity have been observed in FA cells. Here we demonstrated that FANCD2 protein inhibits NF-κB activity in its monoubiquitination-dependent manner. Furthermore, we detected a specific association between FANCD2 and an NF-κB consensus element in the TNF-α promoter by electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) assay. Therefore, we propose FANCD2 deficiency promotes transcriptional activity of the TNF-α promoter and induces overproduction of TNF-which then sustains prolonged inflammatory responses. These results also suggest that artificial modulation of TNFα production could be a promising therapeutic approach to FA.
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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.