ArticleJournal of immunology (Baltimore, Md. : 1950)2007
Inflammatory reactive oxygen species-mediated hemopoietic suppression in Fancc-deficient mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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.
The trial behind it
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
43 citing papers in PubMed, 73 citations in OpenAlex.
- Trial
- HES1 regulates bone marrow mesenchymal stromal cell function by suppressing NFATc2-mediated inflammation.Haematologica · 2026Article
- Genomic insights into chromosomal fusion and its evolutionary implications for zokors.Molecular biology and evolution · 2026Article
- Distinct developmental outcomes in DNA repair-deficient FANCC c.67delG mutant and FANCCCell death and differentiation · 2025Article
- Phase 1 study of quercetin, a natural antioxidant for children and young adults with Fanconi anemia.Blood advances · 2025Article
- Autophagy prevents graft failure during murine graft-versus-host disease.Blood advances · 2024Article
- FANCC deficiency mediates microglial pyroptosis and secondary neuronal apoptosis in spinal cord contusion.Cell & bioscience · 2022Article
- Type-I Interferon Signaling in Fanconi Anemia.Frontiers in cellular and infection microbiology · 2022Review
- Inflammatory Pathophysiology as a Contributor to Myeloproliferative Neoplasms.Frontiers in immunology · 2021Review
- Reduced Cell Division Control Protein 42 Activity Compromises Hematopoiesis-Supportive Function of Fanconi Anemia Mesenchymal Stromal Cells.Stem cells (Dayton, Ohio) · 2018Article
- Recent advances in understanding hematopoiesis in Fanconi Anemia.F1000Research · 2018Review
- Persistent response of Fanconi anemia haematopoietic stem and progenitor cells to oxidative stress.Cell cycle (Georgetown, Tex.) · 2017Article
- Cytokine overproduction and crosslinker hypersensitivity are unlinked in Fanconi anemia macrophages.Journal of leukocyte biology · 2016Article
- Oxidative stress-associated protein tyrosine kinases and phosphatases in Fanconi anemia.Antioxidants & redox signaling · 2014Review
- TNF-α, a good or bad factor in hematological diseases?Stem cell investigation · 2014Review
- Learning from a paradox: recent insights into Fanconi anaemia through studying mouse models.Disease models & mechanisms · 2013Review
- Article
- Association of FANCC polymorphisms with FEV1 decline in aspirin exacerbated respiratory disease.Molecular biology reports · 2012Article
- Article
- Impaired function of Fanconi anemia type C-deficient macrophages.Journal of leukocyte biology · 2012Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
Abstract
Patients with the genomic instability syndrome Fanconi anemia (FA) commonly develop progressive bone marrow (BM) failure and have a high risk of cancer. Certain manifestations of the disease suggest that the FA immune system is dysfunctional and may contribute to the pathogenesis of both BM failure and malignancies. In this study, we have investigated inflammation and innate immunity in FA hemopoietic cells using mice deficient in Fanconi complementation group C gene (Fancc). We demonstrate that Fancc-deficient mice exhibit enhanced inflammatory response and are hypersensitive to LPS-induced septic shock as a result of hemopoietic suppression. This exacerbated inflammatory phenotype is intrinsic to the hemopoietic system and can be corrected by the re-expression of a wild-type FANCC gene, suggesting a potential role of the FANCC protein in innate immunity. LPS-mediated hemopoietic suppression requires two major inflammatory agents, TNF-alpha and reactive oxygen species. In addition, LPS-induced excessive accumulation of reactive oxygen species in Fancc(-/-) BM cells overactivates the stress kinase p38 and requires prolonged activation of the JNK. Our data implicate a role of inflammation in pathogenesis of FA and BM failure diseases in general.
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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.