ArticleBlood2009
TLR8-dependent TNF-(alpha) overexpression in Fanconi anemia group C cells.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 72 citations in OpenAlex.
- miR-29a-3p and TGF-β Axis in Fanconi anemia: mechanisms driving metabolic dysfunction and genome stability.Cellular and molecular life sciences : CMLS · 2025Article
- Inflammatory pathways and the bone marrow microenvironment in inherited bone marrow failure syndromes.Stem cells (Dayton, Ohio) · 2025Review
- Human REXO4 is Required for Cell Cycle Progression.bioRxiv : the preprint server for biology · 2025Article
- Chronic Inflammation in Primary Myelofibrosis: In-Depth Insights Into Pathogenesis and Promising Anti-Inflammatory Therapeutic Strategies.Mediators of inflammation · 2025Review
- RUNX1 mutations mitigate quiescence to promote transformation of hematopoietic progenitors in Fanconi anemia.Leukemia · 2023Article
- Review
- Global miRNA expression of bone marrow mesenchymal stem/stromal cells derived from Fanconi anemia patients.Human cell · 2022Article
- Distinct SARS-CoV-2 RNA fragments activate Toll-like receptors 7 and 8 and induce cytokine release from human macrophages and microglia.Frontiers in immunology · 2022Article
- The role of inflammation in hematopoiesis and bone marrow failure: What can we learn from mouse models?Frontiers in immunology · 2022Review
- An induced pluripotent stem cell model of Fanconi anemia reveals mechanisms of p53-driven progenitor cell differentiation.Blood advances · 2020Article
- Using mechanistic models for the clinical interpretation of complex genomic variation.Scientific reports · 2019Article
- Exploring the druggable space around the Fanconi anemia pathway using machine learning and mechanistic models.BMC bioinformatics · 2019Article
- Natural Killer Cell Degranulation Defect: A Cause for Impaired NK-Cell Cytotoxicity and Hyperinflammation in Fanconi Anemia Patients.Frontiers in immunology · 2019Article
- Inhibition of interleukin-1 receptor-associated kinase-1 is a therapeutic strategy for acute myeloid leukemia subtypes.Leukemia · 2018Article
- Cell-Cycle-Specific Function of p53 in Fanconi Anemia Hematopoietic Stem and Progenitor Cell Proliferation.Stem cell reports · 2018Article
- Recent advances in understanding hematopoiesis in Fanconi Anemia.F1000Research · 2018Review
- PlGF enhances TLR-dependent inflammatory responses in human mononuclear phagocytes.American journal of reproductive immunology (New York, N.Y. : 1989) · 2017Article
- Acquired cross-linker resistance associated with a novel spliced BRCA2 protein variant for molecular phenotyping of BRCA2 disruption.Cell death & disease · 2017Article
- In Vivo RNAi Screen Unveils PPARγ as a Regulator of Hematopoietic Stem Cell Homeostasis.Stem cell reports · 2017Article
- Cytokine overproduction and crosslinker hypersensitivity are unlinked in Fanconi anemia macrophages.Journal of leukocyte biology · 2016Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
Tumor necrosis factor alpha (TNF-alpha) production is abnormally high in Fanconi anemia (FA) cells and contributes to the hematopoietic defects seen in FA complementation group C-deficient (Fancc(-/-)) mice. Applying gene expression microarray and proteomic methods to studies on FANCC-deficient cells we found that genes encoding proteins directly involved in ubiquitinylation are overrepresented in the signature of FA bone marrow cells and that ubiquitinylation profiles of FA-C and complemented cells were substantially different. Finding that Toll-like receptor 8 (TLR8) was one of the proteins ubiquitinylated only in mutant cells, we confirmed that TLR8 (or a TLR8-associated protein) is ubiquitinylated in mutant FA-C cells and that TNF-alpha production in mutant cells depended upon TLR8 and the canonical downstream signaling intermediates interleukin 1 receptor-associated kinase (IRAK) and IkappaB kinase-alpha/beta. FANCC-deficient THP-1 cells and macrophages from Fancc(-/-) mice overexpressed TNF-alpha in response to TLR8 agonists but not other TLR agonists. Ectopically expressed FANCC point mutants were capable of fully complementing the mitomycin-C hypersensitivity phenotype of FA-C cells but did not suppress TNF-alpha overproduction. In conclusion, FANCC suppresses TNF-alpha production in mononuclear phagocytes by suppressing TLR8 activity and this particular function of FANCC is independent of its function in protecting the genome from cross-linking agents.
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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.