ArticleOncogene2004
Fanconi anemia C gene product regulates expression of genes involved in differentiation and inflammation.
Article in Oncogene, 2004. 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.
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
20 citing papers in PubMed, 48 citations in OpenAlex.
- The tight bond between Fanconi anemia and aging.Frontiers in aging · 2026Review
- Inflammatory pathways and the bone marrow microenvironment in inherited bone marrow failure syndromes.Stem cells (Dayton, Ohio) · 2025Review
- Contribution of p53-dependent and -independent mechanisms to upregulation of p21 in Fanconi anemia.PLoS genetics · 2024Article
- Crosstalk between DNA Damage Repair and Metabolic Regulation in Hematopoietic Stem Cells.Cells · 2024Review
- FANCA deficiency promotes leukaemic progression by allowing the emergence of cells carrying oncogenic driver mutations.Oncogene · 2023Article
- Fanca deficiency is associated with alterations in osteoclastogenesis that are rescued by TNFα.Cell & bioscience · 2023Article
- Polyclonal evolution of Fanconi anemia to MDS and AML revealed at single cell resolution.Experimental hematology & oncology · 2022Article
- 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
- Mitoprotective Clinical Strategies in Type 2 Diabetes and Fanconi Anemia Patients: Suggestions for Clinical Management of Mitochondrial Dysfunction.Antioxidants (Basel, Switzerland) · 2020Review
- Fancd2-deficient hematopoietic stem and progenitor cells depend on augmented mitochondrial translation for survival and proliferation.Stem cell research · 2019Article
- Fanconi anaemia and cancer: an intricate relationship.Nature reviews. Cancer · 2018Review
- Fancd2 in vivo interaction network reveals a non-canonical role in mitochondrial function.Scientific reports · 2017Article
- V(D)J recombination process and the Pre-B to immature B-cells transition are altered in FancaScientific reports · 2016Article
- Fanconi anemia: a signal transduction and DNA repair pathway.The Yale journal of biology and medicine · 2013Review
- The inherited bone marrow failure syndromes.Pediatric clinics of North America · 2013Review
- Article
- Fanconi anemia.Hematology/oncology clinics of North America · 2009Review
- A never-ending story: the steadily growing family of the FA and FA-like genes.Genetics and molecular biologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of Fanconi anemia (FA) proteins activity by recessive inherited mutations in one of the FA genes leads to a disease characterized by bone marrow failure, myeloid leukemia and DNA damage hypersensitivity. The aim of this work was to improve our understanding of the FA syndrome defining the transcription profile of the FA complementation group C (FANCC)-deficient cells in comparison to their ectopically corrected counterpart using oligonucleotide microarrays. In this way, 49 RNAs have been isolated, which showed a consistent differential pattern of expression among FANCC mutated and corrected cells. The observed specific changes in gene expression suggest that FANCC regulates specifically myeloid differentiation and unmasks a previously unsuspected anti-inflammatory role for the FA proteins. In spite of the DNA damage hypersensitivity of the syndrome, no gene coding for a protein directly involved in DNA repair/damage response was found to be deregulated in our analysis. This observation suggests that FANCC does not directly control genes involved in DNA repair at the transcriptional level, but does not exclude a regulation at the translational or post-translational level, or by protein/protein interactions. The potential role of the differentially expressed genes in FA phenotype as well as a functional- and cellular-based clustering of the identified genes are presented and discussed.
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What OpenQuestion holds
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.