ArticleMutation research2009
Fanconi anemia proteins and endogenous stresses.
Article in Mutation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
- Fanconi Anemia: Interplay Between DNA Repair Defects, Mitochondrial Dysfunction, and Oxidative Stress.Cells · 2026Review
- Article
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
- Correction of Fanconi Anemia Mutations Using Digital Genome Engineering.International journal of molecular sciences · 2022Article
- A Multidrug Approach to Modulate the Mitochondrial Metabolism Impairment and Relative Oxidative Stress in Fanconi Anemia Complementation Group A.Metabolites · 2021Article
- A Mendelian randomization study of telomere length and blood-cell traits.Scientific reports · 2020Article
- 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
- FANCJ is essential to maintain microsatellite structure genome-wide during replication stress.Nucleic acids research · 2016Article
- Cellular response to DNA interstrand crosslinks: the Fanconi anemia pathway.Cellular and molecular life sciences : CMLS · 2016Review
- Increased red cell distribution width in Fanconi anemia: a novel marker of stress erythropoiesis.Orphanet journal of rare diseases · 2016Article
- Fanconi anemia proteins in telomere maintenance.DNA repair · 2016Review
- TGF-β Inhibition Rescues Hematopoietic Stem Cell Defects and Bone Marrow Failure in Fanconi Anemia.Cell stem cell · 2016Article
- TGF-β: a master regulator of the bone marrow failure puzzle in Fanconi anemia.Stem cell investigation · 2016Article
- Hematopoietic RIPK1 deficiency results in bone marrow failure caused by apoptosis and RIPK3-mediated necroptosis.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Oxidative stress-associated protein tyrosine kinases and phosphatases in Fanconi anemia.Antioxidants & redox signaling · 2014Review
- What is wrong with Fanconi anemia cells?Cell cycle (Georgetown, Tex.) · 2014Review
- The inherited bone marrow failure syndromes.Pediatric clinics of North America · 2013Review
- Reduced FANCD2 influences spontaneous SCE and RAD51 foci formation in uveal melanoma and Fanconi anaemia.Oncogene · 2013Article
- Inflammation-mediated notch signaling skews fanconi anemia hematopoietic stem cell differentiation.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Each of the thirteen identified Fanconi anemia (FA) genes is required for resistance to DNA interstrand crosslinking agents, such as mitomycin C, cisplatin, and melphalan. While these agents are excellent tools for understanding the function of FA proteins in DNA repair, it is uncertain whether a defect in the removal of DNA interstrand crosslinks (ICLs) is the basis for the pathophysiology of FA. For example, DNA interstrand crosslinking agents induce other types of DNA damage, in addition to ICLs. Further, other DNA-damaging agents, such as ionizing or ultraviolet radiation, activate the FA pathway, leading to monoubiquitination of FANCD2 and FANCI. Also, FA patients display congenital abnormalities, hematologic deficiencies, and a predisposition to cancer in the absence of an environmental source of ICLs that is external to cells. Here we consider potential sources of endogenous DNA damage, or endogenous stresses, to which FA proteins may respond. These include ICLs formed by products of lipid peroxidation, and other forms of oxidative DNA damage. FA proteins may also potentially respond to telomere shortening or replication stress. Defining these endogenous sources of DNA damage or stresses is critical for understanding the pathogenesis of deficiencies for FA proteins.We propose that FA proteins are centrally involved in the response to replication stress, including replication stress arising from oxidative DNA damage.
Indexed as
Identifiers
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.