ArticleAmerican journal of human genetics1997
Evidence for at least eight Fanconi anemia genes.
Article in American journal of human genetics, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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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Who cites it
38 citing papers in PubMed, 284 citations in OpenAlex.
- Genetic Testing of Japanese Patients with Serrated Polyposis Syndrome: A Multicentric Study.Journal of the anus, rectum and colon · 2024Article
- ERCC1 mutations impede DNA damage repair and cause liver and kidney dysfunction in patients.The Journal of experimental medicine · 2021Article
- Stem cell-derived clade F AAVs mediate high-efficiency homologous recombination-based genome editing.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Recent discoveries in the molecular pathogenesis of the inherited bone marrow failure syndrome Fanconi anemia.Blood reviews · 2017Review
- Male fertility and skin diseases.Reviews in endocrine & metabolic disorders · 2016Review
- Concurrent progress of reprogramming and gene correction to overcome therapeutic limitation of mutant ALK2-iPSC.Experimental & molecular medicine · 2016Article
- FANCJ protein is important for the stability of FANCD2/FANCI proteins and protects them from proteasome and caspase-3 dependent degradation.Oncotarget · 2015Article
- AMD3100 synergizes with G-CSF to mobilize repopulating stem cells in Fanconi anemia knockout mice.Experimental hematology · 2008Article
- FANCD2 monoubiquitination and activation by hexavalent chromium [Cr(VI)] exposure: activation is not required for repair of Cr(VI)-induced DSBs.Mutation research · 2006Article
- Article
- In vivo repopulation ability of genetically corrected bone marrow cells from Fanconi anemia patients.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Topics in pediatric leukemia--Fanconi's anemia: new insights.MedGenMed : Medscape general medicine · 2005Review
- FANCG is phosphorylated at serines 383 and 387 during mitosis.Molecular and cellular biology · 2004Article
- Deletion and reduced expression of the Fanconi anemia FANCA gene in sporadic acute myeloid leukemia.Leukemia · 2004Article
- A Rad50-dependent pathway of DNA repair is deficient in Fanconi anemia fibroblasts.Nucleic acids research · 2004Article
- Fanconi anemia in Ashkenazi Jews.Familial cancer · 2004Review
- Epithelial cancer in Fanconi anemia complementation group D2 (Fancd2) knockout mice.Genes & development · 2003Article
- Fanconi anaemia.Journal of medical genetics · 2003Review
- Fanconi anemia in Tunisia: high prevalence of group A and identification of new FANCA mutations.Journal of human genetics · 2003Article
- FANCE: the link between Fanconi anaemia complex assembly and activity.The EMBO journal · 2002Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 4 countries.
Funding
Abstract
Fanconi anemia (FA) is an autosomal recessive chromosomal breakage disorder with diverse clinical symptoms including progressive bone marrow failure and increased cancer risk. FA cells are hypersensitive to crosslinking agents, which has been exploited to assess genetic heterogeneity through complementation analysis. Five complementation groups (FA-A through FA-E) have so far been distinguished among the first 20 FA patients analyzed. Complementation groups in FA are likely to represent distinct disease genes, two of which (FAC and FAA) have been cloned. Following the identification of the first FA-E patient, additional patients were identified whose cell lines complemented groups A-D. To assess their possible assignment to the E group, we introduced selection markers into the original FA-E cell line and analyzed fusion hybrids with three cell lines classified as non-ABCD. All hybrids were complemented for cross-linker sensitivity, indicating nonidentity with group E. We then marked the three non-ABCDE cell lines and examined all possible hybrid combinations for complementation, which indicated that each individual cell line represented a separate complementation group. These results thus define three new groups, FA-F, FA-G, and FA-H, providing evidence for a minimum of eight distinct FA genes.
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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.