ArticleProceedings of the National Academy of Sciences of the United States of America1999
A physical complex of the Fanconi anemia proteins FANCG/XRCC9 and FANCA.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 153 citations in OpenAlex.
- Bridging sequence-structure motifs and genetic variants for genome-wide dynamic RNA-protein interaction profiling.Nature communications · 2026Article
- A C57BL/6J Fancg-KO Mouse Model Generated by CRISPR/Cas9 Partially Captures the Human Phenotype.International journal of molecular sciences · 2023Article
- Structural basis of the fanconi anemia-associated mutations within the FANCA and FANCG complex.Nucleic acids research · 2020Article
- FANCA Promotes DNA Double-Strand Break Repair by Catalyzing Single-Strand Annealing and Strand Exchange.Molecular cell · 2018Article
- The Fanconi anemia proteins FANCD2 and FANCJ interact and regulate each other's chromatin localization.The Journal of biological chemistry · 2014Article
- Modularized functions of the Fanconi anemia core complex.Cell reports · 2014Article
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- The Fanconi anemia ID2 complex: dueling saxes at the crossroads.Cell cycle (Georgetown, Tex.) · 2014Review
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- Facioscapulohumeral muscular dystrophy region gene 1 is a dynamic RNA-associated and actin-bundling protein.Journal of molecular biology · 2011Article
- The cellular phenotype of Roberts syndrome fibroblasts as revealed by ectopic expression of ESCO2.PloS one · 2009Article
- The fanconi anemia core complex acts as a transcriptional co-regulator in hairy enhancer of split 1 signaling.The Journal of biological chemistry · 2009Article
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- FANCG promotes formation of a newly identified protein complex containing BRCA2, FANCD2 and XRCC3.Oncogene · 2008Article
- Loss of expression of FANCD2 protein in sporadic and hereditary breast cancer.Breast cancer research and treatment · 2008Article
- FAAP100 is essential for activation of the Fanconi anemia-associated DNA damage response pathway.The EMBO journal · 2007Article
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- Fanconi anemia A is a nucleocytoplasmic shuttling molecule required for gonadotropin-releasing hormone (GnRH) transduction of the GnRH receptor.Endocrinology · 2006Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Fanconi anemia (FA) is a recessively inherited disease characterized at the cellular level by spontaneous chromosomal instability and specific hypersensitivity to cross-linking agents. FA is genetically heterogeneous, comprising at least eight complementation groups (A-H). We report that the protein encoded by the gene mutated in complementation group G (FANCG) localizes to the cytoplasm and nucleus of the cell and assembles in a molecular complex with the FANCA protein, both in vivo and in vitro. Endogenous FANCA/FANCG complex was detected in both non-FA cells and in FA cells from groups D and E. By contrast, no complex was detected in specific cell lines belonging to groups A and G, whereas reduced levels were found in cells from groups B, C, F, and H. Wild-type levels of FANCA/FANCG complex were restored upon correction of the cellular phenotype by transfection or cell fusion experiments, suggesting that this complex is of functional significance in the FA pathway. These results indicate that the cellular FA phenotype can be connected to three biochemical subtypes based on the levels of FANCA/FANCG complex. Disruption of the complex may provide an experimental strategy for chemosensitization of neoplastic cells.
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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.