ArticleThe Journal of biological chemistry2014
The carboxyl terminus of FANCE recruits FANCD2 to the Fanconi Anemia (FA) E3 ligase complex to promote the FA DNA repair pathway.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Multi-omics analysis in suspected hereditary breast and ovarian cancer cases reveals novel candidate susceptibility factors.NPJ breast cancer · 2026Article
- Integrated analysis of FANCE expression and its regulatory role in the immune microenvironment of oral squamous cell carcinoma.Oncology letters · 2025Article
- Reduced FANCE Confers Genomic Instability and Malignant Behavior by Regulating Cell Cycle Progression in Endometrial Cancer.Journal of Cancer · 2023Article
- Structure of the FA core ubiquitin ligase closing the ID clamp on DNA.Nature structural & molecular biology · 2021Article
- Long Noncoding RNAFrontiers in oncology · 2021Article
- TGF-β2-induced NEAT1 regulates lens epithelial cell proliferation, migration and EMT by the miR-26a-5p/FANCE axis.International journal of ophthalmology · 2021Article
- Structural basis of the fanconi anemia-associated mutations within the FANCA and FANCG complex.Nucleic acids research · 2020Article
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- The FA Core Complex Contains a Homo-dimeric Catalytic Module for the Symmetric Mono-ubiquitination of FANCI-FANCD2.Cell reports · 2017Article
- Dearth and Delayed Maturation of Testicular Germ Cells in Fanconi Anemia E Mutant Male Mice.PloS one · 2016Article
- Update of the human and mouse Fanconi anemia genes.Human genomics · 2015Review
- FANCJ protein is important for the stability of FANCD2/FANCI proteins and protects them from proteasome and caspase-3 dependent degradation.Oncotarget · 2015Article
- Exploiting the Fanconi Anemia Pathway for Targeted Anti-Cancer Therapy.Molecules and cells · 2015Review
- The genetic and biochemical basis of FANCD2 monoubiquitination.Molecular cell · 2014Article
- Damaged mitochondria in Fanconi anemia - an isolated event or a general phenomenon?Oncoscience · 2014Article
- The Fanconi anemia ID2 complex: dueling saxes at the crossroads.Cell cycle (Georgetown, Tex.) · 2014Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Fanconi anemia (FA) is a genome instability syndrome characterized by bone marrow failure and cellular hypersensitivity to DNA cross-linking agents. In response to DNA damage, the FA pathway is activated through the cooperation of 16 FA proteins. A central player in the pathway is a multisubunit E3 ubiquitin ligase complex or the FA core complex, which monoubiquitinates its substrates FANCD2 and FANCI. FANCE, a subunit of the FA core complex, plays an essential role by promoting the integrity of the complex and by directly recognizing FANCD2. To delineate its role in substrate ubiquitination from the core complex assembly, we analyzed a series of mutations within FANCE. We report that a phenylalanine located at the highly conserved extreme C terminus, referred to as Phe-522, is a critical residue for mediating the monoubiquitination of the FANCD2-FANCI complex. Using the FANCE mutant that specifically disrupts the FANCE-FANCD2 interaction as a tool, we found that the interaction-deficient mutant conferred cellular sensitivity in reconstituted FANCE-deficient cells to a similar degree as FANCE null cells, suggesting the significance of the FANCE-FANCD2 interaction in promoting cisplatin resistance. Intriguingly, ectopic expression of the FANCE C terminus fragment alone in FA normal cells disrupts DNA repair, consolidating the importance of the FANCE-FANCD2 interaction in the DNA cross-link repair.
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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.