ArticleThe Journal of biological chemistry2008
Tip60 is required for DNA interstrand cross-link repair in the Fanconi anemia pathway.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 38 citations in OpenAlex.
- Pancancer analysis of the prognostic and immunological role of FANCD2: a potential target for carcinogenesis and survival.BMC medical genomics · 2024Article
- The FANC/BRCA Pathway Releases Replication Blockades by Eliminating DNA Interstrand Cross-Links.Genes · 2020Review
- Acetylation of XPF by TIP60 facilitates XPF-ERCC1 complex assembly and activation.Nature communications · 2020Article
- Understanding the Histone DNA Repair Code: H4K20me2 Makes Its Mark.Molecular cancer research : MCR · 2018Review
- The Nature of Actin-Family Proteins in Chromatin-Modifying Complexes.Frontiers in genetics · 2018Review
- Chronic treatment with cisplatin induces chemoresistance through the TIP60-mediated Fanconi anemia and homologous recombination repair pathways.Scientific reports · 2017Article
- Impaired TIP60-mediated H4K16 acetylation accounts for the aberrant chromatin accumulation of 53BP1 and RAP80 in Fanconi anemia pathway-deficient cells.Nucleic acids research · 2016Article
- Forkhead transcription factor FoxF1 interacts with Fanconi anemia protein complexes to promote DNA damage response.Oncotarget · 2016Article
- The Fanconi anemia ID2 complex: dueling saxes at the crossroads.Cell cycle (Georgetown, Tex.) · 2014Review
- Histone chaperone activity of Fanconi anemia proteins, FANCD2 and FANCI, is required for DNA crosslink repair.The EMBO journal · 2012Article
- DNA transcription and repair: a confluence.The Journal of biological chemistry · 2012Review
- DNA interstrand crosslink repair in mammalian cells: step by step.Critical reviews in biochemistry and molecular biology · 2010Review
- DNA interstrand crosslink repair in mammalian cells.Journal of cellular physiology · 2009Review
- Cellular and molecular consequences of defective Fanconi anemia proteins in replication-coupled DNA repair: mechanistic insights.Mutation research · 2009Review
- The Fanconi anemia protein interaction network: casting a wide net.Mutation research · 2009Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The disease Fanconi anemia is a genome instability syndrome characterized by cellular sensitivity to DNA interstrand cross-linking agents, manifest by decreased cellular survival and chromosomal aberrations after such treatment. There are at least 13 proteins acting in the pathway, with the FANCD2 protein apparently functioning as a late term effecter in the maintenance of genome stability. We find that the chromatin remodeling protein, Tip60, interacts directly with the FANCD2 protein in a yeast two-hybrid system. This interaction has been confirmed by co-immunoprecipitation and co-localization using both endogenous and epitope-tagged FANCD2 and Tip60 from human cells. The observation of decreased cellular survival after exposure to mitomycin C in normal fibroblasts depleted for Tip60 indicates a direct function in interstrand cross-link repair. The coincident function of Tip60 and FANCD2 in one pathway is supported by the finding that depletion of Tip60 in Fanconi anemia cells does not increase sensitivity to DNA cross-links. However, depletion of Tip60 did not reduce monoubiquitination of FANCD2 or its localization to nuclear foci following DNA damage. The observations indicate that Fanconi anemia proteins act in concert with chromatin remodeling functions to maintain genome stability after DNA cross-link damage.
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Registered trials
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