ArticleMolecular and cellular biology2008
Cellular concentrations of DDB2 regulate dynamic binding of DDB1 at UV-induced DNA damage.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Multifunctional acyltransferase HBO1: a key regulatory factor for cellular functions.Cellular & molecular biology letters · 2024Review
- Differential processing of RNA polymerase II at DNA damage correlates with transcription-coupled repair syndrome severity.Nucleic acids research · 2024Article
- PTEN-negative endometrial cancer cells protect their genome through enhanced DDB2 expression associated with augmented nucleotide excision repair.BMC cancer · 2023Article
- Cross-continental admixture in the Kho population from northwest Pakistan.European journal of human genetics : EJHG · 2022Article
- MEKK1-Dependent Activation of the CRL4 Complex Is Important for DNA Damage-Induced Degradation of p21 and DDB2 and Cell Survival.Molecular and cellular biology · 2021Article
- Transcriptional Profiling of Porcine Blastocysts Produced In Vitro in a Chemically Defined Culture Medium.Animals : an open access journal from MDPI · 2021Article
- Review
- [Bioinformatics analysis of expression and function of EXD3 gene in gastric cancer].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- Cereblon attenuates DNA damage-induced apoptosis by regulating the transcription-independent function of p53.Cell death & disease · 2019Article
- Phosphorylated HBO1 at UV irradiated sites is essential for nucleotide excision repair.Nature communications · 2017Article
- Independent mechanisms recruit the cohesin loader protein NIPBL to sites of DNA damage.Journal of cell science · 2017Article
- Orchestral maneuvers at the damaged sites in nucleotide excision repair.Cellular and molecular life sciences : CMLS · 2015Review
- Damaged DNA-binding protein down-regulates epigenetic mark H3K56Ac through histone deacetylase 1 and 2.Mutation research · 2015Article
- Sequential and ordered assembly of a large DNA repair complex on undamaged chromatin.The Journal of cell biology · 2014Article
- Single-molecule analysis reveals human UV-damaged DNA-binding protein (UV-DDB) dimerizes on DNA via multiple kinetic intermediates.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- DDB2 association with PCNA is required for its degradation after UV-induced DNA damage.Cell cycle (Georgetown, Tex.) · 2014Article
- Damaged DNA induced UV-damaged DNA-binding protein (UV-DDB) dimerization and its roles in chromatinized DNA repair.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- DDB2 promotes chromatin decondensation at UV-induced DNA damage.The Journal of cell biology · 2012Article
- Recognition of DNA damage by XPC coincides with disruption of the XPC-RAD23 complex.The Journal of cell biology · 2012Article
- Regulation of nucleotide excision repair by UV-DDB: prioritization of damage recognition to internucleosomal DNA.PLoS biology · 2011Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleotide excision repair (NER) is the principal pathway for counteracting cytotoxic and mutagenic effects of UV irradiation. To provide insight into the in vivo regulation of the DNA damage recognition step of global genome NER (GG-NER), we constructed cell lines expressing fluorescently tagged damaged DNA binding protein 1 (DDB1). DDB1 is a core subunit of a number of cullin 4-RING ubiquitin ligase complexes. UV-activated DDB1-DDB2-CUL4A-ROC1 ubiquitin ligase participates in the initiation of GG-NER and triggers the UV-dependent degradation of its subunit DDB2. We found that DDB1 rapidly accumulates on DNA damage sites. However, its binding to damaged DNA is not static, since DDB1 constantly dissociates from and binds to DNA lesions. DDB2, but not CUL4A, was indispensable for binding of DDB1 to DNA damage sites. The residence time of DDB1 on the damage site is independent of the main damage-recognizing protein of GG-NER, XPC, as well as of UV-induced proteolysis of DDB2. The amount of DDB1 that is temporally immobilized on damaged DNA critically depends on DDB2 levels in the cell. We propose a model in which UV-dependent degradation of DDB2 is important for the release of DDB1 from continuous association to unrepaired DNA and makes DDB1 available for its other DNA damage response functions.
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