ArticleMolecular and cellular biology2005
Xeroderma pigmentosum complementation group E protein (XPE/DDB2): purification of various complexes of XPE and analyses of their damaged DNA binding and putative DNA repair properties.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 60 citations in OpenAlex.
- Development of Peptide Displacement Assays to Screen for Antagonists of DDB1 Interactions.Biochemistry · 2024Article
- Targeted CUL4A inhibition synergizes with cisplatin to yield long-term survival in models of head and neck squamous cell carcinoma through a DDB2-mediated mechanism.Cell death & disease · 2022Article
- Rational, Unbiased Selection of Reference Genes for Pluripotent Stem Cell-Derived Cardiomyocytes.Tissue engineering. Part C, Methods · 2021Article
- Involvement of the nuclear structural proteins in aging-related responses of human skin to the environmental stress.Clinical, cosmetic and investigational dermatology · 2018Review
- DNA Damage and Deficiencies in the Mechanisms of Its Repair: Implications in the Pathogenesis of Systemic Lupus Erythematosus.Journal of immunology research · 2018Review
- Timing of DNA lesion recognition: Ubiquitin signaling in the NER pathway.Cell cycle (Georgetown, Tex.) · 2017Review
- A Novel Mutation inFrontiers in pediatrics · 2017Article
- Real-Time Tracking of Parental Histones Reveals Their Contribution to Chromatin Integrity Following DNA Damage.Molecular cell · 2016Article
- Cooperative motion of a key positively charged residue and metal ions for DNA replication catalyzed by human DNA Polymerase-η.Nucleic acids research · 2016Article
- Xeroderma pigmentosum group C sensor: unprecedented recognition strategy and tight spatiotemporal regulation.Cellular and molecular life sciences : CMLS · 2016Review
- Global-genome Nucleotide Excision Repair Controlled by Ubiquitin/Sumo Modifiers.Frontiers in genetics · 2016Review
- Ultraviolet Radiation-Induced Skin Aging: The Role of DNA Damage and Oxidative Stress in Epidermal Stem Cell Damage Mediated Skin Aging.Stem cells international · 2016Review
- DNA damage-binding complex recruits HDAC1 to repress Bcl-2 transcription in human ovarian cancer cells.Molecular cancer research : MCR · 2014Article
- A novel DDB2-ATM feedback loop regulates human cytomegalovirus replication.Journal of virology · 2014Article
- p21 cooperates with DDB2 protein in suppression of ultraviolet ray-induced skin malignancies.The Journal of biological chemistry · 2012Article
- Regulation of nucleotide excision repair by UV-DDB: prioritization of damage recognition to internucleosomal DNA.PLoS biology · 2011Article
- Turn-on DNA damage sensors for the direct detection of 8-oxoguanine and photoproducts in native DNA.Journal of the American Chemical Society · 2011Article
- Mechanisms of trinucleotide repeat instability during human development.Nature reviews. Genetics · 2010Review
- Similar nucleotide excision repair capacity in melanocytes and melanoma cells.Cancer research · 2010Article
- DDB2, an essential mediator of premature senescence.Molecular and cellular biology · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Xeroderma pigmentosum is characterized by increased sensitivity of the affected individuals to sunlight and light-induced skin cancers and, in some cases, to neurological abnormalities. The disease is caused by a mutation in genes XPA through XPG and the XP variant (XPV) gene. The proteins encoded by the XPA, -B, -C, -D, -F, and -G genes are required for nucleotide excision repair, and the XPV gene encodes DNA polymerase eta, which carries out translesion DNA synthesis. In contrast, the mechanism by which the XPE gene product prevents sunlight-induced cancers is not known. The gene (XPE/DDB2) encodes the small subunit of a heterodimeric DNA binding protein with high affinity to UV-damaged DNA (UV-damaged DNA binding protein [UV-DDB]). The DDB2 protein exists in at least four forms in the cell: monomeric DDB2, DDB1-DDB2 heterodimer (UV-DDB), and as a protein associated with both the Cullin 4A (CUL4A) complex and the COP9 signalosome. To better define the role of DDB2 in the cellular response to DNA damage, we purified all four forms of DDB2 and analyzed their DNA binding properties and their effects on mammalian nucleotide excision repair. We find that DDB2 has an intrinsic damaged DNA binding activity and that under our assay conditions neither DDB2 nor complexes that contain DDB2 (UV-DDB, CUL4A, and COP9) participate in nucleotide excision repair carried out by the six-factor human excision nuclease.
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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.