ArticleMolecular and cellular biology1998
Relationship of the xeroderma pigmentosum group E DNA repair defect to the chromatin and DNA binding proteins UV-DDB and replication protein A.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 111 citations in OpenAlex.
- Nucleotide excision repair: a versatile and smart toolkit.Acta biochimica et biophysica Sinica · 2022Review
- Review
- Damage sensor role of UV-DDB during base excision repair.Nature structural & molecular biology · 2019Article
- UV radiation-induced SUMOylation of DDB2 regulates nucleotide excision repair.Carcinogenesis · 2017Article
- Autophagic UVRAG Promotes UV-Induced Photolesion Repair by Activation of the CRL4(DDB2) E3 Ligase.Molecular cell · 2016Article
- Fluorescence detection of cellular nucleotide excision repair of damaged DNA.Scientific reports · 2014Article
- DNA damage tolerance and a web of connections with DNA repair at Yale.The Yale journal of biology and medicine · 2013Article
- The deubiquitinating protein USP24 interacts with DDB2 and regulates DDB2 stability.Cell cycle (Georgetown, Tex.) · 2012Article
- PARP1 promotes nucleotide excision repair through DDB2 stabilization and recruitment of ALC1.The Journal of cell biology · 2012Article
- Multiple skin cancers in adults with mutations in the XP-E (DDB2) DNA repair gene.The Journal of investigative dermatology · 2011Article
- DDB2 complex-mediated ubiquitylation around DNA damage is oppositely regulated by XPC and Ku and contributes to the recruitment of XPA.Molecular and cellular biology · 2010Article
- Physical and functional interaction between DDB and XPA in nucleotide excision repair.Nucleic acids research · 2009Article
- Article
- The xeroderma pigmentosum group E gene product DDB2 activates nucleotide excision repair by regulating the level of p21Waf1/Cip1.Molecular and cellular biology · 2008Article
- DDB1 and Cul4A are required for human immunodeficiency virus type 1 Vpr-induced G2 arrest.Journal of virology · 2007Article
- Ubiquitylation-independent degradation of Xeroderma pigmentosum group C protein is required for efficient nucleotide excision repair.Nucleic acids research · 2007Article
- The DDB1-CUL4ADDB2 ubiquitin ligase is deficient in xeroderma pigmentosum group E and targets histone H2A at UV-damaged DNA sites.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- 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.Molecular and cellular biology · 2005Article
- DDB2 gene disruption leads to skin tumors and resistance to apoptosis after exposure to ultraviolet light but not a chemical carcinogen.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Recognition and repair of the cyclobutane thymine dimer, a major cause of skin cancers, by the human excision nuclease.Genes & development · 2003Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cells from complementation groups A through G of the heritable sun-sensitive disorder xeroderma pigmentosum (XP) show defects in nucleotide excision repair of damaged DNA. Proteins representing groups A, B, C, D, F, and G are subunits of the core recognition and incision machinery of repair. XP group E (XP-E) is the mildest form of the disorder, and cells generally show about 50% of the normal repair level. We investigated two protein factors previously implicated in the XP-E defect, UV-damaged DNA binding protein (UV-DDB) and replication protein A (RPA). Three newly identified XP-E cell lines (XP23PV, XP25PV, and a line formerly classified as an XP variant) were defective in UV-DDB binding activity but had levels of RPA in the normal range. The XP-E cell extracts did not display a significant nucleotide excision repair defect in vitro, with either UV-irradiated DNA or a uniquely placed cisplatin lesion used as a substrate. Purified UV-DDB protein did not stimulate repair of naked DNA by DDB- XP-E cell extracts, but microinjection of the protein into DDB- XP-E cells could partially correct the repair defect. RPA stimulated repair in normal, XP-E, or complemented extracts from other XP groups, and so the effect of RPA was not specific for XP-E cell extracts. These data strengthen the connection between XP-E and UV-DDB. Coupled with previous results, the findings suggest that UV-DDB has a role in the repair of DNA in chromatin.
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