1997
DOI: 10.1093/emboj/16.21.6559
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Abstract: During nucleotide excision repair in human cells, a damaged DNA strand is cleaved by two endonucleases, XPG on the 3Ј side of the lesion and ERCC1-XPF on the 5Ј side. These structure-specific enzymes act at junctions between duplex and single-stranded DNA. ATP-dependent formation of an open DNA structure of~25 nt around the adduct precedes this dual incision. We investigated the mechanism of open complex formation and find that mutations in XPB or XPD, the DNA helicase subunits of the transcription and repair … Show more

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Cited by 429 publications
(380 citation statements)
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References 51 publications
(86 reference statements)
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“…We next addressed the role of ATP, which is required for the activity of the XPB and XPD helicases of TFIIH (33)(34)(35) in modulating the footprinting pattern of the damaged DNA around the lesion (36). We first observed that ATP does not modify the XPC/HR23B footprinting pattern of the damaged DNA (Fig.…”
Section: Resultsmentioning
confidence: 99%
“…We next addressed the role of ATP, which is required for the activity of the XPB and XPD helicases of TFIIH (33)(34)(35) in modulating the footprinting pattern of the damaged DNA around the lesion (36). We first observed that ATP does not modify the XPC/HR23B footprinting pattern of the damaged DNA (Fig.…”
Section: Resultsmentioning
confidence: 99%
“…According to scanning force microscopy studies, the binding of XPC protein to DNA induces a kink of 39-49º in the nucleic acid backbone regardless of whether the substrate is damaged or not 7 [37]. Permanganate footprinting studies demonstrate that the observed sharp bending is accompanied by partial melting of the duplex extending over 4-7 base pairs [34,38].…”
Section: Initiation Of Ggr Activity By the Xpc Complexmentioning
confidence: 99%
“…44 Since a variety of lesions are recognized, it has been suggested that the NER factors do not recognize the lesion itself, but the local distortions in the DNA that are associated with the lesions. 15,[44][45][46] In this connection, we have shown recently that the human NER factor XPC/HR23B is the first mammalian NER factor that recognizes anti- [BP]-N 2 -dG lesions; this factor distinguishes between the BD (+)-cis-, and MG (+)-trans-and (−)-trans-[BP]-N 2 -dG lesions by opening the duplex to different extents and at different sites in the vicinity of the lesions. 47 Gunz et al have proposed a thermodynamic probing mechanism based on their observations that differences of more than 3 orders of magnitude are observed in the efficiency by which helix-destabilizing and helix-stabilizing adducts are excised by the NER mechanism.…”
Section: Dynamic Flexibility and Ner Damage Recognitionmentioning
confidence: 99%