2020
DOI: 10.1016/j.dnarep.2020.102985
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The DNA damage-sensing NER repair factor XPC-RAD23B does not recognize bulky DNA lesions with a missing nucleotide opposite the lesion

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Cited by 5 publications
(5 citation statements)
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“…There were several reasons to choose the E. coli system to demonstrate the clear picture of the dG-AF adduct’s biological properties in cell; first, a single-stranded DNA vector was chosen to avoid repair of the bulky dG-AF adduct that would be recognized by NER proteins such as XPC in specific secondary structures, namely the single strand–double strand DNA junction ( 49–51 ). Thus, the cellular data reflected the biological properties of dG-AF adduct without complications from NER repair.…”
Section: Resultsmentioning
confidence: 99%
“…There were several reasons to choose the E. coli system to demonstrate the clear picture of the dG-AF adduct’s biological properties in cell; first, a single-stranded DNA vector was chosen to avoid repair of the bulky dG-AF adduct that would be recognized by NER proteins such as XPC in specific secondary structures, namely the single strand–double strand DNA junction ( 49–51 ). Thus, the cellular data reflected the biological properties of dG-AF adduct without complications from NER repair.…”
Section: Resultsmentioning
confidence: 99%
“…The protein XPA plays a structural role in the assembly of this multi-protein-DNA complex [ 33 ] that, in turn, recruits the endonucleases XPF and XPG that catalyze the dual incisions of these oligonucleotide sequences that is followed by the excision of oligonucleotides ~24–32 nucleotides in length. We employed standard Western Blot methods for comparing the expressions of three of the critically important TFIIH proteins XPA, XPB and XPD in BRBE-treated and untreated HeLa cells; XPC-Rad23B was omitted because the binding affinity of XPC-Rad23B to structurally distorted DNA sequences is not proportional to the overall observed NER dual incision efficiencies [ 34 ], and because of its affinity for binding to unmodified DNA and to structural DNA distortions even in the absence of DNA lesions or adducts [ 34 , 35 , 36 ].…”
Section: Resultsmentioning
confidence: 99%
“…We reasoned that Gh would be interesting to study because the BER and NER mechanisms appear to compete for excising the same lesion [ 24 , 34 ]. In our experiments, the BER activity of Gh in our DNA repair pathways are robust ( Figure 3 A) and overshadows the NER activity.…”
Section: Discussionmentioning
confidence: 99%
“…Like other repair systems, there are two steps involved: recognition of the damage and the reparation step. Bulky adducts cause DNA distortions recognized by XPC-RAD23B, but only if the nucleotide opposing the lesion is not missing [ 15 ]. Once XPC-RAD23B recognizes the bulky adduct, a small bubble is formed, and TFIIH, a complex of 10 proteins, is recruited [ 16 ].…”
Section: The Dna Damage Responsementioning
confidence: 99%