scholarly journals Oxidative Damage to RPA Limits the Nucleotide Excision Repair Capacity of Human Cells

2015 ◽  
Vol 135 (11) ◽  
pp. 2834-2841 ◽  
Author(s):  
Melisa Guven ◽  
Reto Brem ◽  
Peter Macpherson ◽  
Matthew Peacock ◽  
Peter Karran
Keyword(s):  
Oxidative Damage ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Human Cells ◽  
Repair Capacity ◽  
Nucleotide Excision

scholarly journals Nucleotide Excision Repair in Human Cells

2013 ◽  
Vol 288 (29) ◽  
pp. 20918-20926 ◽  
Author(s):  
Jinchuan Hu ◽  
Jun-Hyuk Choi ◽  
Shobhan Gaddameedhi ◽  
Michael G. Kemp ◽  
Joyce T. Reardon ◽  
...  
Keyword(s):  
Nucleotide Excision Repair ◽  
Genomic Dna ◽  
Excision Repair ◽  
Human Cells ◽  
Naked Dna ◽  
Nucleotide Excision ◽  
Uv Photoproducts ◽  
Mutant Cells

Nucleotide excision repair is the sole mechanism for removing the major UV photoproducts from genomic DNA in human cells. In vitro with human cell-free extract or purified excision repair factors, the damage is removed from naked DNA or nucleosomes in the form of 24- to 32-nucleotide-long oligomers (nominal 30-mer) by dual incisions. Whether the DNA damage is removed from chromatin in vivo in a similar manner and what the fate of the excised oligomer was has not been known previously. Here, we demonstrate that dual incisions occur in vivo identical to the in vitro reaction. Further, we show that transcription-coupled repair, which operates in the absence of the XPC protein, also generates the nominal 30-mer in UV-irradiated XP-C mutant cells. Finally, we report that the excised 30-mer is released from the chromatin in complex with the repair factors TFIIH and XPG. Taken together, our results show the congruence of in vivo and in vitro data on nucleotide excision repair in humans.

O V A.1 Nucleotide excision repair mechanism in human cells: Analysis by in vitro assays

1997 ◽  
Vol 379 (1) ◽  
pp. S33
Author(s):  
Bernard Salles ◽  
Patrick Calsou ◽  
Philippe Frit ◽  
Ruo-Ya Li ◽  
Catherine Muller ◽  
...  
Keyword(s):  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Human Cells ◽  
In Vitro Assays ◽  
Repair Mechanism ◽  
Nucleotide Excision

scholarly journals DNA damage and nucleotide excision repair capacity in healthy individuals

2011 ◽  
Vol 52 (7) ◽  
pp. 511-517 ◽  
Author(s):  
Jana Slyskova ◽  
Alessio Naccarati ◽  
Veronika Polakova ◽  
Barbara Pardini ◽  
Ludmila Vodickova ◽  
...  
Keyword(s):  
Dna Damage ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Healthy Individuals ◽  
Repair Capacity ◽  
Nucleotide Excision

scholarly journals Nucleotide Excision Repair or Polymerase V-Mediated Lesion Bypass Can Act To Restore UV-Arrested Replication Forks in Escherichia coli

2005 ◽  
Vol 187 (20) ◽  
pp. 6953-6961 ◽  
Author(s):  
Charmain T. Courcelle ◽  
Jerilyn J. Belle ◽  
Justin Courcelle
Keyword(s):  
Dna Synthesis ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Translesion Synthesis ◽  
Replication Forks ◽  
Repair Capacity ◽  
Translesion Dna Synthesis ◽  
Pol V ◽  
Nucleotide Excision ◽  
Translesion Dna

ABSTRACT Nucleotide excision repair and translesion DNA synthesis are two processes that operate at arrested replication forks to reduce the frequency of recombination and promote cell survival following UV-induced DNA damage. While nucleotide excision repair is generally considered to be error free, translesion synthesis can result in mutations, making it important to identify the order and conditions that determine when each process is recruited to the arrested fork. We show here that at early times following UV irradiation, the recovery of DNA synthesis occurs through nucleotide excision repair of the lesion. In the absence of repair or when the repair capacity of the cell has been exceeded, translesion synthesis by polymerase V (Pol V) allows DNA synthesis to resume and is required to protect the arrested replication fork from degradation. Pol II and Pol IV do not contribute detectably to survival, mutagenesis, or restoration of DNA synthesis, suggesting that, in vivo, these polymerases are not functionally redundant with Pol V at UV-induced lesions. We discuss a model in which cells first use DNA repair to process replication-arresting UV lesions before resorting to mutagenic pathways such as translesion DNA synthesis to bypass these impediments to replication progression.

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