Abstract 3021: FoxP1 increases nucleotide excision repair capacity through activating xeroderma pigmentosum group C in human breast cancer

2015 ◽  
Author(s):  
Haesung Kim ◽  
Lee-Su Kim ◽  
Jae-yong Lee ◽  
Jeong-Hyeon Kim ◽  
Jeong-Min Lee ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Nucleotide Excision Repair ◽  
Xeroderma Pigmentosum ◽  
Human Breast Cancer ◽  
Excision Repair ◽  
Human Breast ◽  
Repair Capacity ◽  
Nucleotide Excision

scholarly journals Xeroderma Pigmentosum Diagnosis Using a Flow Cytometry-Based Nucleotide Excision Repair Assay

2018 ◽  
Vol 138 (2) ◽  
pp. 467-470 ◽  
Author(s):  
Eiji Nakano ◽  
Seiji Takeuchi ◽  
Ryusuke Ono ◽  
Mariko Tsujimoto ◽  
Taro Masaki ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Nucleotide Excision Repair ◽  
Xeroderma Pigmentosum ◽  
Excision Repair ◽  
Nucleotide Excision

Nucleotide Excision Repair in the Three Domains of Life

2011 ◽  
Vol 2 (1) ◽  
Author(s):  
David A Farnell
Keyword(s):  
Dna Repair ◽  
Nucleotide Excision Repair ◽  
Xeroderma Pigmentosum ◽  
Excision Repair ◽  
Human Diseases ◽  
Repair Pathway ◽  
Functional Conservation ◽  
Wide Range ◽  
Nucleotide Excision ◽  
Domains Of Life

Nucleotide excision repair (NER) is a vital DNA repair pathway which acts on a wide range of helix-distorting lesions. The importance of this pathway is highlighted by its functional conservation throughout evolution and by several human diseases, such as xeroderma pigmentosum, which are caused by a defective NER pathway. This review summarizes the NER mechanisms present in all three domains of life: eukaryotes, bacteria, and archaea.

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.

scholarly journals Centrin 2 Stimulates Nucleotide Excision Repair by Interacting with Xeroderma Pigmentosum Group C Protein

2005 ◽  
Vol 25 (13) ◽  
pp. 5664-5674 ◽  
Author(s):  
Ryotaro Nishi ◽  
Yuki Okuda ◽  
Eriko Watanabe ◽  
Toshio Mori ◽  
Shigenori Iwai ◽  
...  
Keyword(s):  
Nucleotide Excision Repair ◽  
Xeroderma Pigmentosum ◽  
Excision Repair ◽  
Physical Interaction ◽  
C Protein ◽  
Damage Recognition ◽  
C Terminus ◽  
Nucleotide Excision ◽  
Dna Damage Recognition

ABSTRACT Xeroderma pigmentosum group C (XPC) protein plays a key role in DNA damage recognition in global genome nucleotide excision repair (NER). The protein forms in vivo a heterotrimeric complex involving one of the two human homologs of Saccharomyces cerevisiae Rad23p and centrin 2, a centrosomal protein. Because centrin 2 is dispensable for the cell-free NER reaction, its role in NER has been unclear. Binding experiments with a series of truncated XPC proteins allowed the centrin 2 binding domain to be mapped to a presumed α-helical region near the C terminus, and three amino acid substitutions in this domain abrogated interaction with centrin 2. Human cell lines stably expressing the mutant XPC protein exhibited a significant reduction in global genome NER activity. Furthermore, centrin 2 enhanced the cell-free NER dual incision and damaged DNA binding activities of XPC, which likely require physical interaction between XPC and centrin 2. These results reveal a novel vital function for centrin 2 in NER, the potentiation of damage recognition by XPC.

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