scholarly journals Combination of Aβ Secretion and Oxidative Stress in an Alzheimer-Like Cell Line Leads to the Over-Expression of the Nucleotide Excision Repair Proteins DDB2 and XPC

2015 ◽  
Vol 16 (8) ◽  
pp. 17422-17444 ◽  
Author(s):  
Anne Forestier ◽  
Thierry Douki ◽  
Viviana De Rosa ◽  
David Béal ◽  
Walid Rachidi
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Over Expression ◽  
Nucleotide Excision ◽  
And Oxidative Stress

scholarly journals The effect of oxidative stress on nucleotide-excision repair in colon tissue of newborn piglets

2010 ◽  
Vol 695 (1-2) ◽  
pp. 75-80 ◽  
Author(s):  
Sabine A.S. Langie ◽  
Pawel Kowalczyk ◽  
Barbara Tudek ◽  
Romuald Zabielski ◽  
Tomasz Dziaman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Colon Tissue ◽  
Newborn Piglets ◽  
Nucleotide Excision

Molecular cloning and biological characterization of a human gene, ERCC2, that corrects the nucleotide excision repair defect in CHO UV5 cells

1988 ◽  
Vol 8 (3) ◽  
pp. 1137-1146
Author(s):  
C A Weber ◽  
E P Salazar ◽  
S A Stewart ◽  
L H Thompson
Keyword(s):  
Cell Line ◽  
Nucleotide Excision Repair ◽  
Human Gene ◽  
Excision Repair ◽  
Hybrid Cell ◽  
Repetitive Sequences ◽  
Chinese Hamster ◽  
Wild Type ◽  
Wild Type Level ◽  
Nucleotide Excision

The UV-sensitive Chinese hamster ovary (CHO) cell line UV5, which is defective in the incision step of nucleotide excision repair, was used to identify and clone a complementing human gene, ERCC2, and to study the repair process. Genomic DNA from a human-hamster hybrid cell line was sheared and cotransferred with pSV2gpt plasmid DNA into UV5 cells to obtain five primary transformants. Transfer of sheared DNA from one primary transformant resulted in a secondary transformant expressing both gpt and ERCC2. The human repair gene was identified with a probe for Alu-family repetitive sequences. For most primary, secondary, and cosmid transformants, survival after UV exposure showed a return to wild-type levels of resistance. The levels of UV-induced mutation at the aprt locus for secondary and cosmid transformants varied from 50 to 130% of the wild-type level. Measurements of the initial rate of UV-induced strand incision by alkaline elution indicated that, whereas the UV5 rate was 3% of the wild-type level, rates of cosmid-transformed lines were similar to that of the wild type, and the secondary transformant rate was about 165% of the wild-type rate. Analysis of overlapping cosmids determined that ERCC2 is between 15.5 and 20 kilobases and identified a closely linked gpt gene. Cosmids were obtained with functional copies of both ERCC2 and gpt. ERCC2 corrects only the first of the five CHO complementation groups of incision-defective mutants.

scholarly journals 8-Oxo-7,8-Dihydroguanine Is Removed by a Nucleotide Excision Repair-Like Mechanism in Porphyromonas gingivalis W83

2004 ◽  
Vol 186 (22) ◽  
pp. 7697-7703 ◽  
Author(s):  
N. A. Johnson ◽  
R. McKenzie ◽  
L. McLean ◽  
L. C. Sowers ◽  
H. M. Fletcher
Keyword(s):  
Oxidative Stress ◽  
Nucleotide Excision Repair ◽  
Porphyromonas Gingivalis ◽  
Excision Repair ◽  
Periodontal Pocket ◽  
Periodontal Pathogens ◽  
Chromosomal Dna ◽  
Inflammatory Microenvironment ◽  
Cell Extracts ◽  
Nucleotide Excision

ABSTRACT A consequence of oxidative stress is DNA damage. The survival of Porphyromonas gingivalis in the inflammatory microenvironment of the periodontal pocket requires an ability to overcome oxidative stress caused by reactive oxygen species (ROS). 8-Oxo-7,8-dihydroguanine (8-oxoG) is typical of oxidative damage induced by ROS. There is no information on the presence of 8-oxoG in P. gingivalis under oxidative stress conditions or on a putative mechanism for its repair. High-pressure liquid chromatography with electrochemical detection analysis of chromosomal DNA revealed higher levels of 8-oxoG in P. gingivalis FLL92, a nonpigmented isogenic mutant, than in the wild-type strain. 8-OxoG repair activity was also increased in cell extracts from P. gingivalis FLL92 compared to those from the parent strain. Enzymatic removal of 8-oxoG was catalyzed by a nucleotide excision repair (NER)-like mechanism rather than the base excision repair (BER) observed in Escherichia coli. In addition, in comparison with other anaerobic periodontal pathogens, the removal of 8-oxoG was unique to P. gingivalis. Taken together, the increased 8-oxoG levels in P. gingivalis FLL92 could further support a role for the hemin layer as a unique mechanism in oxidative stress resistance in this organism. In addition, this is the first observation of an NER-like mechanism as the major mechanism for removal of 8-oxoG in P. gingivalis.

The role of glutathione in the regulation of nucleotide excision repair during oxidative stress

2007 ◽  
Vol 168 (3) ◽  
pp. 302-309 ◽  
Author(s):  
Sabine A.S. Langie ◽  
Ad M. Knaapen ◽  
Joyce M.J. Houben ◽  
Frederik C. van Kempen ◽  
Joep P.J. de Hoon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Nucleotide Excision

scholarly journals Regulation of ddb2 expression in blind cavefish and zebrafish reveals plasticity in the control of sunlight-induced DNA damage repair

PLoS Genetics ◽  
2021 ◽  
Vol 17 (2) ◽  
pp. e1009356
Author(s):  
Haiyu Zhao ◽  
Hongxiang Li ◽  
Juan Du ◽  
Giuseppe Di Mauro ◽  
Sebastian Lungu-Mitea ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Transcriptional Activation ◽  
Excision Repair ◽  
Environmental Challenges ◽  
Damage Repair ◽  
Nucleotide Excision ◽  
Surface Dwelling ◽  
Blind Cavefish ◽  
And Oxidative Stress

We have gained considerable insight into the mechanisms which recognize and repair DNA damage, but how they adapt to extreme environmental challenges remains poorly understood. Cavefish have proven to be fascinating models for exploring the evolution of DNA repair in the complete absence of UV-induced DNA damage and light. We have previously revealed that the Somalian cavefish Phreatichthys andruzzii, lacks photoreactivation repair via the loss of light, UV and ROS-induced photolyase gene transcription mediated by D-box enhancer elements. Here, we explore whether other systems repairing UV-induced DNA damage have been similarly affected in this cavefish model. By performing a comparative study using P. andruzzii and the surface-dwelling zebrafish, we provide evidence for a conservation of sunlight-regulated Nucleotide Excision Repair (NER). Specifically, the expression of the ddb2 gene which encodes a key NER recognition factor is robustly induced following exposure to light, UV and oxidative stress in both species. As in the case of the photolyase genes, D-boxes in the ddb2 promoter are sufficient to induce transcription in zebrafish. Interestingly, despite the loss of D-box-regulated photolyase gene expression in P. andruzzii, the D-box is required for ddb2 induction by visible light and oxidative stress in cavefish. However, in the cavefish ddb2 gene this D-box-mediated induction requires cooperation with an adjacent, highly conserved E2F element. Furthermore, while in zebrafish UV-induced ddb2 expression results from transcriptional activation accompanied by stabilization of the ddb2 mRNA, in P. andruzzii UV induces ddb2 expression exclusively via an increase in mRNA stability. Thus, we reveal plasticity in the transcriptional and post transcriptional mechanisms regulating the repair of sunlight-induced DNA damage under long-term environmental challenges.

scholarly journals Genomic Characterization of Cisplatin Response Uncovers Priming of Cisplatin-Induced Genes in a Resistant Cell Line

2021 ◽  
Vol 22 (11) ◽  
pp. 5814
Author(s):  
Hadar Golan Berman ◽  
Pooja Chauhan ◽  
Shira Shalev ◽  
Hiba Hassanain ◽  
Avital Parnas ◽  
...  
Keyword(s):  
Cell Line ◽  
Nucleotide Excision Repair ◽  
Cisplatin Resistance ◽  
Excision Repair ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Nucleotide Excision ◽  
Genomic Characterization ◽  
Resistant Cells

Cisplatin is a chemotherapy drug that kills cancer cells by damaging their DNA. In human cells, this damage is repaired primarily by nucleotide excision repair. While cisplatin is generally effective, many cancers exhibit initial or acquired resistance to it. Here, we studied cisplatin resistance in a defined cell line system. We conducted a comprehensive genomic characterization of the cisplatin-sensitive A2780 ovarian cancer cell line compared to A2780cis, its resistant derivative. The resistant cells acquired less damage, but had similar repair kinetics. Genome-wide mapping of nucleotide excision repair showed a shift in the resistant cells from global genome towards transcription-coupled repair. By mapping gene expression changes following cisplatin treatment, we identified 56 upregulated genes that have higher basal expression in the resistant cell line, suggesting they are primed for a cisplatin response. More than half of these genes are novel to cisplatin- or damage-response. Six out of seven primed genes tested were upregulated in response to cisplatin in additional cell lines, making them attractive candidates for future investigation. These novel candidates for cisplatin resistance could prove to be important prognostic markers or targets for tailored combined therapy in the future.

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