scholarly journals Oxidative DNA damage is concurrently repaired by base excision repair (BER) and apyrimidinic endonuclease 1 (APE1)‐initiated nonhomologous end joining (NHEJ) in cortical neurons

2019 ◽  
Vol 46 (4) ◽  
pp. 375-390 ◽  
Author(s):  
J.‐L. Yang ◽  
W.‐Y. Chen ◽  
S. Mukda ◽  
Y.‐R. Yang ◽  
S.‐F. Sun ◽  
...  
Keyword(s):  
Dna Damage ◽  
Base Excision Repair ◽  
Cortical Neurons ◽  
Oxidative Dna Damage ◽  
Excision Repair ◽  
Nonhomologous End Joining ◽  
End Joining ◽  
Base Excision

scholarly journals Dynamic Compartmentalization of Base Excision Repair Proteins in Response to Nuclear and Mitochondrial Oxidative Stress

2008 ◽  
Vol 29 (3) ◽  
pp. 794-807 ◽  
Author(s):  
Lyra M. Griffiths ◽  
Dan Swartzlander ◽  
Kellen L. Meadows ◽  
Keith D. Wilkinson ◽  
Anita H. Corbett ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Repair ◽  
Base Excision Repair ◽  
Oxidative Dna Damage ◽  
Excision Repair ◽  
Intracellular Localization ◽  
Genotoxic Stress ◽  
Mitochondrial Oxidative Stress ◽  
Base Excision

ABSTRACT DNAs harbored in both nuclei and mitochondria of eukaryotic cells are subject to continuous oxidative damage resulting from normal metabolic activities or environmental insults. Oxidative DNA damage is primarily reversed by the base excision repair (BER) pathway, initiated by N-glycosylase apurinic/apyrimidinic (AP) lyase proteins. To execute an appropriate repair response, BER components must be distributed to accommodate levels of genotoxic stress that may vary considerably between nuclei and mitochondria, depending on the growth state and stress environment of the cell. Numerous examples exist where cells respond to signals, resulting in relocalization of proteins involved in key biological transactions. To address whether such dynamic localization contributes to efficient organelle-specific DNA repair, we determined the intracellular localization of the Saccharomyces cerevisiae N-glycosylase/AP lyases, Ntg1 and Ntg2, in response to nuclear and mitochondrial oxidative stress. Fluorescence microscopy revealed that Ntg1 is differentially localized to nuclei and mitochondria, likely in response to the oxidative DNA damage status of the organelle. Sumoylation is associated with targeting of Ntg1 to nuclei containing oxidative DNA damage. These studies demonstrate that trafficking of DNA repair proteins to organelles containing high levels of oxidative DNA damage may be a central point for regulating BER in response to oxidative stress.

scholarly journals Base excision repair of oxidative DNA damage and association with cancer and aging

2008 ◽  
Vol 30 (1) ◽  
pp. 2-10 ◽  
Author(s):  
S. Maynard ◽  
S. H. Schurman ◽  
C. Harboe ◽  
N. C. de Souza-Pinto ◽  
V. A. Bohr
Keyword(s):  
Dna Damage ◽  
Base Excision Repair ◽  
Oxidative Dna Damage ◽  
Excision Repair ◽  
Base Excision

scholarly journals Databases and Bioinformatics Tools for the Study of DNA Repair

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Kaja Milanowska ◽  
Kristian Rother ◽  
Janusz M. Bujnicki
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Excision Repair ◽  
Uv Light ◽  
Dna Lesions ◽  
Environmental Chemicals ◽  
Nonhomologous End Joining ◽  
End Joining ◽  
Repair Mechanisms ◽  
Base Excision

DNA is continuously exposed to many different damaging agents such as environmental chemicals, UV light, ionizing radiation, and reactive cellular metabolites. DNA lesions can result in different phenotypical consequences ranging from a number of diseases, including cancer, to cellular malfunction, cell death, or aging. To counteract the deleterious effects of DNA damage, cells have developed various repair systems, including biochemical pathways responsible for the removal of single-strand lesions such as base excision repair (BER) and nucleotide excision repair (NER) or specialized polymerases temporarily taking over lesion-arrested DNA polymerases during the S phase in translesion synthesis (TLS). There are also other mechanisms of DNA repair such as homologous recombination repair (HRR), nonhomologous end-joining repair (NHEJ), or DNA damage response system (DDR). This paper reviews bioinformatics resources specialized in disseminating information about DNA repair pathways, proteins involved in repair mechanisms, damaging agents, and DNA lesions.

scholarly journals The Effect ofMsh2Knockdown on Toxicity Induced bytert-Butyl-hydroperoxide, Potassium Bromate, and Hydrogen Peroxide in Base Excision Repair Proficient and Deficient Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
N. Cooley ◽  
R. H. Elder ◽  
A. C. Povey
Keyword(s):  
Dna Damage ◽  
Base Excision Repair ◽  
Oxidative Dna Damage ◽  
Excision Repair ◽  
Shrna Expression ◽  
Cellular Toxicity ◽  
Dna Mismatch ◽  
Shrna Expression Vector ◽  
Repair Systems ◽  
Base Excision

The DNA mismatch repair (MMR) and base excision repair (BER) systems are important determinants of cellular toxicity following exposure to agents that cause oxidative DNA damage. To examine the interactions between these different repair systems, we examined whether toxicity, induced byt-BOOH and KBrO3, differs in BER proficient (Mpg+/+,Nth1+/+) and deficient (Mpg−/−,Nth1−/−) mouse embryonic fibroblasts (MEFs) followingMsh2knockdown of between 79 and 88% using an shRNA expression vector.Msh2knockdown inNth1+/+cells had no effect ont-BOOH and KBrO3induced toxicity as assessed by an MTT assay; knockdown inNth1−/−cells resulted in increased resistance tot-BOOH and KBrO3, a result consistent with Nth1 removing oxidised pyrimidines.Msh2knockdown inMpg+/+cells had no effect ont-BOOH toxicity but increased resistance to KBrO3; inMpg−/−cells,Msh2knockdown increased cellular sensitivity to KBrO3but increased resistance to t-BOOH, suggesting a role forMpgin removing DNA damage induced by these agents. MSH2 dependent and independent pathways then determine cellular toxicity induced by oxidising agents. A complex interaction between MMR and BER repair systems, that is, exposure dependent, also exists to determine cellular toxicity.

Roles of base excision repair enzymes Nth1p and Apn2p from Schizosaccharomyces pombe in processing alkylation and oxidative DNA damage

DNA Repair ◽  
2005 ◽  
Vol 4 (11) ◽  
pp. 1270-1280 ◽  
Author(s):  
Takanori Sugimoto ◽  
Emi Igawa ◽  
Haruna Tanihigashi ◽  
Mayumi Matsubara ◽  
Hiroshi Ide ◽  
...  
Keyword(s):  
Dna Damage ◽  
Schizosaccharomyces Pombe ◽  
Base Excision Repair ◽  
Oxidative Dna Damage ◽  
Excision Repair ◽  
Repair Enzymes ◽  
Base Excision

Mammalian DNA base excision repair proteins: their interactions and role in repair of oxidative DNA damage

Toxicology ◽  
2003 ◽  
Vol 193 (1-2) ◽  
pp. 43-65 ◽  
Author(s):  
Tadahide Izumi ◽  
Lee R. Wiederhold ◽  
Gargi Roy ◽  
Rabindra Roy ◽  
Arun Jaiswal ◽  
...  
Keyword(s):  
Dna Damage ◽  
Base Excision Repair ◽  
Oxidative Dna Damage ◽  
Excision Repair ◽  
Dna Base Excision Repair ◽  
Dna Base ◽  
Base Excision
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