scholarly journals Stimulation of NEIL2-mediated Oxidized Base Excision Repair via YB-1 Interaction during Oxidative Stress

2007 ◽  
Vol 282 (39) ◽  
pp. 28474-28484 ◽  
Author(s):  
Soumita Das ◽  
Ranajoy Chattopadhyay ◽  
Kishor K. Bhakat ◽  
Istvan Boldogh ◽  
Kimitoshi Kohno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Base Excision Repair ◽  
Excision Repair ◽  
Base Excision ◽  
Stimulation Of

scholarly journals Effect of DNA Glycosylases OGG1 and Neil1 on Oxidized G-Rich Motif in the KRAS Promoter

2021 ◽  
Vol 22 (3) ◽  
pp. 1137
Author(s):  
Annalisa Ferino ◽  
Luigi E. Xodo
Keyword(s):  
Oxidative Stress ◽  
Base Excision Repair ◽  
Excision Repair ◽  
Start Site ◽  
Dna Glycosylases ◽  
Repair Pathway ◽  
Transcription Start ◽  
G Quadruplex ◽  
Base Excision ◽  
Regulatory Functions

The promoter of the Kirsten ras (KRAS) proto-oncogene contains, upstream of the transcription start site, a quadruplex-forming motif called 32R with regulatory functions. As guanine under oxidative stress can be oxidized to 8-oxoguanine (8OG), we investigated the capacity of glycosylases 8-oxoguanine glycosylase (OGG1) and endonuclease VIII-like 1 (Neil1) to excise 8OG from 32R, either in duplex or G-quadruplex (G4) conformation. We found that OGG1 efficiently excised 8OG from oxidized 32R in duplex but not in G4 conformation. By contrast, glycosylase Neil1 showed more activity on the G4 than the duplex conformation. We also found that the excising activity of Neil1 on folded 32R depended on G4 topology. Our data suggest that Neil1, besides being involved in base excision repair pathway (BER), could play a role on KRAS transcription.

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 Oxidative stress triggers the preferential assembly of base excision repair complexes on open chromatin regions

2010 ◽  
Vol 38 (9) ◽  
pp. 2878-2890 ◽  
Author(s):  
Rachel Amouroux ◽  
Anna Campalans ◽  
Bernd Epe ◽  
J. Pablo Radicella
Keyword(s):  
Oxidative Stress ◽  
Base Excision Repair ◽  
Excision Repair ◽  
Open Chromatin ◽  
Base Excision

scholarly journals Long Patch Base Excision Repair proceeds via coordinated stimulation of the multienzyme repair complex

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Lata Balakrishnan ◽  
Patrick Brandt ◽  
Laura Lindsey‐Boltz ◽  
Aziz Sancar ◽  
Robert Bambara
Keyword(s):  
Base Excision Repair ◽  
Excision Repair ◽  
Base Excision ◽  
Stimulation Of
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