scholarly journals Nucleotide excision repair deficiency increases levels of acrolein-derived cyclic DNA adduct and sensitizes cells to apoptosis induced by docosahexaenoic acid and acrolein

Author(s):  
Jishen Pan ◽  
Elizabeth Sinclair ◽  
Zhuoli Xuan ◽  
Marcin Dyba ◽  
Ying Fu ◽  
...  
2012 ◽  
Vol 132 (12) ◽  
pp. 2738-2747 ◽  
Author(s):  
Arash Etemadi ◽  
Farhad Islami ◽  
David H. Phillips ◽  
Roger Godschalk ◽  
Asieh Golozar ◽  
...  

Author(s):  
Heather C. Murray ◽  
Vicki E. Maltby ◽  
Doug W. Smith ◽  
Nikola A. Bowden

2010 ◽  
Vol 107 (50) ◽  
pp. 21725-21730 ◽  
Author(s):  
J. J. Latimer ◽  
J. M. Johnson ◽  
C. M. Kelly ◽  
T. D. Miles ◽  
K. A. Beaudry-Rodgers ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Trevor van Eeuwen ◽  
Yoonjung Shim ◽  
Hee Jong Kim ◽  
Tingting Zhao ◽  
Shrabani Basu ◽  
...  

AbstractThe versatile nucleotide excision repair (NER) pathway initiates as the XPC–RAD23B–CETN2 complex first recognizes DNA lesions from the genomic DNA and recruits the general transcription factor complex, TFIIH, for subsequent lesion verification. Here, we present a cryo-EM structure of an NER initiation complex containing Rad4–Rad23-Rad33 (yeast homologue of XPC–RAD23B–CETN2) and 7-subunit coreTFIIH assembled on a carcinogen-DNA adduct lesion at 3.9–9.2 Å resolution. A ~30-bp DNA duplex could be mapped as it straddles between Rad4 and the Ssl2 (XPB) subunit of TFIIH on the 3' and 5' side of the lesion, respectively. The simultaneous binding with Rad4 and TFIIH was permitted by an unwinding of DNA at the lesion. Translocation coupled with torque generation by Ssl2 and Rad4 would extend the DNA unwinding at the lesion and deliver the damaged strand to Rad3 (XPD) in an open form suitable for subsequent lesion scanning and verification.


2013 ◽  
Vol 26 (11) ◽  
pp. 1746-1754 ◽  
Author(s):  
Jacek Krzeminski ◽  
Konstantin Kropachev ◽  
Dara Reeves ◽  
Aleksandr Kolbanovskiy ◽  
Marina Kolbanovskiy ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document