Nucleotide Excision Repair Proteins May Be Involved in the Fixation of Glyoxal-Induced Mutagenesis inEscherichia coli

1998 ◽  
Vol 248 (2) ◽  
pp. 412-417 ◽  
Author(s):  
Naoko Murata-Kamiya ◽  
Hiroyuki Kamiya ◽  
Hiroshi Kaji ◽  
Hiroshi Kasai
2013 ◽  
Vol 9 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Mi-Sun Kang ◽  
Sung-Lim Yu ◽  
Ho-Yeol Kim ◽  
Hyun-Sook Lim ◽  
Sung-Keun Lee

2016 ◽  
Vol 44 (22) ◽  
pp. 10711-10726 ◽  
Author(s):  
Stuart G. Jarrett ◽  
Erin M. Wolf Horrell ◽  
John A. D'Orazio

Abstract Loss-of-function in melanocortin 1 receptor (MC1R), a GS protein-coupled receptor that regulates signal transduction through cAMP and protein kinase A (PKA) in melanocytes, is a major inherited melanoma risk factor. Herein, we report a novel cAMP-mediated response for sensing and responding to UV-induced DNA damage regulated by A-kinase-anchoring protein 12 (AKAP12). AKAP12 is identified as a necessary participant in PKA-mediated phosphorylation of ataxia telangiectasia mutated and Rad3-related (ATR) at S435, a post-translational event required for cAMP-enhanced nucleotide excision repair (NER). Moreover, UV exposure promotes ATR-directed phosphorylation of AKAP12 at S732, which promotes nuclear translocation of AKAP12–ATR-pS435. This complex subsequently recruits XPA to UV DNA damage and enhances 5΄ strand incision. Preventing AKAP12's interaction with PKA or with ATR abrogates ATR-pS435 accumulation, delays recruitment of XPA to UV-damaged DNA, impairs NER and increases UV-induced mutagenesis. Our results define a critical role for AKAP12 as an UV-inducible scaffold for PKA-mediated ATR phosphorylation, and identify a repair complex consisting of AKAP12–ATR-pS435-XPA at photodamage, which is essential for cAMP-enhanced NER.


2008 ◽  
Vol 60 (1) ◽  
pp. 93-102 ◽  
Author(s):  
Jasna Stanojevic ◽  
Tanja Beric ◽  
Biljana Opacic ◽  
Branka Vukovic-Gacic ◽  
Draga Simic ◽  
...  

The antimutagenic potential of essential oil (EO) of basil (Ocimum basilicum L.) and its major constituent linalool were studied with the E. coli K12 and S.cerevisiae D7 assays. In the E. coli assay, EO and linalool inhibited UV-induced mutagenesis in a repair-proficient strain, but had no effect on spontaneous mutagenesis in repair-proficient, nucleotide excision repair-deficient, and mismatch-deficient strains. By testing participation of different mechanisms involved in antimutagenesis, it was concluded that the antimutagenic effect against UV-induced mutagenesis involved decrease of protein synthesis and cell proliferation which led to increased efficiency of nucleotide excision repair. An antimutagenic effect of basil derivatives in S. cerevisiae was not detected.


Author(s):  
Anita F. W. Frijhoff ◽  
Cyrille A. M. Krul ◽  
Annemieke de Vries ◽  
Marco C. J. M. Kelders ◽  
Geert Weeda ◽  
...  

2015 ◽  
Vol 364 ◽  
pp. 7-20 ◽  
Author(s):  
Aleksandr N. Bugay ◽  
Evgeny A. Krasavin ◽  
Aleksandr Yu. Parkhomenko ◽  
Maria A. Vasilyeva

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