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关键词:'C0496'
显示 1-7 共 7 条结果 关于 "C0496" 范围 论文
Prachi Verma et al.
Biochimie, 144, 122-133 (2017-11-04)
Dihydroxy-1-selenolane (DHS) previously reported to exhibit radioprotective activity was investigated to understand its mechanism of action in CHO cells of epithelial origin. DHS pre-treatment at 25 μM for 16 h significantly protected CHO cells from radiation (4-11 Gy)-induced delayed mitotic cell death. Further
Lidan Li et al.
Nanoscale, 11(3), 1343-1350 (2019-01-04)
The transition of DNA nanomachines from test tubes to living cells would realize the ultimate goal of smart therapeutic dynamic DNA nanotechnology. The operation of DNA nanomachines in living cells remains challenging because it is difficult to utilize an endogenous
Leonardo Pereira Franchi et al.
Journal of photochemistry and photobiology. B, Biology, 211, 111992-111992 (2020-08-18)
Photodynamic therapy (PDT) is an anticancer modality depicting an induced oxidative stress as the mechanism of action that ultimately culminates in cell death. The apurinic/apyrimidinic endonuclease 1/redox factor-1 (APE1/Ref-1) is a key protein promoting bad prognostic in several cancer types.
De-Sheng Pei et al.
Nucleic acids research, 39(8), 3156-3165 (2010-12-22)
DNA repair is required to maintain genome stability in stem cells and early embryos. At critical junctures, oxidative damage to DNA requires the base excision repair (BER) pathway. Since early zebrafish embryos lack the major polymerase in BER, DNA polymerase
Junqiu Zhai et al.
Nucleic acids research, 45(6), e45-e45 (2016-12-08)
Human apurinic/apyrimidinic endonuclease/redox effector factor 1 (APE1) is an essential DNA repair protein. Herein, we demonstrate that avidin-oriented abasic site-containing DNA strands (AP-DNA) on the surface of silica coated magnetic nanoparticles (SiMNP) can selectively respond to APE1 while resist the
Meryem Alagoz et al.
Nucleic acids research, 42(5), 3089-3103 (2013-12-18)
Base damage and topoisomerase I (Top1)-linked DNA breaks are abundant forms of endogenous DNA breakage, contributing to hereditary ataxia and underlying the cytotoxicity of a wide range of anti-cancer agents. Despite their frequency, the overlapping mechanisms that repair these forms
Jeroen E J Guikema et al.
The Journal of experimental medicine, 204(12), 3017-3026 (2007-11-21)
Antibody class switch recombination (CSR) occurs by an intrachromosomal deletion requiring generation of double-stranded breaks (DSBs) in switch-region DNA. The initial steps in DSB formation have been elucidated, involving cytosine deamination by activation-induced cytidine deaminase and generation of abasic sites
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