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1 (AZB), a potent antimicrobial and antitumor genotoxin.
2 t were and those that were not producing the genotoxin.
3 dialdehyde (MDA) is a natural and widespread genotoxin.
4 RAILR2) occur following exposure of cells to genotoxins.
5 air and oncogenic responses to environmental genotoxins.
6 A, ruvC, and recA for sensitivity to various genotoxins.
7 revented the cleavage of endogenous MEKK1 by genotoxins.
8 block cell cycle progression in response to genotoxins.
9 for Hus1 in mediating cellular responses to genotoxins.
10 KK1 contributes to the apoptotic response to genotoxins.
11 ent of the cellular response to a variety of genotoxins.
12 roposed to mediate the apoptopic response to genotoxins.
13 ed with hypersensitivity to DNA-crosslinking genotoxins.
14 cover how the embryo is protected from these genotoxins.
15 s exhibit increased sensitivity to oxidising genotoxins.
16 nstability in people exposed to carcinogenic genotoxins.
17 may be of general importance beyond estrogen genotoxins.
18 SB) generated endogenously or by exposure to genotoxins.
19 acute exposure to a limited number of potent genotoxins.
20 carcinogenicity may therefore exist for such genotoxins.
21 er DNA damage and causes hypersensitivity to genotoxins.
22 ,beta-unsaturated aldehydes are bifunctional genotoxins.
25 In vivo, exposure of mice to CO followed by genotoxin (Adriamycin) or radiation-induced injury led t
26 estricted to ionizing radiation, as chemical genotoxins also induce heritable and transmissible genom
27 tion of nts1 causes increased sensitivity to genotoxins and deregulated expression of Tf2 elements, l
28 t3 level is downregulated in the presence of genotoxins and ectopic expression of HST3 blocks genotox
30 196N) mutants exhibit greater sensitivity to genotoxins and higher levels of crossing over during DSB
31 gs implicate susceptibility to environmental genotoxins and inadequate DNA repair as novel mechanisms
34 ing mouse Hus1 are hypersensitive to certain genotoxins, and we have explored the molecular basis for
36 hese findings show that signals generated by genotoxins are transduced by multiple, independent pathw
37 establish that CDTs are likely to be potent genotoxins, as indicated by in vivo degradation of chrom
41 ancer stem cells are resistant to killing by genotoxins, but the mechanism for this resistance is poo
48 l pathogenic E. coli (ExPEC) and encodes the genotoxin colibactin, is epidemiologically associated wi
50 urthermore, these studies suggest the active genotoxins (colibactins) are unsaturated imines that are
51 detoxification of this ubiquitous endogenous genotoxin creates a benign 1C unit that can sustain esse
57 site, which is phosphorylated in response to genotoxins, had no effect on survival or checkpoint acti
58 ene Hus1 results in chromosomal instability, genotoxin hypersensitivity, and embryonic lethality.
59 nt identification of aldehydes as endogenous genotoxins in Fanconi anemia has provided new insight in
61 affect both the activity of nonintercalating genotoxins in vivo and the accessibility of glutathione
62 er after exposure to cisplatin but not other genotoxins including another cross-linking agent, mitomy
63 sing transgenic atpollambda-2 mutants toward genotoxins indicated the importance of the BRCT domain o
67 ne disruption was caused by sensitization to genotoxin-induced (p53-mediated) apoptosis or by p53-ind
68 the inner ring of HUS1 that were crucial for genotoxin-induced 9-1-1 chromatin localization and ATR s
69 est that ATM is a major signal initiator for genotoxin-induced apoptosis but, paradoxically, also con
70 breast epithelium and carcinomas to undergo genotoxin-induced apoptosis correlates strongly with cel
71 th receptors is a significant contributor to genotoxin-induced apoptosis in human epithelial carcinom
72 iquitination of NEMO significantly increased genotoxin-induced apoptosis, resulting in enhanced sensi
81 These findings suggest that ATM is the major genotoxin-induced CREB kinase in mammalian cells and tha
83 ed RAD51 nuclear foci and were able to limit genotoxin-induced genomic instability, both hallmarks of
89 terozygosity confers broad susceptibility to genotoxin-induced tumorigenesis, and this paradigm serve
90 ient mice are particularly susceptibility to genotoxin-induced tumors, suggesting a role for p27 in t
91 uirement for LXCXE binding in suppression of genotoxin-initiated hepatocellular carcinoma in vivo.
93 ubunit REV3L is important in defense against genotoxins, little is known of its biological function.
94 metrial carcinogenesis may proceed through a genotoxin-mediated pathway, although the detection of en
99 logous proteins (CdtA, CdtB, and CdtC) and a genotoxin mode of action distinguish the Cdt from others
100 LME6 (lacking p53) cells were exposed to the genotoxin N-methyl-N-nitro-N-nitrosoguanidine (MNNG), bo
101 man gut produce colibactin, a small-molecule genotoxin of unknown structure that has been implicated
102 etabolism, as a consequence of environmental genotoxins or radiation, or during programmed recombinat
103 compose a subclass of intracellularly acting genotoxins produced by many Gram-negative pathogenic bac
107 ppaB activation in H157 cells in response to genotoxin resulted in loss of cell surface expression of
110 found the srs2Delta mutant to have a similar genotoxin sensitivity profile and replicative lifespan t
111 d G1 cells was not associated with increased genotoxin sensitivity, indicating that back-up DSB repai
112 ipid hydroperoxides gives rise to endogenous genotoxins such as 4-oxo-2(E)-nonenal, which cause the f
114 benzo(a)pyrene dihydrodiol epoxide (BPDE), a genotoxin that causes bulky DNA adducts, Hus1-null cells
115 ynthesis of colibactin, a polyketide-peptide genotoxin that causes genomic instability in eukaryotic
116 were also hypersensitive to camptothecin, a genotoxin that generates breaks specifically at the repl
118 cells depleted of SLX4 are hypersensitive to genotoxins that cause DSBs and show defects in the resol
120 (DDR) protein gammaH2AX induced by selective genotoxins that promote DNA replication stress or SSBs.
122 conclude that the AhR shuttles PAH o-quinone genotoxins to the nucleus and enhances oxidative DNA dam
125 damage tolerance throughout the genome under genotoxin treatment, its function during unperturbed gro
127 ranslational modification, we also show that genotoxin-triggered 9-1-1 chromatin binding does not dep
130 nvironment of DNA affects it as a target for genotoxins, we have used ligation-mediated PCR to map DN
132 53-mediated cell-cycle arrest in response to genotoxins while loss of HSF1 attenuates apoptosis in re
133 erforming cell-based functional sensing of a genotoxin with high sensitivity and short incubation tim
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