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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 ,beta-unsaturated aldehydes are bifunctional genotoxins.
5 RAILR2) occur following exposure of cells to genotoxins.
6 air and oncogenic responses to environmental genotoxins.
7 A, ruvC, and recA for sensitivity to various genotoxins.
8 revented the cleavage of endogenous MEKK1 by genotoxins.
9  block cell cycle progression in response to genotoxins.
10  for Hus1 in mediating cellular responses to genotoxins.
11 KK1 contributes to the apoptotic response to genotoxins.
12 ent of the cellular response to a variety of genotoxins.
13 roposed to mediate the apoptopic response to genotoxins.
14 DNA repair capacities that sensitize them to genotoxins.
15 response, making cells vulnerable to various genotoxins.
16 ich showed a reduction in most, but not all, genotoxins.
17 chromatin exchanges but are not sensitive to genotoxins.
18 vival and SSBR following exposure to various genotoxins.
19 atural products, including many DNA-damaging genotoxins.
20 lanar genotoxicity profiling that can detect genotoxins.
21 A damage in eliciting a specific response to genotoxins.
22 s exhibit increased sensitivity to oxidising genotoxins.
23 ed with hypersensitivity to DNA-crosslinking genotoxins.
24 cover how the embryo is protected from these genotoxins.
25 nstability in people exposed to carcinogenic genotoxins.
26 may be of general importance beyond estrogen genotoxins.
27 SB) generated endogenously or by exposure to genotoxins.
28 acute exposure to a limited number of potent genotoxins.
29 carcinogenicity may therefore exist for such genotoxins.
30 er DNA damage and causes hypersensitivity to genotoxins.
31 onstrate that an intratumor-bacteria-derived genotoxin accelerates tumor metastasis, potentially open
32             Some phenotypes induced by these genotoxins (actin cytoskeleton remodeling, stress fibers
33                     Rad9, a key component of genotoxin-activated checkpoint signaling pathways, assoc
34                       Usp is a novel E. coli genotoxin active against mammalian cells.
35  In vivo, exposure of mice to CO followed by genotoxin (Adriamycin) or radiation-induced injury led t
36                                         This genotoxin alkylates deoxyadenosines on opposite strands
37 estricted to ionizing radiation, as chemical genotoxins also induce heritable and transmissible genom
38 tion of nts1 causes increased sensitivity to genotoxins and deregulated expression of Tf2 elements, l
39 t3 level is downregulated in the presence of genotoxins and ectopic expression of HST3 blocks genotox
40 drial DNA (mtDNA) by important environmental genotoxins and endogenous metabolites.
41 196N) mutants exhibit greater sensitivity to genotoxins and higher levels of crossing over during DSB
42 gs implicate susceptibility to environmental genotoxins and inadequate DNA repair as novel mechanisms
43         Cells are under constant attack from genotoxins and rely on a multifaceted DNA damage respons
44      Several studies suggest colibactins are genotoxins and support a role for clb metabolites in col
45 ing mouse Hus1 are hypersensitive to certain genotoxins, and we have explored the molecular basis for
46 ifferent DNA alterations induced by the same genotoxin are mended by separate repair pathways.
47 ty, cell cycle regulation, and resistance to genotoxins are genetically separable.
48 hese findings show that signals generated by genotoxins are transduced by multiple, independent pathw
49  establish that CDTs are likely to be potent genotoxins, as indicated by in vivo degradation of chrom
50  an endogenous one-carbon unit but potential genotoxin, at different rates in living systems.
51 ibitors (HDACi) on cancer cell resistance to genotoxin based therapies.
52  cells treated with the bulky adduct-forming genotoxin benzo[a]pyrene dihydrodiol epoxide (BPDE).
53  exposure to intracellular and environmental genotoxins but also as intermediates of normal DNA metab
54 nt of MEKK1 in the induction of apoptosis by genotoxins but not microtubule altering drugs.
55 ancer stem cells are resistant to killing by genotoxins, but the mechanism for this resistance is poo
56  CdtB into the host cell, where it acts as a genotoxin by creating DNA lesions.
57 s do not show elevated susceptibility to the genotoxins camptothecin or 4-NQO.
58                                              Genotoxins cause DNA damage, which can result in genomic
59               Replication errors and various genotoxins cause DNA double-strand breaks (DSBs) where e
60  exposure to intracellular and environmental genotoxins, causing damage in one or two strands of the
61 e, which we call RING (response induced by a genotoxin), characterized by accumulation of phosphoryla
62                                          The genotoxin cisplatin is commonly used in chemotherapy to
63         We find that cell treatment with the genotoxin cisplatin leads to concurrent relocalization o
64   We further identified the pathogen-derived genotoxin colibactin as a potential source of DNA breaks
65 ng subsequently allows the production of the genotoxin colibactin in close proximity to host epitheli
66                      The human gut bacterial genotoxin colibactin is a possible key driver of colorec
67  pks(+) Escherichia coli, which produces the genotoxin colibactin that induces characteristic mutatio
68  Escherichia coli (ExPEC), which encodes the genotoxin colibactin, are incompletely defined.
69 l pathogenic E. coli (ExPEC) and encodes the genotoxin colibactin, is epidemiologically associated wi
70                                          The genotoxin colibactin, synthesized by Escherichia coli, i
71 entification of an Escherichia coli-produced genotoxin, colibactin, and its specific targeted killing
72 urthermore, these studies suggest the active genotoxins (colibactins) are unsaturated imines that are
73 detoxification of this ubiquitous endogenous genotoxin creates a benign 1C unit that can sustain esse
74                                The bacterial genotoxins cytolethal distending toxin (CDT) and colibac
75                                The bacterial genotoxin, cytolethal distending toxin (CDT), causes DNA
76 p fusion were used as sensing components for genotoxin detection.
77                    The identification of the genotoxin determinant clb coding for colibactin exhibite
78 he hepatocellular carcinoma model induced by genotoxin diethylnitrosamine.
79                                          The genotoxin doxorubicin increased AdEV protein and FABP4 s
80                                 We show that genotoxin-enhanced Rad1 sumoylation occurs after the nuc
81 broblasts exposed to increasing doses of the genotoxin etoposide and identified SRC as a key kinase c
82                              A wide range of genotoxins exists, including radiations and chemicals fo
83 te, BRCA1meth cancers are highly adaptive to genotoxin exposure and, through reversal of promoter met
84                                              Genotoxin exposure causes pol III but not Paf1 loss from
85 ighly conserved signaling pathway induced by genotoxin exposure or endogenous genome stress.
86 actions affecting mitochondrial health after genotoxin exposure.
87              Vitamin C-mediated formation of genotoxins from lipid hydroperoxides in the absence of t
88 site, which is phosphorylated in response to genotoxins, had no effect on survival or checkpoint acti
89 ene Hus1 results in chromosomal instability, genotoxin hypersensitivity, and embryonic lethality.
90                        Up to eight different genotoxins (i.e., genotoxic compound zones) have been de
91 man gut produce colibactin, a small-molecule genotoxin implicated in colorectal cancer pathogenesis.
92 SSB intermediates after exposure to specific genotoxins in certain cell lines, likely due to altered
93 nt identification of aldehydes as endogenous genotoxins in Fanconi anemia has provided new insight in
94 for such a response is to ensure aversion to genotoxins in food.
95    In addition, HSPCs developed tolerance to genotoxins in hepatocyte-conditioned medium, suggesting
96 range from sterility to increased killing by genotoxins in humans, mice, and Drosophila.
97 show the feasibility of inhibiting bacterial genotoxins in the gut, establishing a starting point for
98 affect both the activity of nonintercalating genotoxins in vivo and the accessibility of glutathione
99 er after exposure to cisplatin but not other genotoxins including another cross-linking agent, mitomy
100 nformation is protected against a variety of genotoxins including ionizing radiation (IR) through the
101  repair defective backgrounds, exposed to 11 genotoxins, including UV-B and ionizing radiation, alkyl
102 sing transgenic atpollambda-2 mutants toward genotoxins indicated the importance of the BRCT domain o
103                             Chemotherapeutic genotoxins induce apoptosis in epithelial-cell-derived c
104                           This finding links genotoxin induced switching to Hst3 regulation.
105 toxins and ectopic expression of HST3 blocks genotoxin induced switching.
106 ne disruption was caused by sensitization to genotoxin-induced (p53-mediated) apoptosis or by p53-ind
107 the inner ring of HUS1 that were crucial for genotoxin-induced 9-1-1 chromatin localization and ATR s
108 est that ATM is a major signal initiator for genotoxin-induced apoptosis but, paradoxically, also con
109  breast epithelium and carcinomas to undergo genotoxin-induced apoptosis correlates strongly with cel
110 th receptors is a significant contributor to genotoxin-induced apoptosis in human epithelial carcinom
111 iquitination of NEMO significantly increased genotoxin-induced apoptosis, resulting in enhanced sensi
112 expressed in HEK293 cells effectively blocks genotoxin-induced apoptosis.
113 xpression of kinase-inactive MEKK1 inhibited genotoxin-induced apoptosis.
114 translesion synthesis causes the majority of genotoxin-induced base substitutions, but averts larger
115 DNA adducts, a molecular initiating event in genotoxin-induced carcinogenesis.
116                            Here we show that genotoxin-induced Chk1 activation requires Cut5 (Mus101/
117 D1-RAD9 (9-1-1) complex that participates in genotoxin-induced CHK1 activation.
118 ge signaling events and functions to promote genotoxin-induced Chk1 phosphorylation.
119           Likewise, Hus1 was dispensable for genotoxin-induced Chk2 phosphorylation.
120                            Here we show that genotoxin-induced chromatin binding of 9-1-1 does not re
121 These findings suggest that ATM is the major genotoxin-induced CREB kinase in mammalian cells and tha
122 e core component of Pol II and show that its genotoxin-induced degradation is impaired in ddi1.
123  method to measure the prevalence of genomic genotoxin-induced DNA damage.
124 ed RAD51 nuclear foci and were able to limit genotoxin-induced genomic instability, both hallmarks of
125 eration but slightly increased resistance to genotoxin-induced growth arrest.
126         To test this hypothesis, we measured genotoxin-induced mutations and chromosome damage in p27
127 t by examining how Hus1 inactivation affects genotoxin-induced signaling events.
128  selective pathway of autophagy that we term genotoxin-induced targeted autophagy (GTA).
129 ify Noxa and Puma as important regulators of genotoxin-induced telencephalic NPC death.
130 terozygosity confers broad susceptibility to genotoxin-induced tumorigenesis, and this paradigm serve
131 ient mice are particularly susceptibility to genotoxin-induced tumors, suggesting a role for p27 in t
132 uirement for LXCXE binding in suppression of genotoxin-initiated hepatocellular carcinoma in vivo.
133                   The regulation of MEKK1 by genotoxins involves its activation, which may be part of
134  purified CdtB protein demonstrates that the genotoxin is essential for C. jejuni's pro-metastatic pr
135 , premature infant, and found to contain the genotoxin island pks associated with development of colo
136 ubunit REV3L is important in defense against genotoxins, little is known of its biological function.
137 metrial carcinogenesis may proceed through a genotoxin-mediated pathway, although the detection of en
138                      Following activation by genotoxins, MEKK1 was cleaved in a caspase-dependent man
139  markedly exacerbated in the presence of the genotoxin menadione.
140 easing dramatically after treatment with the genotoxin methyl methanesulfonate (MMS).
141 ed constitutively and in the presence of the genotoxin MMS.
142 logous proteins (CdtA, CdtB, and CdtC) and a genotoxin mode of action distinguish the Cdt from others
143 LME6 (lacking p53) cells were exposed to the genotoxin N-methyl-N-nitro-N-nitrosoguanidine (MNNG), bo
144 orphologies, including cytoskeletal poisons, genotoxins, nonspecific electrophiles, and redox-active
145 man gut produce colibactin, a small-molecule genotoxin of unknown structure that has been implicated
146 etabolism, as a consequence of environmental genotoxins or radiation, or during programmed recombinat
147 rnal genotoxic agents (ionizing radiation or genotoxins) or by internal processes (recombination inte
148 cumulation of RPA, ATR, ETAA1, and TOPBP1 at genotoxin-perturbed RFs, decreases CHK1 activation, and
149 compose a subclass of intracellularly acting genotoxins produced by many Gram-negative pathogenic bac
150 Overall, these data show that infection with genotoxin-producing bacteria elicits EMT process activat
151 Overall, these data show that infection with genotoxin-producing bacteria involves the YAP/TAZ-TEAD s
152                                    Bacterial genotoxins provoke DNA damage and carcinogenesis.
153 unstressed cells, the role of hHR23B in post-genotoxin regulation of p53 was investigated.
154  MLH1 proteins in preventing spontaneous and genotoxin-related mutations.
155 ational repair and critically contributes to genotoxin resistance.
156 ppaB activation in H157 cells in response to genotoxin resulted in loss of cell surface expression of
157                     Dimerization mutants are genotoxin sensitive and defective in checkpoint signalin
158                          The slow growth and genotoxin sensitivity of a musN null mutant can be parti
159 found the srs2Delta mutant to have a similar genotoxin sensitivity profile and replicative lifespan t
160 d G1 cells was not associated with increased genotoxin sensitivity, indicating that back-up DSB repai
161 dings elucidate the mechanisms through which genotoxins shape microbial communities and provide a pla
162 ipid hydroperoxides gives rise to endogenous genotoxins such as 4-oxo-2(E)-nonenal, which cause the f
163 ant to cell death caused by NAD(+)-depleting genotoxins such as hydrogen peroxide and methylmethane s
164 moylation has recently been shown to promote genotoxin survival.
165 (MMR) results in lack of sensitivity to this genotoxin (termed alkylation tolerance).
166 amage and discovered a distinctive family of genotoxins-termed the indolimines-produced by the CRC-as
167 benzo(a)pyrene dihydrodiol epoxide (BPDE), a genotoxin that causes bulky DNA adducts, Hus1-null cells
168 ynthesis of colibactin, a polyketide-peptide genotoxin that causes genomic instability in eukaryotic
169 acteria produce colibactin, a small-molecule genotoxin that causes interstrand cross-links in host ce
170  were also hypersensitive to camptothecin, a genotoxin that generates breaks specifically at the repl
171 ctin is a chemically unstable small-molecule genotoxin that is produced by several different bacteria
172 s involved in cellular response to a complex genotoxin that may not directly induce DSBs.
173 cells depleted of SLX4 are hypersensitive to genotoxins that cause DSBs and show defects in the resol
174 1a overexpression also provided tolerance to genotoxins that induce double-strand break.
175 (DDR) protein gammaH2AX induced by selective genotoxins that promote DNA replication stress or SSBs.
176                Reactive aldehydes are potent genotoxins that threaten the integrity of hematopoietic
177 f C53 rendered cells susceptible to multiple genotoxins that usually trigger G(2)/M arrest.
178 conclude that the AhR shuttles PAH o-quinone genotoxins to the nucleus and enhances oxidative DNA dam
179 mic changes in the phosphoprotein profile of genotoxin-treated cells, largely mediated by the ATAXIA
180 in a checkpoint kinase 1-dependent manner in genotoxin-treated cells.
181                                        Thus, genotoxin treatment in combination with TRAIL is an effe
182 Activation of the DNA damage checkpoint upon genotoxin treatment induces a multitude of cellular chan
183 damage tolerance throughout the genome under genotoxin treatment, its function during unperturbed gro
184                              After prolonged genotoxin treatment, the checkpoint can be downregulated
185  not inappropriately enter mitosis following genotoxin treatment.
186 ranslational modification, we also show that genotoxin-triggered 9-1-1 chromatin binding does not dep
187  and examined the role of phosphorylation in genotoxin-triggered checkpoint activation.
188                        Following exposure to genotoxins, tumor cells undergo terminal growth arrest a
189 nvironment of DNA affects it as a target for genotoxins, we have used ligation-mediated PCR to map DN
190             Dose-response curves for several genotoxins were obtained.
191 53-mediated cell-cycle arrest in response to genotoxins while loss of HSF1 attenuates apoptosis in re
192 Colibactin is an assumed human gut bacterial genotoxin, whose biosynthesis is linked to the clb genom
193 erforming cell-based functional sensing of a genotoxin with high sensitivity and short incubation tim
194  of double-stranded breaks (DSBs) induced by genotoxins with various modes of action.

 
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