ライフサイエンスコーパス: genotoxin

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.

23 Rad9, a key component of genotoxin-activated checkpoint signaling pathways, assoc

24 Usp is a novel E. coli genotoxin active against mammalian cells.

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

29 drial DNA (mtDNA) by important environmental genotoxins and endogenous metabolites.

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

32 Cells are under constant attack from genotoxins and rely on a multifaceted DNA damage respons

33 Several studies suggest colibactins are genotoxins and support a role for clb metabolites in col

34 ing mouse Hus1 are hypersensitive to certain genotoxins, and we have explored the molecular basis for

35 ty, cell cycle regulation, and resistance to genotoxins are genetically separable.

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

38 ibitors (HDACi) on cancer cell resistance to genotoxin based therapies.

39 cells treated with the bulky adduct-forming genotoxin benzo[a]pyrene dihydrodiol epoxide (BPDE).

40 nt of MEKK1 in the induction of apoptosis by genotoxins but not microtubule altering drugs.

41 ancer stem cells are resistant to killing by genotoxins, but the mechanism for this resistance is poo

42 CdtB into the host cell, where it acts as a genotoxin by creating DNA lesions.

43 s do not show elevated susceptibility to the genotoxins camptothecin or 4-NQO.

44 Genotoxins cause DNA damage, which can result in genomic

45 The genotoxin cisplatin is commonly used in chemotherapy to

46 We find that cell treatment with the genotoxin cisplatin leads to concurrent relocalization o

47 Escherichia coli (ExPEC), which encodes the genotoxin colibactin, are incompletely defined.

48 l pathogenic E. coli (ExPEC) and encodes the genotoxin colibactin, is epidemiologically associated wi

49 The genotoxin colibactin, synthesized by Escherichia coli, i

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

52 p fusion were used as sensing components for genotoxin detection.

53 We show that genotoxin-enhanced Rad1 sumoylation occurs after the nuc

54 A wide range of genotoxins exists, including radiations and chemicals fo

55 actions affecting mitochondrial health after genotoxin exposure.

56 Vitamin C-mediated formation of genotoxins from lipid hydroperoxides in the absence of t

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

60 range from sterility to increased killing by genotoxins in humans, mice, and Drosophila.

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

64 Chemotherapeutic genotoxins induce apoptosis in epithelial-cell-derived c

65 This finding links genotoxin induced switching to Hst3 regulation.

66 toxins and ectopic expression of HST3 blocks genotoxin induced switching.

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

73 expressed in HEK293 cells effectively blocks genotoxin-induced apoptosis.

74 xpression of kinase-inactive MEKK1 inhibited genotoxin-induced apoptosis.

75 DNA adducts, a molecular initiating event in genotoxin-induced carcinogenesis.

76 Here we show that genotoxin-induced Chk1 activation requires Cut5 (Mus101/

77 D1-RAD9 (9-1-1) complex that participates in genotoxin-induced CHK1 activation.

78 ge signaling events and functions to promote genotoxin-induced Chk1 phosphorylation.

79 Likewise, Hus1 was dispensable for genotoxin-induced Chk2 phosphorylation.

80 Here we show that genotoxin-induced chromatin binding of 9-1-1 does not re

81 These findings suggest that ATM is the major genotoxin-induced CREB kinase in mammalian cells and tha

82 method to measure the prevalence of genomic genotoxin-induced DNA damage.

83 ed RAD51 nuclear foci and were able to limit genotoxin-induced genomic instability, both hallmarks of

84 eration but slightly increased resistance to genotoxin-induced growth arrest.

85 To test this hypothesis, we measured genotoxin-induced mutations and chromosome damage in p27

86 t by examining how Hus1 inactivation affects genotoxin-induced signaling events.

87 selective pathway of autophagy that we term genotoxin-induced targeted autophagy (GTA).

88 ify Noxa and Puma as important regulators of genotoxin-induced telencephalic NPC death.

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.

92 The regulation of MEKK1 by genotoxins involves its activation, which may be part of

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

95 Following activation by genotoxins, MEKK1 was cleaved in a caspase-dependent man

96 markedly exacerbated in the presence of the genotoxin menadione.

97 easing dramatically after treatment with the genotoxin methyl methanesulfonate (MMS).

98 ed constitutively and in the presence of the genotoxin MMS.

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

104 Bacterial genotoxins provoke DNA damage and carcinogenesis.

105 unstressed cells, the role of hHR23B in post-genotoxin regulation of p53 was investigated.

106 MLH1 proteins in preventing spontaneous and genotoxin-related mutations.

107 ppaB activation in H157 cells in response to genotoxin resulted in loss of cell surface expression of

108 Dimerization mutants are genotoxin sensitive and defective in checkpoint signalin

109 The slow growth and genotoxin sensitivity of a musN null mutant can be parti

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

113 (MMR) results in lack of sensitivity to this genotoxin (termed alkylation tolerance).

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

117 s involved in cellular response to a complex genotoxin that may not directly induce DSBs.

118 cells depleted of SLX4 are hypersensitive to genotoxins that cause DSBs and show defects in the resol

119 1a overexpression also provided tolerance to genotoxins that induce double-strand break.

120 (DDR) protein gammaH2AX induced by selective genotoxins that promote DNA replication stress or SSBs.

121 f C53 rendered cells susceptible to multiple genotoxins that usually trigger G(2)/M arrest.

122 conclude that the AhR shuttles PAH o-quinone genotoxins to the nucleus and enhances oxidative DNA dam

123 in a checkpoint kinase 1-dependent manner in genotoxin-treated cells.

124 Thus, genotoxin treatment in combination with TRAIL is an effe

125 damage tolerance throughout the genome under genotoxin treatment, its function during unperturbed gro

126 not inappropriately enter mitosis following genotoxin treatment.

127 ranslational modification, we also show that genotoxin-triggered 9-1-1 chromatin binding does not dep

128 and examined the role of phosphorylation in genotoxin-triggered checkpoint activation.

129 Following exposure to genotoxins, tumor cells undergo terminal growth arrest a

130 nvironment of DNA affects it as a target for genotoxins, we have used ligation-mediated PCR to map DN

131 Dose-response curves for several genotoxins were obtained.

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