ライフサイエンスコーパス: genotoxic

1 fied from soil extracts was determined to be genotoxic.

2 s, when inappropriate cyclin E expression is genotoxic.

3 oses, whereas of 12 compounds not considered genotoxic, 11 (92%) are negative.

4 documents the replacement of the potentially genotoxic 3-nitro group by 3-chloro and 3-fluoro substit

5 irectly or after metabolic activation; 2) be genotoxic; 3) alter DNA repair or cause genomic instabil

6 antagonistic endocrine activities, mutagenic/genotoxic activities, cytotoxic activities, further acti

7 olerance potentially through its RAG-coupled genotoxic activity in self-reactive immature B cells.

8 irradiated animals, covering three types of genotoxic activity.

9 -deficient mutants are hypersensitive to the genotoxic agent methyl methanesulfonate (MMS), but the m

10 FOXM1 in breast cancer and has a key role in genotoxic agent resistance.

11 both OTUB1 and FOXM1 expression reduced upon genotoxic agent treatment in MCF-7 cells, but remained r

12 hromatin relaxation and further activated by genotoxic agent-induced DSBs.

13 hanism of rescue following the withdrawal of genotoxic agent.

14 MMR-deficient cancer cells are resistant to genotoxic agents and have microsatellite instability (MS

15 ms by which FOXM1 expression is regulated by genotoxic agents and how they are deregulated in resista

16 l and occupational monitoring of exposure to genotoxic agents and their complex mixtures.

17 poT-deficient cells are sensitive to diverse genotoxic agents and ultraviolet radiation, whereas ppGp

18 levated ILF2 expression exerts resistance to genotoxic agents by modulating YB-1 nuclear localization

19 We previously reported that genotoxic agents induce nuclear localization of NF-kappa

20 ours towards therapeutic treatments based on genotoxic agents or PARP inhibitors following a syntheti

21 In contrast to genotoxic agents that induce damage in a cell cycle stag

22 Genotoxic agents trigger a 'nuclear-to-cytoplasmic' NF-k

23 he potential to enhance the effectiveness of genotoxic agents used in AML therapy.

24 more sensitive both in vitro and in vivo to genotoxic agents used in clinical therapy: daunorubicin

25 Our results show that genotoxic agents used in the therapy of MM (i.e., doxoru

26 ntext of therapeutic strategies that combine genotoxic agents with immune checkpoint blockade.

27 ased chromosomal breaks, hypersensitivity to genotoxic agents, and chromosomal instability.

28 exhibit decreased viability, sensitivity to genotoxic agents, and decreased stability of the Mcd1 co

29 man exposure to endogenous and environmental genotoxic agents, and for DNA repair studies were also d

30 ion of KAP1 and p53) in response to multiple genotoxic agents, including camptothecin, H2O2, and nitr

31 n products have been implicated as causative genotoxic agents, no specific product has been identifie

32 Macrophages produce genotoxic agents, such as reactive oxygen and nitrogen s

33 e counterparts in response to treatment with genotoxic agents, suggesting that FAN1 mutations cause c

34 a critical function in cellular response to genotoxic agents, we aimed to analyze the role of Chk1 i

35 9M allele that sensitizes tel1Delta cells to genotoxic agents.

36 adenovirus or herpesvirus) or treatment with genotoxic agents.

37 tensive study of proliferation dynamics of a genotoxic and a non-genotoxic compound.

38 Aflatoxins are the most potent genotoxic and carcinogenic mycotoxins.

39 first insight into how we might measure the genotoxic and cytotoxic effect of plasma jet treatments

40 mparatively little research on the potential genotoxic and cytotoxic effects of plasma jet treatment.

41 n response, and accordingly are resistant to genotoxic and ER stress.

42 In genotoxic and genetic models, HCCs arose exclusively fro

43 ences in proliferative responses between non-genotoxic and genotoxic carcinogens during the initial s

44 As non-genotoxic and genotoxic carcinogens have different cance

45 ivation of p53 and increased apoptosis under genotoxic and hematopoietic stress.

46 Low-dose BPA exerted c-Myc-dependent genotoxic and mitogenic effects on ERalpha-negative mamm

47 Lucidin is a genotoxic and mutagenic hydroxyanthraquinone metabolite,

48 cept not only enabled a simple prediction of genotoxic and non-genotoxic carcinogens, but also had th

49 deacylation; the latter are postulated to be genotoxic and to contribute to colorectal cancer formati

50 indicates that GEBR-32a is not cytotoxic and genotoxic, and does not seem to possess emetic-like side

51 Induction of the SOS response by the genotoxic antibiotic ciprofloxacin changes the E. coli r

52 In this study, we focused on a genotoxic aspect of exposure of esophageal cells to acid

53 Euterpe oleracea) provide prebiotic and anti-genotoxic benefits in the colon.

54 organic extract were found to act mutagenic/genotoxic, but the amplitudes of the effects differed co

55 Individually, these compounds are genotoxic, but the consequences of exposure to mixtures

56 The variety of non-genotoxic cancer pathways complicates the search for rel

57 Genotoxic cancer therapies, such as chemoradiation, caus

58 Inflammatory gene expression following genotoxic cancer therapy is well documented, yet the eve

59 ferative responses between non-genotoxic and genotoxic carcinogens during the initial stages of the r

60 As non-genotoxic and genotoxic carcinogens have different cancer risks, the o

61 led a simple prediction of genotoxic and non-genotoxic carcinogens, but also had the power to discrim

62 rcinoma samples and liver samples exposed to genotoxic carcinogens.

63 cinogenicity assays is the prediction of non-genotoxic carcinogens.

64 Most organisms are exposed to the genotoxic chemical formaldehyde, either from endogenous

65 Mixtures of these genotoxic chemicals produced mutation responses that dif

66 Because rLOX-PP can enhance effects of a genotoxic chemotherapeutic on breast cancer cell apoptos

67 cell lines induced synthetic lethality with genotoxic chemotherapeutics, including PARP inhibitors,

68 found that in response to UV irradiation or genotoxic chemotherapeutics, SOX9 is actively degraded i

69 ATM, are associated with resistance against genotoxic chemotherapy (del17p) and poor outcome (del11q

70 immunity through TLR signaling in modulating genotoxic chemotherapy-induced small intestinal injury i

71 r mechanism promoting acquired resistance to genotoxic chemotherapy.

72 nce suggests precolibactins are converted to genotoxic colibactins by colibactin peptidase (ClbP)-med

73 liferation dynamics of a genotoxic and a non-genotoxic compound.

74 meat is likely to result in the formation of genotoxic compounds during digestion and should, therefo

75 This non-genotoxic conditioning method may provide an attractive

76 rmediate-sized repeats both under normal and genotoxic conditions.

77 Both, ATR- and CHK1 inhibitors induce genotoxic damage and apoptosis in human and murine SCLC

78 ematopoietic cells from TOP2 poison-mediated genotoxic damage and, therefore, reduce the rate of ther

79 ng budding yeast, we demonstrate that global genotoxic damage or even a single unrepaired double-stra

80 ng them to undergo cell death in response to genotoxic damage.

81 on of the lead compounds showed that in vivo genotoxic degradants might be generated.

82 ar proteins producing proteotoxic stress and genotoxic DNA-histone crosslinks.

83 Premenopausal women undergoing commonly used genotoxic (DNA-damaging) chemotherapy experience an acce

84 Treatment of preexisting CSCs with a genotoxic drug combination (5-fluorouracil, doxorubicin,

85 eregulated overexpression is associated with genotoxic drug resistance in breast cancer.

86 atment of tumours with ionizing radiation or genotoxic drugs drives p21-activated kinase 1 (PAK1)-med

87 he use of G9a inhibitors in combination with genotoxic drugs to treat p53-positive tumors.

88 rapy regimens commonly include radiation and genotoxic drugs, tumour cells typically develop resistan

89 cusing on a matrix of DNA repair mutants and genotoxic drugs, we quantify 76 gene-drug interactions b

90 itizes tumour cells to ionizing radiation or genotoxic drugs.

91 d milk did not cause any changes in cyto- or genotoxic effects and antigenotoxic capability of protec

92 a vital step in determining their potential genotoxic effects and developing safer vectors for thera

93 lopropane has been shown to be essential for genotoxic effects in vitro, this ClbS-catalyzed ring-ope

94 tal exposure, only few animal studies on the genotoxic effects of chronic LDR radiation have been per

95 also protects Ras-transformed cells from the genotoxic effects of doxorubicin in culture and immune-d

96 ed a meat based diet to compare the possible genotoxic effects of red vs. white meat, and the interfe

97 o the response mechanism for coping with the genotoxic effects of zebularine and identify several com

98 Genotoxic effects were seen after continuous radiation (

99 mation of reactive metabolites that may have genotoxic effects.

100 d PDE4C2 enzymes, without both cytotoxic and genotoxic effects.

101 Ethanol blending appears to reduce genotoxic emissions on this specific flex-fuel GDI vehic

102 aralysis of meiotic chromosome mobility in a genotoxic environment is not a universal response among

103 genes encoding drug targets across multiple genotoxic environments.

104 isted, and TERT-positive ALT cells surviving genotoxic events propagated through subsequent generatio

105 These genotoxic events were accompanied by changes in plasma c

106 sequestration of free iron necessary for the genotoxic Fenton reaction.

107 hemicals at low concentrations that were not genotoxic for the individual chemicals, as well as the n

108 al biosensor recApr-Luc2 was built to detect genotoxic hazard in recycled ash.

109 red functional RecA expression to respond to genotoxic heavy metals (Cr>Cd approximately Pb), and pol

110 sed to oxidative stress, and are most likely genotoxic if not removed by cellular defense mechanisms.

111 The quantification of genotoxic impurities (GIs) such as hydrazine (HZ) is of

112 d important consequences for bioanalysis and genotoxic impurity quantification.

113 nstrates that chronic LDR gamma radiation is genotoxic in an exposure scenario realistic for humans,

114 Out of 25 compounds that are known to be genotoxic in vitro and in vivo, 21 (84%) are detected as

115 stress of transplantation, inflammation, and genotoxic injury, and associated with distinctive transc

116 anced ectopic progenitor proliferation after genotoxic injury, thereby preventing both IR- and cyclop

117 d by bone marrow-derived progenitors after a genotoxic insult, these cells are replenished by an extr

118 nt kinase 1 (Chk1) by this pathway after the genotoxic insult.

119 involved in regulating cellular responses to genotoxic insult.

120 es DNA repair to facilitate survival against genotoxic insults and found that FASN suppresses NF-kapp

121 that CMA is also upregulated in response to genotoxic insults and that declined CMA functionality le

122 abilization conferred cellular resistance to genotoxic insults and was required for the recruitment o

123 hat FASN regulates cellular response against genotoxic insults by up-regulating PARP-1 and DNA repair

124 ositive ALT cells showed higher tolerance to genotoxic insults compared with their TERT-negative coun

125 itions, such as growth factor deprivation or genotoxic insults or hormone deprivation.

126 ession has been found to cause resistance to genotoxic insults.

127 for the maintenance of genomic stability on genotoxic insults.

128 chanism of fork stabilization in response to genotoxic insults.

129 The genome is constantly attacked by genotoxic insults.

130 Arthur and colleagues identified a genotoxic island in Escherichia coli NC101 that appeared

131 mutated strain of E. coli NC101 lacking the genotoxic island, and showed that those mice suffered fr

132 y of ATM and p53 through the accumulation of genotoxic levels of DNA damage.

133 The genotoxic metabolites, 2-hydroxyamino-9H-pyrido[2,3-b]in

134 duces the secondary metabolite colibactin, a genotoxic molecule(s) causing double-stranded DNA breaks

135 sed meat has been linked to the formation of genotoxic N-nitroso compounds (NOCs) and lipid peroxidat

136 While N-chloroacetamide was not found to be genotoxic, N,2-dichloroacetamide genotoxic potency (5.19

137 roach to the bacterial colibactin pathway, a genotoxic NRPS-PKS hybrid pathway found in certain Esche

138 sociated with breast cancer all demonstrated genotoxic or endocrine activity, but not necessarily bot

139 mitant defects in p53 accumulation following genotoxic or ribosomal stress.

140 r, the disruption of topoisomerases leads to genotoxic outcomes.

141 Treatment of mammalian cells with genotoxic oxidants that generate dL in DNA led to the fo

142 trating that CerS6 is a component of the non-genotoxic p53-dependent cellular stress response.

143 found to be genotoxic, N,2-dichloroacetamide genotoxic potency (5.19 x 10(-3) M) was on the same orde

144 study elucidates a mechanism behind the low genotoxic potential of foamy virus, identifies a unique

145 That observation underscores the genotoxic potential of oxidative Polbeta-DPC and the bio

146 rs are required.IMPORTANCE Understanding the genotoxic potential of viral vectors is important in des

147 ts described suggest that DP poses a greater genotoxic potential than BDE-209.

148 s retained significant anti-oxidant and anti-genotoxic potential through digestion and fermentation.

149 yl- and nitro-PAH emissions and assess their genotoxic potential.

150 96% with E10 and by 82-96% with E85, and the genotoxic potentials dropped by 72 and 83%, respectively

151 ecolibactins, leads to the production of non-genotoxic pyridone-based isolates derived from the diver

152 regulation suppresses aberrant, potentially genotoxic recombination activities, and the mobilization

153 All major genotoxic responses to FA, including replication inhibit

154 cApr-Luc2 could be useful for evaluating the genotoxic risk of pollutants present in ash that might b

155 ctive intermediates are converted to a known genotoxic scaffold, providing metabolic support of our m

156 , replication defects due to Rtt107 loss and genotoxic sensitivities in mutants of Rtt107 and its ass

157 Genotoxic small molecules from this pathway that are cap

158 se and can be oxidatively transformed to the genotoxic spiroiminodihydantoin (Sp) and 5-guanidinohyda

159 ust to external stresses, and in the case of genotoxic stress (i.e. DNA damage), the circadian clock

160 bly arrested proliferation, often induced by genotoxic stress [1].

161 triggered by a combination of metabolic and genotoxic stress acts as an intrinsic barrier to EBV-med

162 5-fluorouracil, which induces metabolic and genotoxic stress and activates p53, further implicated C

163 s in adult tissues are constantly exposed to genotoxic stress and also accumulate DNA damage with age

164 Wss1 is vacuolar, suggesting a link between genotoxic stress and autophagy involving the Doa1 adapte

165 PSGs enhance resistance to genotoxic stress and confer fitness during aging.

166 Yeast cells activate RNR in response to genotoxic stress and iron deficiency by facilitating red

167 enomenon that occurs in cells in response to genotoxic stress and is also a hallmark of several cance

168 noubiquitylation of Nup60 is stimulated upon genotoxic stress and regulates the DNA-damage response a

169 Antioxidants attenuate genotoxic stress and rescue cell proliferation, implying

170 re characterized by increased sensitivity to genotoxic stress associated with sustained induction of

171 Genotoxic stress can promote antitumor NK cell responses

172 eport that ZNF281 expression increased after genotoxic stress caused by DNA-damaging drugs.

173 of programmed cell death under salinity and genotoxic stress conditions.

174 vation via PDCD5-dependent HDAC3 decay under genotoxic stress conditions.

175 suggest that regulation of p53 responses to genotoxic stress contributes to the tumour suppressor fu

176 We investigated whether genotoxic stress could promote the release of NK group 2

177 Genotoxic stress drives damaged DNA out of the nucleus b

178 -expressing cells, and arises in response to genotoxic stress due to the production of reactive oxyge

179 s or in a repair-competent background due to genotoxic stress from celluar processes such as transcri

180 Upon genotoxic stress in G2, high levels of H2A.X lead to per

181 rks as a pivotal RAD51-regulated response to genotoxic stress in human cells and as a promising targe

182 s to silence repetitive elements and prevent genotoxic stress in the germ line.

183 Exogenous overexpression of SOX9 after genotoxic stress increases cell survival.

184 Thus, genotoxic stress increases the Cry1/Cry2 ratio, suggesti

185 breaks in developing lymphocytes exposed to genotoxic stress increases the risk for aberrant recombi

186 Genotoxic stress induces alternative splicing of the onc

187 Genotoxic stress induces p57Kip2 expression via the bone

188 EMO is disengaged from IKK complex following genotoxic stress induction.

189 sistent PARP-1 hyperactivation during severe genotoxic stress is associated with cell death.

190 Indeed, the transcriptional response to genotoxic stress is enhanced in Cry1-/- and blunted in C

191 esulfonate (MMS), but the molecular basis of genotoxic stress is unclear.

192 In this study, we assessed the effect of genotoxic stress on RAG1/2 expression in pre-B cells and

193 In response to genotoxic stress p53 activates DNA repair, cell cycle ar

194 Genotoxic stress reduces this ubiquitination in cytosol

195 Sumoylation during genotoxic stress regulates the composition of DNA repair

196 However, whether ATR affects the genotoxic stress response in non-replicating, non-cyclin

197 energy, in addition to cell development and genotoxic stress response.

198 their functions in time and space during the genotoxic stress response.

199 innate immunity, lymphocyte development and genotoxic stress response.

200 , immunophenotyping studies, and analysis of genotoxic stress responses.

201 We demonstrate that genotoxic stress stimulates Cry1 phosphorylation and its

202 , CTCF-deficient cells are hypersensitive to genotoxic stress such as ionizing radiation (IR).

203 genes determine antimicrobial resistance and genotoxic stress survival.

204 constantly threatened by multiple sources of genotoxic stress that cause DNA damage.

205 In response to genotoxic stress the TP53 tumour suppressor activates ta

206 Cmr1/WDR76 plays a role in the recovery from genotoxic stress through regulation of the turnover of s

207 vement of ZNF281 in the cellular response to genotoxic stress through the control exercised on the ex

208 efective TERT variants that bestowed similar genotoxic stress tolerance, indicating that telomere syn

209 Late origin firing occurs under genotoxic stress when the controls on Mcm4, Sld3, and Db

210 ectly sense DNA damage and act as signal for genotoxic stress without loss of cell integrity.

211 l-extrinsic (chemical- or metabolism-induced genotoxic stress) challenges.

212 zes, the evolution of extreme sensitivity to genotoxic stress, and a hyperactive TP53 signaling pathw

213 Therefore, in response to genotoxic stress, bacterial cells give priority to TLS,

214 and break (DSB) is the most critical type of genotoxic stress, but the involvement of DSB repair in P

215 In response to genotoxic stress, cells employ diverse adaptive mechanis

216 Under genotoxic stress, cells showed increased expression of b

217 Following genotoxic stress, disruption of PRMT5-mediated KLF4 meth

218 Upon genotoxic stress, dynamic relocalization events control

219 Following genotoxic stress, FBXO31 is phosphorylated by the DNA da

220 w that KRAS-mutant cancer displays intrinsic genotoxic stress, leading to tonic Chk1- and MK2 activit

221 In response to genotoxic stress, p53 levels increase and induce cell-cy

222 In response to genotoxic stress, phosphorylation of the ATM/CK cluster

223 l a function for TAF1 in plant resistance to genotoxic stress, providing further insight into the mol

224 traviolet radiation, or to asbestos, survive genotoxic stress, resulting in a higher rate of cellular

225 onversely, SIRT1 activity is inhibited under genotoxic stress, resulting in increased TopBP1 acetylat

226 nt cells (SCs) accumulate with age and after genotoxic stress, such as total-body irradiation (TBI).

227 nse normally used by the host cell to combat genotoxic stress, to aid its own replication.

228 and organelle quality control, prevention of genotoxic stress, tumor suppression, pathogen eliminatio

229 ng germination, indicative of high levels of genotoxic stress, which is induced following maturation

230 In the absence of genotoxic stress, wild-type and mutant MEFs showed simil

231 Upon genotoxic stress, Wss1 is vacuolar, suggesting a link be

232 Sam68 sensitizes human colon cancer cells to genotoxic stress-induced apoptosis and genetic deletion

233 arrested myeloid differentiation, inhibited genotoxic stress-induced apoptosis, and facilitated accu

234 x1-FBXO31) ubiquitin ligase complex mediates genotoxic stress-induced cyclin D1 degradation.

235 in cells lacking LKB1 protects them against genotoxic stress-induced DNA damage and prevents the acc

236 NEMO and whose reduced expression prevented genotoxic stress-induced NEMO nuclear translocation, IKK

237 Here we show that Sam68 is critical for genotoxic stress-induced NF-kappaB activation in the gam

238 the critical role of Sam68 in orchestrating genotoxic stress-initiated NF-kappaB activation signalin

239 data reveal a novel function of Sam68 in the genotoxic stress-initiated nuclear signaling, which is c

240 m68/KHDRBS1) is a key NF-kappaB regulator in genotoxic stress-initiated signaling pathway.

241 3 stabilization and activity following acute genotoxic stress.

242 from radiotherapy- and chemotherapy-induced genotoxic stress.

243 acilitating its stabilization in response to genotoxic stress.

244 e deficiencies, and increased sensitivity to genotoxic stress.

245 which has a direct impact on the response to genotoxic stress.

246 hylation landscape in the absence of applied genotoxic stress.

247 ded and p53 levels do not increase following genotoxic stress.

248 hat influences hp53's downstream response to genotoxic stress.

249 t signals to decide cell fate in response to genotoxic stress.

250 ic features, and increased susceptibility to genotoxic stress.

251 Per2 modulates hp53 signaling in response to genotoxic stress.

252 Here, we show that LKB1 protects cells from genotoxic stress.

253 fork processing and restart after prolonged genotoxic stress.

254 suggest that PRC2 modulates the response to genotoxic stress.

255 Filia expression is induced by genotoxic stress.

256 attern during development and in response to genotoxic stress.

257 lated and sumoylated proteins in response to genotoxic stress.

258 ction in orchestrating cellular responses to genotoxic stress.

259 uired for nuclear oxidation induced by acute genotoxic stress.

260 required for cell growth and survival during genotoxic stress.

261 CA1 rescues LKB1 loss-induced sensitivity to genotoxic stress.

262 ell cycle, peaking in late S phase and under genotoxic stress.

263 hway in cycling CLL cells in the presence of genotoxic stress.

264 in the Escherichia coli genome during acute genotoxic stress.

265 its role in the deacetylation of APE1 after genotoxic stress.

266 ll cycle arrest and apoptosis in response to genotoxic stress.

267 le minute 2 (MDM2) is induced in response to genotoxic stress.

268 ulators of DNA replication in the absence of genotoxic stress.

269 p53-binding kinetics are modulated following genotoxic stress.

270 ished functions in sensing and responding to genotoxic stress.

271 is but also with increased susceptibility to genotoxic stress.

272 sponse to metformin, hypoxia-like (CoCl2) or genotoxic stress.

273 on with the DROSHA-processing complex during genotoxic stress.

274 form for caspase-2 activation in response to genotoxic stress.

275 limiting H2A.X synthesis and cell death upon genotoxic stress.

276 Oxidative and genotoxic stresses caused by ionizing radiation are detr

277 st decrease in apoptosis in response to most genotoxic stresses compared with wild-type p53 but exhib

278 Genotoxic stresses lead to centrosome amplification, a f

279 ion of IkappaB kinase (IKK) and NF-kappaB by genotoxic stresses modulates apoptotic responses and pro

280 cesses including resistance to oxidative and genotoxic stresses, protection against aging-related pat

281 A damage detection and repair in response to genotoxic stresses, the field has expanded to include th

282 key intracellular molecule participating in genotoxic stresses-induced NF-kappaB activation.

283 durance of naked mole rat tissues to various genotoxic stresses.

284 synthesis pathway and monitor environmental genotoxic substances, which can ultimately provide insig

285 h chloramination that are more cytotoxic and genotoxic than regulated DBPs.

286 comparable to chloramination, 3.9 times more genotoxic than the nondisinfected controls.

287 zonated wastewater was at least 3 times less genotoxic than the samples treated with chlorine-based d

288 ted species are typically more cytotoxic and genotoxic than their chlorinated analogs.

289 emely high CIN are less tolerant to specific genotoxic therapies.

290 (CSC) drive tumorigenesis and contribute to genotoxic therapy resistance, diffuse infiltrative invas

291 gulation across cancer types correlates with genotoxic therapy resistance.

292 to normal versus mutated cells and were only genotoxic to normal cells.

293 How genotoxic TOP2 DNA-protein cross-links are resolved is u

294 an cells in response to a panel of sublethal genotoxic treatments, using other topoisomerase poisons,

295 produced by human primary fibroblasts after genotoxic treatments.

296 examined for combined effects in response to genotoxic treatments.

297 coupling and reversal as global responses to genotoxic treatments.

298 Treatment of cells with the non-genotoxic UPR agonist thapsigargin led to a rapid inhibi

299 nd foamy virus vectors to be remarkably less genotoxic, well below what was expected from their integ

300 HANs, previously demonstrated to be genotoxic, were investigated for their effects on the ma