ライフサイエンスコーパス: genotoxic stress

1 from radiotherapy- and chemotherapy-induced genotoxic stress.

2 acilitating its stabilization in response to genotoxic stress.

3 e deficiencies, and increased sensitivity to genotoxic stress.

4 sensitive to DNA double-strand break-induced genotoxic stress.

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

6 hylation landscape in the absence of applied genotoxic stress.

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

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

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

10 Per2 modulates hp53 signaling in response to genotoxic stress.

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

12 fork processing and restart after prolonged genotoxic stress.

13 suggest that PRC2 modulates the response to genotoxic stress.

14 Filia expression is induced by genotoxic stress.

15 attern during development and in response to genotoxic stress.

16 lated and sumoylated proteins in response to genotoxic stress.

17 ction in orchestrating cellular responses to genotoxic stress.

18 uired for nuclear oxidation induced by acute genotoxic stress.

19 required for cell growth and survival during genotoxic stress.

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

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

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

23 in the Escherichia coli genome during acute genotoxic stress.

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

25 an increase in the cell's susceptibility to genotoxic stress.

26 ier lncRNA, which regulates cell response to genotoxic stress.

27 sors, IFNRs, Ag-specific TCR activation, and genotoxic stress.

28 nction through modulation of the response to genotoxic stress.

29 repress the apoptotic cell death response to genotoxic stress.

30 double strand DNA break-repair pathway after genotoxic stress.

31 ells, rely on the alt-NHEJ repair pathway on genotoxic stress.

32 capacities to survive the damage induced by genotoxic stress.

33 n of MDM2, p21, and proapoptotic genes after genotoxic stress.

34 n this surface result in hypersensitivity to genotoxic stress.

35 ial for growth and important for coping with genotoxic stress.

36 3-dependent apoptotic pathway in response to genotoxic stress.

37 A damage response and cellular recovery from genotoxic stress.

38 ne-selective functions of p53 in response to genotoxic stress.

39 ent sensitivity of growing hair follicles to genotoxic stress.

40 thus may facilitate tumor development under genotoxic stress.

41 -regulators, in turn mediating resistance to genotoxic stress.

42 0, which interacts with NEMO via MCPIP1 upon genotoxic stress.

43 dependent RNR regulation under conditions of genotoxic stress.

44 d induction of apoptosis in response to this genotoxic stress.

45 nificant variations in cellular responses to genotoxic stress.

46 and be required for optimal p53 response to genotoxic stress.

47 n important role in the cellular response to genotoxic stress.

48 BAP1 loss sensitizes RCC cells in vitro to genotoxic stress.

49 s lose the ability to induce apoptosis after genotoxic stress.

50 naling cell survival or death in response to genotoxic stress.

51 and recruitment to the miR-21 promoter upon genotoxic stress.

52 dergo dramatic genome changes in response to genotoxic stress.

53 ->TNFalpha that was activated in response to genotoxic stress.

54 attenuating apoptosis following exposure to genotoxic stress.

55 ensures efficient DNA repair in response to genotoxic stress.

56 quitin signaling in the cellular response to genotoxic stress.

57 ssing p53-dependent apoptosis in response to genotoxic stress.

58 Rad53 is phosphorylated and activated upon genotoxic stress.

59 anism for protecting the nervous system from genotoxic stress.

60 Mule-deficient B cells and MEFs subjected to genotoxic stress.

61 lex in budding yeast cells in the absence of genotoxic stress.

62 ntain homeostasis of survival pathways under genotoxic stress.

63 re it alters membrane permeability following genotoxic stress.

64 in the root meristem, even in the absence of genotoxic stress.

65 d degradation, is necessary for responses to genotoxic stress.

66 l organisms might be a significant source of genotoxic stress.

67 responses are crucial for plant growth under genotoxic stress.

68 d histone modification in plant growth under genotoxic stress.

69 leolytic degradation only in the presence of genotoxic stress.

70 r non-corrected cells, even without imposing genotoxic stress.

71 cetylation of a key elongation factor during genotoxic stress.

72 2AX phosphorylation for plant survival under genotoxic stress.

73 while sosA inactivation sensitizes cells to genotoxic stress.

74 taining cellular homeostasis and response to genotoxic stress.

75 , with the gene induced by multiple types of genotoxic stress.

76 tial new regulator of RNAPII turnover during genotoxic stress.

77 ia have evolved a network of genes to combat genotoxic stress.

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

79 ic features, and increased susceptibility to genotoxic stress.

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

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

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

83 p53-binding kinetics are modulated following genotoxic stress.

84 ished functions in sensing and responding to genotoxic stress.

85 is but also with increased susceptibility to genotoxic stress.

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

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

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

89 3 stabilization and activity following acute genotoxic stress.

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

91 sites, thus enhancing cellular resistance to genotoxic stresses.

92 vealing a variant that improves growth under genotoxic stresses.

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

94 and found that depleting cells of HP1 caused genotoxic stress, a delay in the repair of DSBs and elev

95 In response to genotoxic stress, a transient arrest in cell-cycle progr

96 nt control and repair signals in response to genotoxic stress, acting as an efficient control mechani

97 Notably, genotoxic stress activated ATM and VDR through phosphory

98 ULIN Tyr56 phosphorylation, which depends on genotoxic stress-activated ABL1/c-Abl.

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

100 to sublethal low-dose ionizing radiation, a genotoxic stress affecting the soma and the germ line, a

101 5-fluorouracil, which induces metabolic and genotoxic stress and activates p53, further implicated C

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

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

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

105 deficiency leads to increased sensitivity to genotoxic stress and delayed DNA double-strand break (DS

106 A damage in placental cells, suggesting that genotoxic stress and ensuing placental senescence and cy

107 orrespondingly, 1,25-VD protected cells from genotoxic stress and growth inhibition by promoting doub

108 y can allow premalignant cells to escape the genotoxic stress and inflammation that promote tumorigen

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

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

111 pressor p53 becomes activated in response to genotoxic stress and is essential for arresting the cell

112 ulates cellular responses to growth factors, genotoxic stress and neoplastic transformation.

113 Doxorubicin produces genotoxic stress and p53 activation in both carcinoma an

114 tosolic double-stranded (ds)DNA arising from genotoxic stress and pathogen invasion.

115 tress responses are also activated following genotoxic stress and play a crucial role in the outcome

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

117 essor p53 block cell cycle progression after genotoxic stress and represent an intrinsic barrier prev

118 Antioxidants attenuate genotoxic stress and rescue cell proliferation, implying

119 s to heightened apoptotic priming, intrinsic genotoxic stress and susceptibility to DNA damage checkp

120 ageal squamous cells against DNA damage from genotoxic stress and that GSTT2 expression can be induce

121 in transcriptional silencing and response to genotoxic stress and the ability of Rtt106 to bind (H3-H

122 isms important for cancer cell adaptation to genotoxic stress and thereby to achieve cancer cell-spec

123 FANCM that is phosphorylated in response to genotoxic stress and this effect is ATR-dependent.

124 emporal restriction of Yen1 protects against genotoxic stress and, by avoiding competition with the n

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

126 organization, leading to cell cycle arrest, genotoxic stress, and innate immunity.

127 Cells lacking IP6K1 arrest after genotoxic stress, and markers associated with DNA repair

128 In response to catastrophic genotoxic stress, apoptosis prevents the persistence and

129 ays prominent roles in cellular responses to genotoxic stress as well as in the regulation of the act

130 ession of gammaH2A.X and of genes related to genotoxic stress, as well as STAT3 phosphorylation, was

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

132 Genotoxic stress attenuates PKCepsilon effect on ATF2; e

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

134 Under genotoxic stress, BMKO B cells were resistant to apoptos

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

136 cGAS induces potent interferon responses to genotoxic stress, but weaker responses to viral infectio

137 -397, Tyr-576, and Tyr-861 was detected upon genotoxic stress by camptothecin in ADAM15-transfected T

138 Exposure to genotoxic stress by environmental agents or treatments,

139 the nucleoporin Nup98 supports adaptation to genotoxic stress by protecting specific p53-induced mRNA

140 cells from apoptosis induced by oxidative or genotoxic stress by stabilizing the mRNA for Bcl-x(L), a

141 or suppressor PML is induced under viral and genotoxic stresses by interferons and JAK-STAT signaling

142 Genotoxic stress can promote antitumor NK cell responses

143 ne in NIH-3T3 cells that fluoresce to report genotoxic stress caused by a wide variety of agents, fro

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

145 Oxidative and genotoxic stresses caused by ionizing radiation are detr

146 nterestingly, we found that arsenite-induced genotoxic stress causes a PLK1-dependent signaling respo

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

148 Under genotoxic stress, cells showed increased expression of b

149 During genotoxic stress, cellular transformation requires that

150 Following genotoxic stress, cGAS can also respond to endogenous DN

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

152 In response to genotoxic stress, CHK1-mediated phosphorylation of RAD51

153 tic genes in mice were resistant to specific genotoxic stress compared to sister cells recovered from

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

155 wed that CaWss1 promotes cell survival under genotoxic stress conditions that generate DPCs and that

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

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

158 occupies the promoter of the E2F7 gene after genotoxic stress, consistent with E2F7 being a novel p53

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

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

161 tified pathways implicated in cell survival, genotoxic stress, detoxification, and innate and adaptiv

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

163 Genotoxic stress drives damaged DNA out of the nucleus b

164 NFkappaB reduces TGM2 promoter activity, and genotoxic stress drives heightened association of p65 wi

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

166 rea (HU) or camptothecin (CPT), we show that genotoxic stress during S phase specifically induces MBF

167 Upon genotoxic stress, dynamic relocalization events control

168 Upon genotoxic stress, endogenous p63 isoforms were stabilize

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

170 s activated in response to a wide variety of genotoxic stresses, frequently via post-translational mo

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

172 Specifically, there is evidence that genotoxic stress from chemotherapy or radiation therapy,

173 ing infections, C. albicans has to cope with genotoxic stresses generated by the host immune system.

174 How these cells respond to genotoxic stress has only recently begun to be investiga

175 53 potentiates the JNK-dependent response to genotoxic stress; however, the mechanism whereby p53 sti

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

177 wly uncovered counter-regulatory response to genotoxic stress in a chondrocytic survival pathway is p

178 ducer of ErbB2 gene family and is induced by genotoxic stress in a p53- and Checkpoint kinase 1 (CHK1

179 show that SK1 is proteolysed in response to genotoxic stress in a p53-dependent manner.

180 A repair by NHEJ in conferring resistance to genotoxic stress in advanced prostate cancer and suggest

181 ing pathway is associated with resistance to genotoxic stress in aggressive prostate cancer cells.

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

183 patient HSPCs but rescued physiological and genotoxic stress in HSPCs from FA mice, showing that MYC

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

185 ous vegetables, to be a widespread source of genotoxic stress in intestinal epithelial cells.

186 The present findings demonstrate that genotoxic stress in neurons results in elongated mitocho

187 terplay between TP53 and TP63 in response to genotoxic stress in normal cells.

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

189 We evaluated the possible origins of genotoxic stress in the mouse gut by examining factors a

190 wild-type strain, suggesting the presence of genotoxic stress in the mouse gut.

191 H1 depletion had no effect on other forms of genotoxic stress in which DSBs form by means that do not

192 multifaceted roles in cellular responses to genotoxic stress, including DNA repair.

193 iana) AtPollambda in response to abiotic and genotoxic stress, including salinity and the DNA cross-l

194 a key mediator in many cellular responses to genotoxic stresses, including ionizing radiation (IR) an

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

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

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

198 ide analysis of transcriptional responses to genotoxic stress induced by cancer therapeutics, we iden

199 sal role in the development of resistance to genotoxic stress induced by common chemotherapeutic agen

200 populations are expected to be less prone to genotoxic stress induced by these treatments and therefo

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

202 talloproteinase, is capable of counteracting genotoxic stress-induced apoptosis by the suppression of

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

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

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

206 Here, we show that genotoxic stress-induced FANCM phosphorylation is ATR-de

207 er, the consequence of miR-122 deficiency on genotoxic stress-induced liver pathogenesis is poorly un

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

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

210 Cdk1 directly phosphorylate Clp1 to promote genotoxic stress-induced nucleoplasmic accumulation.

211 Clp1 RxxS and TP phosphosites eliminates any genotoxic stress-induced redistribution.

212 typic screening for inhibitors of ligand and genotoxic stress-induced translocations in prostate canc

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

214 Genotoxic stress induces alternative splicing of the onc

215 Genotoxic stress induces p57Kip2 expression via the bone

216 Here we show that genotoxic stress induces TG2 expression through the Atax

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

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

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

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

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

222 The protective role of IRE1alpha under genotoxic stress is conserved in fly and mouse.

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

224 show here that relocalization of Clp1 during genotoxic stress is governed by complex phosphoregulatio

225 ly rapid JNK-dependent apoptotic response to genotoxic stress is significantly delayed in Dmp53 (Dros

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

227 lated cell survival under carcinogen-induced genotoxic stress is vital for cancer development.

228 Genotoxic stresses lead to centrosome amplification, a f

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

230 and that disruption of this immune sensor of genotoxic stress leads to behavioural abnormalities.

231 catalyzed by PAR polymerase 1 in response to genotoxic stress mediates cell death due to necrosis and

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

233 In response to genotoxic stress, multiple kinase signaling cascades are

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

235 unusual event that is often associated with genotoxic stress or viral infection.

236 c integrity despite considerable exposure to genotoxic stress over long life spans, and showed conser

237 Genotoxic stress overactivates this compensatory mechani

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

239 cifically addressed the relationship between genotoxic stress, p53 activation, and the regulation of

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

241 During genotoxic stress, PARP-1 recruits to sites of DNA damage

242 or long periods at the sea surface, activate genotoxic stress pathways in response to UV exposure whe

243 Upon genotoxic stress, PCNA ubiquitination allows for replica

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

245 se whose sustained activation in response to genotoxic stress promotes apoptosis.

246 n of apoptosis following exogenously induced genotoxic stress, prophase-arrested oocytes are highly c

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

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

249 Genotoxic stress reduces this ubiquitination in cytosol

250 Sumoylation during genotoxic stress regulates the composition of DNA repair

251 at HER2/HER3 signaling directly, and not via genotoxic stress, regulates MICA/B expression.

252 yet the mechanisms that protect neurons from genotoxic stress remain largely obscure.

253 le of autophagy following carcinogen-induced genotoxic stress remains unclear.

254 Apoptotic death of cells damaged by genotoxic stress requires regulatory input from surround

255 o indicated the involvement of TRIM21 in the genotoxic stress response and suppressing tumorigenesis.

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

257 sphoproteome datasets revealed activation of genotoxic stress response pathways, including deregulati

258 ctivity between circadian regulation and the genotoxic stress response remains poorly understood.

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

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

261 t role in regulating the level of p53 in the genotoxic stress response.

262 innate immunity, lymphocyte development and genotoxic stress response.

263 lock coordinates cell cycle progression with genotoxic stress responses by synchronizing Cdc2/Cyclin

264 ion of histones by PARP-1 has been linked to genotoxic stress responses, its role in physiological pr

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

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

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

268 We demonstrate that genotoxic stress stimulates Cry1 phosphorylation and its

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

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

271 rylation, which significantly increased upon genotoxic stress, suggesting an early DNA-damage respons

272 y of rad9 and rad24 mutants in conditions of genotoxic stress, suggesting that complex stability impa

273 genes determine antimicrobial resistance and genotoxic stress survival.

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

275 yptococcus cells polyploidize in response to genotoxic stresses that cause DNA double-strand breaks.

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

277 In response to genotoxic stress, the p53 tumor suppressor induces targe

278 Here, we show that following genotoxic stress, the RNA-binding motif protein 7 (RBM7)

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

280 ant metastasis in the presence or absence of genotoxic stress therapy.

281 Even without additional genotoxic stress, these mutants show symptoms of DNA dam

282 is induced in response to various viral and genotoxic stresses, this cytokine may regulate autocrine

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

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

285 protein response transducer IRE1alpha under genotoxic stress to modulate repair programs and sustain

286 d other tauopathies, but the consequences of genotoxic stress to postmitotic neurons are poorly under

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

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

289 rther analyses reveal that in the absence of genotoxic stress TP63 plays an important role in maintai

290 We also show that genotoxic stress triggers aberrant degradation of the pr

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

292 Necdin controls the HSC response to genotoxic stress via both cell-cycle-dependent and cell-

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

294 Under genotoxic stress, when RNF8 is rapidly recruited to site

295 Short term IL-22 production protects against genotoxic stress, whereas uncontrolled IL-22 activity pr

296 ic differentiation results in an overload of genotoxic stress, which causes aborted differentiation a

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

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

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

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