ライフサイエンスコーパス: genotoxic stress

1 Filia expression is induced by genotoxic stress.

2 attern during development and in response to genotoxic stress.

3 lated and sumoylated proteins in response to genotoxic stress.

4 ction in orchestrating cellular responses to genotoxic stress.

5 uired for nuclear oxidation induced by acute genotoxic stress.

6 required for cell growth and survival during genotoxic stress.

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

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

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

10 in the Escherichia coli genome during acute genotoxic stress.

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

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

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

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

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

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

17 nction through modulation of the response to genotoxic stress.

18 repress the apoptotic cell death response to genotoxic stress.

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

20 p53-binding kinetics are modulated following genotoxic stress.

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

22 capacities to survive the damage induced by genotoxic stress.

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

24 n this surface result in hypersensitivity to genotoxic stress.

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

26 ished functions in sensing and responding to genotoxic stress.

27 3-dependent apoptotic pathway in response to genotoxic stress.

28 A damage response and cellular recovery from genotoxic stress.

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

30 ent sensitivity of growing hair follicles to genotoxic stress.

31 thus may facilitate tumor development under genotoxic stress.

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

33 is but also with increased susceptibility to genotoxic stress.

34 0, which interacts with NEMO via MCPIP1 upon genotoxic stress.

35 dependent RNR regulation under conditions of genotoxic stress.

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

37 nificant variations in cellular responses to genotoxic stress.

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

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

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

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

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

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

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

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

46 attenuating apoptosis following exposure to genotoxic stress.

47 ensures efficient DNA repair in response to genotoxic stress.

48 quitin signaling in the cellular response to genotoxic stress.

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

50 Rad53 is phosphorylated and activated upon genotoxic stress.

51 anism for protecting the nervous system from genotoxic stress.

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

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

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

55 ntain homeostasis of survival pathways under genotoxic stress.

56 re it alters membrane permeability following genotoxic stress.

57 can protect adult stem cell populations from genotoxic stress.

58 facilitates NEMO linear ubiquitination upon genotoxic stress.

59 m2 inhibition that impacts p53 dynamics upon genotoxic stress.

60 l-cycle checkpoint activation in response to genotoxic stress.

61 ng cell-cycle progression in the presence of genotoxic stress.

62 ppaB activation by diverse stimuli including genotoxic stress.

63 rated induction of senescence in response to genotoxic stress.

64 integrity of the human genome in response to genotoxic stress.

65 -mediated DNA repair and hypersensitivity to genotoxic stress.

66 survival and genome integrity in the face of genotoxic stress.

67 resistance to DNA damage under conditions of genotoxic stress.

68 pneumophila, competence may be a response to genotoxic stress.

69 functions and for survival of animals under genotoxic stress.

70 the PARG null cell phenotype in response to genotoxic stress.

71 in promoting DNA damage repair subsequent to genotoxic stress.

72 checkpoint signalling and the recovery from genotoxic stress.

73 throughout interphase and after exposure to genotoxic stress.

74 53-directed transcriptomic changes following genotoxic stress.

75 ponse observed following prolonged or severe genotoxic stress.

76 omotes B cell differentiation in response to genotoxic stress.

77 at regulates CREB-dependent transcription in genotoxic stress.

78 tions that are not obviously associated with genotoxic stress.

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

80 d PARG is required for cellular responses to genotoxic stress.

81 ments in which p53 is activated primarily by genotoxic stress.

82 esses downstream p53 activity in response to genotoxic stress.

83 urnover proteins induced by various types of genotoxic stress.

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

85 3 stabilization and activity following acute genotoxic stress.

86 from radiotherapy- and chemotherapy-induced genotoxic stress.

87 acilitating its stabilization in response to genotoxic stress.

88 e deficiencies, and increased sensitivity to genotoxic stress.

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

90 hylation landscape in the absence of applied genotoxic stress.

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

92 ic features, and increased susceptibility to genotoxic stress.

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

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

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

96 Per2 modulates hp53 signaling in response to genotoxic stress.

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

98 fork processing and restart after prolonged genotoxic stress.

99 suggest that PRC2 modulates the response to genotoxic stress.

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

101 sites, thus enhancing cellular resistance to genotoxic stresses.

102 ed cell death triggered by environmental and genotoxic stresses.

103 regulate gene transcription and responses to genotoxic stresses.

104 ccounting for higher sensitivity of cells to genotoxic stresses.

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

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

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

108 Under genotoxic stress, accumulating complexes of RecA, ATP an

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

110 Notably, genotoxic stress activated ATM and VDR through phosphory

111 , these results define a direct link between genotoxic stress-activated c-Abl kinase signaling and Md

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

113 RP inhibition, ionizing radiation, and other genotoxic stress agents.

114 5-fluorouracil, which induces metabolic and genotoxic stress and activates p53, further implicated C

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

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

117 at the p73/PTEN cells were more sensitive to genotoxic stress and cellular death as measured by incre

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

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

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

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

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

123 3 or treated with doxorubicin, which induces genotoxic stress and leads to p53 accumulation.

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

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

126 gmentation indicate the presence of elevated genotoxic stress and p53 activation.

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

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

129 Antioxidants attenuate genotoxic stress and rescue cell proliferation, implying

130 pression at baseline and under conditions of genotoxic stress and that photon flux correlated with mR

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

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

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

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

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

136 al cells in a p38-dependent manner following genotoxic stress, and this acute secretory response prec

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

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

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

140 Unfortunately, the genotoxic stress associated with the GC reaction also pr

141 Genotoxic stress attenuates PKCepsilon effect on ATF2; e

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

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

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

145 ows that tumor-adjacent cells can respond to genotoxic stress by activating a paracrine secretory pro

146 -397, Tyr-576, and Tyr-861 was detected upon genotoxic stress by camptothecin in ADAM15-transfected T

147 The tumor suppressor p53 responds to genotoxic stress by engaging a transcriptional program l

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

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

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

151 Genotoxic stress can promote antitumor NK cell responses

152 the DNA damage response that is triggered by genotoxic stresses capable of inducing DNA double-strand

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

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

155 Oxidative and genotoxic stresses caused by ionizing radiation are detr

156 Following genotoxic stress, cells activate a complex kinase-based

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

158 Under genotoxic stress, cells showed increased expression of b

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

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

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

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

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

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

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

166 After genotoxic stress, Cx43 accumulated in large gap junction

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

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

169 Genotoxic stress drives damaged DNA out of the nucleus b

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

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

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

173 Upon genotoxic stress, dynamic relocalization events control

174 Upon genotoxic stress, endogenous p63 isoforms were stabilize

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

176 Genotoxic stresses (for example, ionizing and ultraviole

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

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

179 n the responses of normal and tumor cells to genotoxic stress has led to the development of new ratio

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

181 53 potentiates the JNK-dependent response to genotoxic stress; however, the mechanism whereby p53 sti

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

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

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

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

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

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

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

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

190 s for the employment of these lines to study genotoxic stress in planta.

191 mitted UV light represents a major source of genotoxic stress in the environment and we found that ex

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

193 orylated at serine 516 by ATR in response to genotoxic stress in the S phase, which disrupts its inte

194 were associated with the PUMA promoter after genotoxic stress in TP53-null cells.

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

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

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

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

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

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

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

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

203 Genotoxic stress induced by chemotherapy or radiation th

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

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

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

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

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

209 and caspase-8, and assembles in response to genotoxic stress-induced depletion of XIAP, cIAP1 and cI

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

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

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

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

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

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

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

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

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

219 Genotoxic stress induces alternative splicing of the onc

220 Genotoxic stress induces p57Kip2 expression via the bone

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

222 Genotoxic stress induces the RecA-dependent SOS response

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

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

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

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

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

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

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

230 se and competence development in response to genotoxic stress is RecA independent.

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

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

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

234 While studying how genotoxic stress kills cancer cells, we discovered a lar

235 Genotoxic stresses lead to centrosome amplification, a f

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

237 ese results show a novel CE cell response to genotoxic stress mediated by marked and rapid changes in

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

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

240 s for the role of SIM peptide in sensitizing genotoxic stress of cancer cells.

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

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

243 Genotoxic stress overactivates this compensatory mechani

244 Under conditions of genotoxic stress, p30 expression was associated with red

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

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

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

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

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

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

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

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

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

254 Genotoxic stress reduces this ubiquitination in cytosol

255 Sumoylation during genotoxic stress regulates the composition of DNA repair

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

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

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

259 e of Molecular Cell, Renner et al. show that genotoxic stress requires SUMOylated IKKvarepsilon to re

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

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

262 innate immunity, lymphocyte development and genotoxic stress response.

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

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

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

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

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

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

269 This complex is disrupted by genotoxic stress, resulting in the displacement of BRCA1

270 We demonstrate that genotoxic stress stimulates Cry1 phosphorylation and its

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

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

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

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

275 genes determine antimicrobial resistance and genotoxic stress survival.

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

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

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

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

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

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

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

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

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

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

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

293 rcadian control of an organism's response to genotoxic stress, which is a major contributor to life-t

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

295 undergoes phosphorylation at serine 139 upon genotoxic stress, which provides a docking site to recru

296 ells from the lethal effect of oxidative and genotoxic stresses, which causes DSBs.

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

298 to a mitochondrial adaptive response to TMZ genotoxic stress with a major contribution from cytochro

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