ライフサイエンスコーパス: DNA-damaging agent

1 s measured using the SOS-Chromotest (detects DNA-damaging agents).

2 erase beta that works synergistically with a DNA damaging agent.

3 mitochondria and nucleus in response to this DNA-damaging agent.

4 RP inhibitors alone or in combination with a DNA-damaging agent.

5 iscovery to benefit cancer therapies using a DNA-damaging agent.

6 n slow growth and renders cells sensitive to DNA damaging agents.

7 ion checkpoint response, upon treatment with DNA damaging agents.

8 t that TCOF1 promotes cellular resistance to DNA damaging agents.

9 1 complex6 cause hypersensitivity to various DNA damaging agents.

10 rs and promotes cell survival in the face of DNA damaging agents.

11 e loci such as centromeres in the absence of DNA damaging agents.

12 ons induced by both endogenous and exogenous DNA damaging agents.

13 ingly, POH1-deficient cells are sensitive to DNA damaging agents.

14 y apoptosis even in the absence of exogenous DNA damaging agents.

15 that are targeted by subsequent exposure to DNA damaging agents.

16 with topoisomerase II poisons but not other DNA damaging agents.

17 both Gcn5 and Rtt109 are highly sensitive to DNA damaging agents.

18 e of active PARP1 in vitro or in response to DNA damaging agents.

19 2 function is associated with sensitivity to DNA damaging agents.

20 t in enhanced sensitivity to a wide range of DNA damaging agents.

21 underlies interindividual susceptibility to DNA damaging agents.

22 n several cancer cell models to a variety of DNA damaging agents.

23 ced growth capacity, and hypersensitivity to DNA damaging agents.

24 stability and is required for resistance to DNA damaging agents.

25 nce to the genotoxic effects of a variety of DNA damaging agents.

26 ymes increases cancer cell susceptibility to DNA damaging agents.

27 are hypersensitive to genotoxicity caused by DNA damaging agents.

28 results in cell death or hypersensitivity to DNA damaging agents.

29 e2w alone are not hypersensitive to the same DNA damaging agents.

30 in additive hypersensitivity to a variety of DNA damaging agents.

31 omic instability and enhanced sensitivity to DNA-damaging agents.

32 to predict cellular resistance to killing by DNA-damaging agents.

33 during normal replication and in response to DNA-damaging agents.

34 me of patients with NPC who are treated with DNA-damaging agents.

35 4 proteins and resistance to cell killing by DNA-damaging agents.

36 se RNA, which is altered upon treatment with DNA-damaging agents.

37 OS levels and by exposing cells to oxidative DNA-damaging agents.

38 ortant for survival of cells challenged with DNA-damaging agents.

39 ponsible for the acquired resistance against DNA-damaging agents.

40 genomic instability and drives resistance to DNA-damaging agents.

41 SP1 deubiquitinating enzyme upon exposure to DNA-damaging agents.

42 maintaining genomic integrity in response to DNA-damaging agents.

43 RNF4 gene displayed increased sensitivity to DNA-damaging agents.

44 repair genes and enhanced cell resistance to DNA-damaging agents.

45 uclear foci patterns observed in response to DNA-damaging agents.

46 the genome and showed higher sensitivity to DNA-damaging agents.

47 d differentially to doxycycline, hypoxia, or DNA-damaging agents.

48 itro and (ii) treatment of cancer cells with DNA-damaging agents.

49 ransformation and survival after exposure to DNA-damaging agents.

50 ble to resensitize PRMT7 knock-down cells to DNA-damaging agents.

51 itor) that sensitizes p53-deficient cells to DNA-damaging agents.

52 romatin after DNA damage or to resistance to DNA-damaging agents.

53 E cells were exposed to mitomycin C or other DNA-damaging agents.

54 nd does not trigger apoptosis in response to DNA-damaging agents.

55 esponse and, thus, sensitize cancer cells to DNA-damaging agents.

56 ed breaks, and recN mutants are sensitive to DNA-damaging agents.

57 d increases the efficacy of chemotherapeutic DNA-damaging agents.

58 olaparib sensitized ATM null tumor cells to DNA-damaging agents.

59 ity syndrome characterized by sensitivity to DNA-damaging agents.

60 rexpression showed changes in sensitivity to DNA-damaging agents.

61 e p53-mediated growth inhibitory response to DNA-damaging agents.

62 in RNA and increases cellular sensitivity to DNA-damaging agents.

63 anner and greatly exacerbated sensitivity to DNA-damaging agents.

64 demonstrate an intrinsic supersensitivity to DNA-damaging agents.

65 ed for cell viability upon acute exposure to DNA-damaging agents.

66 upon DNA damage, RRP1B is induced by several DNA-damaging agents.

67 abolism and is phosphorylated in response to DNA-damaging agents.

68 expression of ALC1 results in sensitivity to DNA-damaging agents.

69 hase I trials of ABT-888 in combination with DNA-damaging agents.

70 ll-cell lung cancer cells sensitized them to DNA-damaging agents.

71 ional regulation of cyclin D1 in response to DNA-damaging agents.

72 rget genes and the induction of apoptosis by DNA-damaging agents.

73 the S131F polymorphism conveys resistance to DNA-damaging agents.

74 e H4 lysine 91 and protects cells exposed to DNA-damaging agents.

75 ll cycle arrest and apoptosis in response to DNA-damaging agents.

76 d the traditional resistance of melanomas to DNA-damaging agents.

77 oisomerase inhibitors and a variety of other DNA-damaging agents.

78 cells are hypersensitive to chemotherapeutic DNA-damaging agents.

79 cation and cell-cycle progression induced by DNA-damaging agents.

80 TOR inhibitors when used in combination with DNA-damaging agents.

81 significantly increased the cytotoxicity of DNA-damaging agents.

82 the pericentromere expands after exposure to DNA-damaging agents.

83 phase DSBs, and increased the sensitivity to DNA-damaging agents.

84 ant flies or their survival upon exposure to DNA-damaging agents.

85 SH2 from cells renders resistance to certain DNA-damaging agents.

86 s proliferation and confers sensitization to DNA-damaging agents.

87 s apoptosis to both endogenous and exogenous DNA-damaging agents.

88 are hypersensitive to genotoxicity caused by DNA-damaging agents.

89 se I-dependent manner, which is activated by DNA-damaging agents.

90 common type of environmental and endogenous DNA-damaging agents.

91 and growth advantage, following exposure to DNA-damaging agents.

92 and is under LexA control, being induced by DNA-damaging agents.

93 cient mice (SKO) are prone to CAC induced by DNA-damaging agents.

94 lar resistance of BRCA1 wild-type tumours to DNA-damaging agents.

95 ested the deletion strain for sensitivity to DNA-damaging agents.

96 tigate their potential as radical-generating DNA-damaging agents.

97 ls can be exploited for cancer therapy using DNA-damaging agents.

98 d apoptosis in response to certain exogenous DNA-damaging agents.

99 downstream function of WEE1 upon exposure to DNA-damaging agents.

100 an cancers, confers resistance to killing by DNA-damaging agents.

101 esulting in hypersensitivity to a variety of DNA damaging agents, a diminished ability to maintain re

102 s receptor (c-Met) protect cells against the DNA-damaging agent adriamycin (ADR) as a model for chemo

103 Finally, we show that a variety of DNA damaging agents all result in a large increase in FB

104 , persistent RAD51 foci, hypersensitivity to DNA damaging agents and accumulation of DNA strand break

105 nance of genome integrity, for resistance to DNA damaging agents and for gene targeting.

106 These mutants are sensitive to DNA damaging agents and have reduced frequencies of appa

107 alpha-helix and observed hypersensitivity to DNA damaging agents and increased frequency of genome re

108 nockdown in vitro sensitizes cancer cells to DNA damaging agents and induces cell death via p53-depen

109 an cells lacking HPF1 exhibit sensitivity to DNA damaging agents and PARP inhibition, thereby suggest

110 ransformed cells are not more susceptible to DNA damaging agents and repair DNA lesions at a rate sim

111 yper-recombination phenotype, sensitivity to DNA damaging agents and synthetic lethality with mutatio

112 wn of CEP164 or ZNF423 causes sensitivity to DNA damaging agents and that cep164 knockdown in zebrafi

113 ants display sensitivity to a broad range of DNA-damaging agents and cell wall-targeting antibiotics.

114 This results in sensitivity to DNA-damaging agents and chromosomal instabilities.

115 ignificantly reduces cellular sensitivity to DNA-damaging agents and decreases cellular DNA mismatch

116 HARP results in hypersensitivity to multiple DNA-damaging agents and defects in fork stability or res

117 apoptosis by expression of IAP-antagonists, DNA-damaging agents and even knockdown of the IAP diap1.

118 roposed to sensitize hypoxic cancer cells to DNA-damaging agents and inhibitors of DNA repair.

119 se models to assess bone marrow toxicity for DNA-damaging agents and inhibitors of the DNA damage res

120 ar response to many mechanistically distinct DNA-damaging agents and is selected against during the p

121 73A mutant conferred cellular sensitivity to DNA-damaging agents and led to defective repair of DNA d

122 r rheostat that determines susceptibility to DNA-damaging agents and other death stimuli.

123 air genes and subsequent hypersensitivity to DNA-damaging agents and PARP1/2 inhibitors.

124 apply to the entire family of monofunctional DNA-damaging agents and pave the way for rational improv

125 own to confer yeast cells with resistance to DNA-damaging agents and play a role in activation of DNA

126 devoid of Set2/H3K36me are hypersensitive to DNA-damaging agents and site-specific DSBs, fail to prop

127 eficient tumor cells to apoptosis induced by DNA-damaging agents and suggests that disruption of cryp

128 They are sensitive to a variety of DNA-damaging agents and to the spindle poison thiabendaz

129 mpaction was proportional to the dose of the DNA damaging agent, and results obtained in cells defect

130 ional silencing and increased sensitivity to DNA damaging agents, and these defects are exacerbated w

131 enzymes, DNA repair capacity, sensitivity to DNA-damaging agents, and iron homeostasis.

132 affects genomic instability, sensitivity to DNA-damaging agents, and migration of tumor cells by rec

133 ess, are more tolerant than the wild type to DNA-damaging agents, and show constitutive induction of

134 s but also recognizes DNA adducts induced by DNA-damaging agents, and triggers cell-cycle arrest and

135 Most DNA-damaging agents are weak inducers of an anticancer i

136 and subcellular localization in response to DNA damaging agents at the single-cell level.

137 in the cytoplasm and, after treatment with a DNA-damaging agent, at the centrosomes.

138 -tailed SSB recovers faster from exposure to DNA damaging agents but accumulates more mutations.

139 Cells lacking CHIP are hypersensitive to DNA-damaging agents, but DNA repair and cell viability a

140 ficient cells, do not exhibit sensitivity to DNA-damaging agents, but do display shortened (but stabl

141 igG sigma factor was induced by a variety of DNA-damaging agents, but inactivation of sigG did not af

142 e apoptotic properties of a chemotherapeutic DNA-damaging agent by regulating the expression, subcell

143 ficient tumors in order to sensitize them to DNA-damaging agents by eliminating Chk1-mediated checkpo

144 of this complex confers hypersensitivity to DNA-damaging agents by undefined mechanisms.

145 in CML and non-CML cells upon treatment with DNA damaging agent camptothecin.

146 Noxa were required for apoptosis induced by DNA damaging agents camptothecin and UV.

147 l mouse cortical neurons, treatment with the DNA-damaging agent camptothecin (CPT) resulted in elonga

148 ockdown exacerbated apoptosis induced by the DNA-damaging agent camptothecin.

149 tc3 exhibit synergistic sensitivities to the DNA-damaging agents camptothecin and methyl methanesulfo

150 how that the sensitivity of rad53 mutants to DNA-damaging agents can be almost completely suppressed

151 DNA-damaging agents can induce premature senescence in c

152 roso compounds (NOCs), an important class of DNA damaging agents, can induce the carboxymethylation o

153 ation of gammaH2AX foci after treatment with DNA-damaging agents cannot, therefore, be used as a dire

154 iates resistance to apoptosis in response to DNA-damaging agents, causing BRCA1 wild-type tumours to

155 Upon exposure to DNA-damaging agents, cells expressing non-phosphorylatab

156 When fission yeast cells are treated with DNA-damaging agents, Chk1 is activated and phosphorylate

157 utations were somewhat less sensitive to the DNA-damaging agent ciprofloxacin than the corresponding

158 The DNA-damaging agent cisplatin caused a concentration-depe

159 RNA)-rich nucleoli in cells treated with the DNA-damaging agents cisplatin and etoposide.

160 )histone2AX (gammaH2AX) after treatment with DNA damaging agents, compared with T cells from controls

161 p12, which occurs in cells upon exposure to DNA-damaging agents, converts Pol delta to a form that h

162 SETD2 mutations led to resistance to DNA-damaging agents, cytarabine, 6-thioguanine, doxorubi

163 eferred cancer regimens combine a MTA with a DNA-damaging agent (DDA).

164 DNA-damaging agents (DDAs) constitute the backbone of tr

165 THRAP3 and/or BCLAF1 leads to sensitivity to DNA damaging agents, defective DNA repair and genomic in

166 ary cells do not show altered sensitivity to DNA damaging agents, defects in gamma-H2AX induction, or

167 on the basis of their sensitivity to various DNA-damaging agents demonstrated that deletion of POL32,

168 ant to apoptosis in response to a variety of DNA-damaging agents, despite activation of p53 and the p

169 dogenous p53-target genes in response to the DNA damaging agent doxorubicin.

170 ex-forming oligonucleotides (TFOs) linked to DNA damaging agents (e.g. psoralen) can stimulate HR, pr

171 d that AZD1775 alone and in combination with DNA-damaging agents (e.g., cisplatin and radiation) decr

172 Treatment of yeast and human cells with DNA-damaging agents elicits Rad6-Rad18-mediated monoubiq

173 approximately 20%) following exposure to the DNA-damaging agent etoposide.

174 nes toward the induction of apoptosis by the DNA-damaging agent etoposide.

175 emonstrate that following treatment with the DNA-damaging agents, etoposide or camptothecin, BRCA1 is

176 ree H3 and H4 concomitant with resistance to DNA damaging agents, even in mutants defective in the DN

177 The addition of a DNA-damaging agent further upregulated p53 protein level

178 DC1, NBS1, mTR or hMLH1) or cells exposed to DNA-damaging agents had elevated IGF-1 expression, resul

179 AZD1775 and DNA-damaging agents have displayed favorable activity in

180 NA lesions that are also formed by exogenous DNA damaging agents, have been evaluated in HeLa and xer

181 stem cells showed sensitivity to a range of DNA-damaging agents, highlighting its role in replicatio

182 mES cells and their effect on sensitivity to DNA-damaging agents, homologous recombination and genomi

183 /BRCA2 loss of function mutations respond to DNA damaging agents, however, some do not.

184 hibition of mTOR results in sensitization to DNA-damaging agents; however, the molecular mechanism is

185 When treated with some DNA-damaging agents, human tumor-derived H1299 cells exp

186 the N-OH bond in 2 may yield the well-known DNA-damaging agent, hydroxyl radical.

187 on when assessed for hypersensitivity to the DNA-damaging agent hydroxyurea (HU).

188 inistration of an ATR kinase inhibitor and a DNA damaging agent impacts the DNA damage induced by the

189 RG depletion causes sensitisation to certain DNA damaging agents, implicating PARG as a potential the

190 he four mammalian FoxO genes, in response to DNA damaging agents in both mouse embryonic fibroblasts

191 l biomarker to predict primary resistance to DNA damaging agents in patients with germline BRCA1 and

192 ese results suggest that Al likely acts as a DNA-damaging agent in vivo and that Al-dependent root gr

193 evere phenotypic effects with sensitivity to DNA-damaging agents in fission yeast and reduced viabili

194 mbination of allosteric PARP inhibitors with DNA-damaging agents in genomically unstable cancer cells

195 vide a clinical application for AZD1775 with DNA-damaging agents in KRAS/LKB1 NSCLC.

196 The causes of sensitivity to DNA-damaging agents in nondividing cell populations, suc

197 enes may be exploited to optimize the use of DNA-damaging agents in patients with high-risk MM.

198 HuR's role in the efficacy of DNA-damaging agents in PDA cells was, in part, attribute

199 gly potentiates the efficacy of a variety of DNA-damaging agents in preclinical models.

200 , PD-1 and CTLA-4 and greater sensitivity to DNA-damaging agents in representative cell line models;

201 and sensitized p53-deficient cancer cells to DNA-damaging agents in vitro and in vivo.

202 k1 inhibitors results in hypersensitivity to DNA-damaging agents in vitro and may provide a potential

203 n cells leads to an increased sensitivity to DNA-damaging agents, in particular interstrand cross-lin

204 RecQ4 upon treatment of cells with different DNA-damaging agents including UV irradiation, 4-nitroqui

205 Since we previously showed that DNA-damaging agents (including chemotherapy and irradiat

206 ta and bdf2Delta cells showed sensitivity to DNA damaging agents, including camptothecin, that cause

207 ation and consequently are hypersensitive to DNA-damaging agents, including cisplatin and poly(ADP-ri

208 sitizes p53-mutant cells to a broad range of DNA-damaging agents, including mitomycin C, a bifunction

209 ane lesion (DOB) is produced by a variety of DNA-damaging agents, including the aforementioned.

210 ta60 supports normal growth and responses to DNA damaging agents, indicating that Smc5/6 does not sim

211 early S phase and are sensitive to multiple DNA-damaging agents, indicating impaired DNA replication

212 Here we show that bulky DNA damaging agents induce localized fork stalling at ye

213 Moreover, DNA-damaging agents induce ABH8 expression in an ATM-dep

214 olog 7 (ALKBH7) gene plays a pivotal role in DNA-damaging agent-induced programmed necrosis by trigge

215 of this variant transforms a bacteriostatic DNA damaging agent into a bactericidal drug, resulting i

216 An effective response to DNA damaging agents involves modulating numerous facets

217 hk1 could potentiate the cytotoxicity of the DNA damaging agent irinotecan in TNBC using xenotranspla

218 is and show that REV3-mediated resistance to DNA-damaging agents is independent of the replication da

219 enomic stability in the absence of exogenous DNA-damaging agents is unclear.

220 doxorubicin, and etoposide, but not to a non-DNA damaging agent, l-asparaginase.

221 ion, C646 is shown to promote sensitivity to DNA damaging agents, leading to the enhanced apoptosis o

222 pleted of NFKBIL2 or MMS22L are sensitive to DNA-damaging agents, load phosphorylated RPA onto chroma

223 sed by the sni1 mutation or treatment with a DNA-damaging agent markedly enhances SA-mediated defense

224 We focus on genomic responses to the DNA damaging agent methyl methanesulfonate (MMS) in comp

225 in recombination rates and resistance to the DNA damaging agent methyl methanesulfonate, suggesting t

226 hen fission yeast cells are treated with the DNA-damaging agent methyl methanesulfonate (MMS), we car

227 h54 is not necessary for the response to the DNA-damaging agent methyl methanesulfonate.

228 e DNA replication stress than by the general DNA-damaging agent methyl methanesulfonate.

229 opper genes are regulated in response to the DNA-damaging agents methyl methanesulfonate (MMS) and hy

230 aradoxically, analysis of cells resistant to DNA damaging agents missing the CTD restore HR proficien

231 ) results in an increased sensitivity to the DNA damaging agent mitomycin C (MMC) that correlates wit

232 lease activity, and affects tolerance to the DNA-damaging agent mitomycin C, argue that this prototyp

233 ponse to elf18 and are hypersensitive to the DNA-damaging agent mitomycin C.

234 reduced their viability upon exposure to the DNA-damaging agents mitomycin C and Irofulven, but not e

235 nces in C(18) ceramide levels induced by two DNA-damaging agents, mitomycin C and daunorubicin, and t

236 cacy of MK-1775 alone or in combination with DNA damaging agents (MMC or oxaliplatin) in PDA cell lin

237 shown to be sensitive to treatment with the DNA damaging agent MMS.

238 Upon addition of a DNA-damaging agent, MMSET-high cells repaired DNA damage

239 a protects against cell death induced by the DNA damaging agent N-methyl-N-nitro-N-nitrosoguanidine (

240 utation are sensitive to radiation and other DNA-damaging agents, no such individual has yet develope

241 types of transformed cells exposed to either DNA damaging agents or CDK4 inhibitors.

242 f cohesin become SUMOylated upon exposure to DNA damaging agents or presence of a DNA double-strand b

243 Exposure of neurons to DNA damaging agents or the excitotoxin NMDA elicited sim

244 athways through transcriptional responses to DNA damaging agents or through predicted miRNA regulatio

245 1 was generated by treatment of cells with a DNA-damaging agent or by addition of NAD(+) to CFEs.

246 R genes, providing a rationale for combining DNA-damaging agents or targeted DDR inhibitors with horm

247 Treatment of HCT116 p53(+/+) cells with the DNA-damaging agent oxaliplatin induced a p53-dependent t

248 lustering of damage is a hallmark of certain DNA-damaging agents, particularly ionizing radiation.

249 tumorigenicity and tumor cell resistance to DNA damaging agents, properties associated with tumor-in

250 Exposure of cells to DNA-damaging agents results in a rapid increase in the f

251 rigin firing is blocked by prior exposure to DNA damaging agents showing that the prevention of origi

252 Characterization of the direct effects of DNA-damaging agents shows how DNA lesions lead to specif

253 Loss of RecO elicits hypersensitivity to DNA damaging agents similar to that caused by deletion o

254 strated to enhance the anti-tumor effects of DNA damaging agents such as gemcitabine.

255 DNA repair and enhances the genotoxicity of DNA-damaging agents such as benzo[a]pyrene and ultraviol

256 n turn, cellular response to treatments with DNA-damaging agents such as cisplatin (cis-dichlorodiamm

257 in turn, cellular response to treatment with DNA-damaging agents such as cisplatin, ionizing radiatio

258 us, BRCA-associated cancers are sensitive to DNA-damaging agents such as cisplatin.

259 en Escherichia coli grows in the presence of DNA-damaging agents such as methyl methanesulphonate (MM

260 hibition of PARP potentiates the activity of DNA-damaging agents such as temozolomide, topoisomerase

261 remains unchanged after cells are exposed to DNA-damaging agents such as UV light (generating UV phot

262 n was distinct from that of more traditional DNA damaging agents, such as camptothecin, as it was p53

263 MiRNA expression is also affected by DNA damaging agents, such as radiation.

264 In contrast, the DNA damaging agent temozolomide (TMZ), which is used as

265 ponse to treatment with the chemotherapeutic DNA-damaging agent temozolomide.

266 eptible to apoptosis induced by etoposide, a DNA-damaging agent, than HIPK2+/+ cells.

267 ignancies by promoting cellular responses to DNA damaging agents that are currently ineffective again

268 his mechanism provides the impetus to design DNA damaging agents that produce DSBs by abstracting a s

269 a chemical basis for the cytotoxicity of the DNA damaging agents that produce this lesion.

270 A DNA-damaging agent that induces DNA double-stranded brea

271 mines formed in well-done cooked meats, as a DNA-damaging agent that may contribute to the etiology o

272 y with a single-strand break by a variety of DNA-damaging agents that abstract a hydrogen atom from t

273 and Rad3-related (ATR) gene is activated by DNA-damaging agents that are frequently used as anticanc

274 2 in B. subtilis sensitized cells to several DNA-damaging agents that can block or impair replication

275 ARCAL1-depleted cells display sensitivity to DNA-damaging agents that induce replication fork collaps

276 s highly inducible in primary fibroblasts by DNA-damaging agents that induce strand breaks, alkylate

277 Lig3-null cells are not sensitive to several DNA-damaging agents that sensitize Xrcc1-deficient cells

278 ssion is required for the normal response to DNA-damaging agents, the nuclear localisation of RAD51 a

279 tins) are unsaturated imines that are potent DNA damaging agents, thereby confirming an earlier mecha

280 ils) are required for cellular resistance to DNA damaging agents; therefore, we examined the role of

281 recipitated senescence following exposure to DNA-damaging agents, thus accounting for higher sensitiv

282 ective WEE1 inhibitor MK-1775 synergize with DNA-damaging agent to inhibit cancer cell growth.

283 b at the BRCA1 promoter that is disrupted by DNA-damaging agents to increase its transcription.

284 kinase that is activated by a wide range of DNA-damaging agents to slow the cell cycle during S phas

285 1 foci formation, sensitizes cancer cells to DNA damaging agents, to Poly (ADP-ribose) polymerase (PA

286 3 that is sufficient, even in the absence of DNA-damaging agents, to increase the expression of proap

287 ) in cellular responses to chronic, low-dose DNA-damaging agent treatment by maintaining MEFs in low

288 However, combined Nutlin3a and chronic DNA-damaging agent treatment is insufficient to promote

289 owever, it is still unclear how CSCs survive DNA-damaging agent treatment.

290 machinery and, consequently, the response to DNA-damaging agents used routinely in the clinic.

291 Induction of ER by DNA-damaging agents was p53 dependent as either ionizing

292 Histone deacetylase (HDAC) inhibitors and DNA-damaging agents were identified as novel Golgi disru

293 r hypersensitivity to replication stress and DNA-damaging agents when combined with mutations in hist

294 non-homologous end joining, and tolerance to DNA-damaging agents when other resection enzymes are abs

295 ent on CDK4/6 were resistant to IR and other DNA-damaging agents when treated with CDK4/6 inhibitors.

296 tion and exposure of cells to mitomycin C, a DNA damaging agent, which interferes with FtsZ ring asse

297 ncreased level of DNA-PKcs and resistance to DNA damaging agents, which is reversed by a DNA-PK inhib

298 wn to provide resistance to a broad range of DNA-damaging agents while also contributing to mismatch

299 be used to measure variations in response to DNA damaging agents within the same cell population.

300 ge response and to sensitize cancer cells to DNA-damaging agents without affecting other functions of