ライフサイエンスコーパス: camptothecin

1 but not to hydroxyurea, neocarzinostatin, or camptothecin.

2 hSSB1 being required for survival to HU and camptothecin.

3 vealed that miR-142-3p was highly induced by camptothecin.

4 and 10-fold lower than that using BSA-coated camptothecin.

5 particles of comparable dimensions made from camptothecin.

6 cells upon treatment with DNA damaging agent camptothecin.

7 ark of damage caused by Top1 poisons such as camptothecin.

8 A crosslinking agents, alkylating agents and camptothecin.

9 itomycin C and the topoisomerase-1 inhibitor camptothecin.

10 rs cellular resistance to DNA crosslinks and camptothecin.

11 aberrations, and (5) sensitivity to MMC and camptothecin.

12 ll resistance to the chemotherapeutic agent, camptothecin.

13 rvival in response to ionizing radiation and camptothecin.

14 notoxic stresses, such as UVC irradiation or camptothecin.

15 n in HL-60 cells exposed to staurosporine or camptothecin.

16 range of hypersensitivities to the toposide camptothecin.

17 ochondria from human cells were treated with camptothecin.

18 and religation activities in the absence of camptothecin.

19 merase I-linked DNA (TLD) in the presence of camptothecin.

20 lin was markedly longer than by etoposide or camptothecin.

21 with the specific topoisomerase I inhibitor camptothecin.

22 ctivity relationships for the 11-position of camptothecin.

23 ity to the DNA topoisomerase I (Top1) poison camptothecin.

24 of endogenous ARF causes desensitization to camptothecin.

25 NA-damaging antitumor agents doxorubicin and camptothecin.

26 n could contribute to cellular resistance to camptothecin.

27 prolonged G2 arrest, and hypersensitivity to camptothecin.

28 en more dramatic increase in the presence of camptothecin.

29 le GSK3beta inhibitors and anti-cancer agent camptothecin.

30 ated ATR signaling in response to NA-AAF and camptothecin.

31 P2 inhibition but also by the TOP1 inhibitor camptothecin.

32 nsitivity to the double-strand break-inducer camptothecin.

33 ory activity equal to or better than that of camptothecin.

34 se population as compare to positive control camptothecin.

35 apoptosis induced by the DNA-damaging agent camptothecin.

36 ribed for the encapsulation of the antitumor camptothecins, 10-hydroxycamptothecin and 7-butyl-10-ami

37 d the DNA-damaging topoisomerase I inhibitor camptothecin-11 (CPT-11) or SN38 (7-ethyl-10-hydroxycamp

38 t, we have successfully prepared crystalline camptothecin-20(S)-O-propionate hydrate (CZ48) by reacti

39 3d inhibited 47% Topo I (camptothecin, 34%) and 20% Topo II (etoposide 24%) at 20

40 splatin (13-fold), 5-fluorouracil (31-fold), camptothecin (7-fold), and gemcitabine (16-fold).

41 sogenic p53 null mutant after treatment with camptothecin, a DNA topoisomerase I inhibitor.

42 ere sensitive to the topoisomerase inhibitor camptothecin, a feature shared only with the FA subtype

43 They were also hypersensitive to camptothecin, a genotoxin that generates breaks specific

44 considering H9e hydrogel's interaction with camptothecin, a hydrophobic drug.

45 lowing treatment with the DNA-damaging agent camptothecin, a rare example of stress stimulating the m

46 s from Rad50(S/S) mice are hypersensitive to camptothecin, a topoisomerase I inhibitor that causes DN

47 PEAMOtecan was synthesized by conjugating camptothecin, a topoisomerase I inhibitor, to our propri

48 ensitized the cancer cells to treatment with camptothecin, a topoisomerase inhibitor that induces DNA

49 H188A, and R167A) were not hypersensitive to camptothecin, a type-1 topoisomerase inhibitor that indu

50 Although the topoisomerase I inhibitor camptothecin also activated ATR in non-cycling cells, ot

51 hat Top1, in addition to being the target of camptothecins, also regulates DNA replication, rDNA stab

52 Boric acid coated nanocrystals of camptothecin, an anticancer drug with poor aqueous solub

53 topoisomerase I activity in the presence of camptothecin analogs.

54 ntaining supersaturation of a poorly soluble camptothecin analogue, AR-67 (7-t-butyldimethylsilyl-10-

55 Although FL118 is a camptothecin analogue, its antitumor potency is much sup

56 rable to that of the neutral form of another camptothecin analogue.

57 tency is much superior to other FDA-approved camptothecin analogues (irinotecan and topotecan).

58 ation domain caused increased sensitivity to camptothecin and 4-nitroquinoline 1-oxide similar to tha

59 A damage, or topoisomerase I-targeted drugs (camptothecin and a noncamptothecin indenoisoquinoline de

60 ng from the topoisomerase I (Top1) inhibitor camptothecin and a variety of other DNA-damaging antican

61 sensitivity to the topoisomerase I inhibitor Camptothecin and accumulate gammaH2A at heterochromatin.

62 lls was induced with sodium nitroprusside or camptothecin and activation of prothrombin tested.

63 ncy only provides partial protection against camptothecin and cisplatin-induced apoptosis and no prot

64 e clinically significant DNA damaging agents camptothecin and cisplatin.

65 tive to cytotoxic drugs including Mitomycin, Camptothecin and Cisplatin.

66 Camptothecin and doxorubicin treatment caused activation

67 f their activities with specific inhibitors (camptothecin and ellipticine) blocked ori-Lyt-dependent

68 to killing by the apoptosis-inducing agents camptothecin and etoposide as a cytokine-sensitive cell

69 t protection against cell killing induced by camptothecin and etoposide but no protection against cyt

70 Inhibition of topoisomerase I and II by camptothecin and etoposide treatment, respectively, incr

71 firmed marked antiproliferative synergy with camptothecin and even greater synergy with LMP-400.

72 While camptothecin and H2O2 both induce DDR activation, nitric

73 ulates DNA supercoiling and is the target of camptothecin and indenoisoquinoline anticancer drugs, as

74 tial ATR-CHK1 activation after DNA damage by camptothecin and ionizing radiation.

75 rent sequence selectivity when compared with camptothecin and its clinical derivatives.

76 Camptothecin and its derivatives, topotecan and irinotec

77 ifically targeted by the anticancer compound camptothecin and its derivatives.

78 lication origin-firing checkpoint induced by camptothecin and LMP-400.

79 tively a "composite" of the natural products camptothecin and luotonin A and the synthetic indenoisoq

80 tic sensitivities to the DNA-damaging agents camptothecin and methyl methanesulfonate, as well as hyd

81 vitro DNA resection and sensitized cells to camptothecin and olaparib treatment.

82 xpression on drug-induced apoptosis, we used camptothecin and oxaliplatin on a panel of colorectal ca

83 f SLX4 causes sensitivity to mitomycin C and camptothecin and reduces the efficiency of DSB repair in

84 Camptothecin and taxane-based regimens combined with rad

85 interaction between the fluorophore part of camptothecin and the hydrogel, especially at concentrati

86 Moreover, unlike camptothecin and the indenoisoquinoline MJ-III-65 (NSC 7

87 ation and "poisoning" mechanism identical to camptothecin and the indenoisoquinolines.

88 for apoptosis induced by DNA damaging agents camptothecin and UV.

89 We found that the Topo I inhibitor camptothecin and, to a lesser extent, the Topo II inhibi

90 loped to overcome some of the limitations of camptothecins and expand their anticancer spectrum.

91 t carry precise molar ratios of doxorubicin, camptothecin, and cisplatin.

92 r of apoptosis) was one such gene induced by camptothecin, and its overexpression was sufficient to i

93 nse to treatment with ICL agents (cisplatin, camptothecin, and mitomycin), lamin A/C-deficient cells

94 verexpression of ARF causes sensitization to camptothecin, and siRNA-mediated down-regulation of endo

95 I is a target for anti-cancer drugs such as camptothecin, and these drugs also target the topoisomer

96 s, antimetabolites, anthracyclines, taxanes, camptothecins, and epipodophyllotoxins.

97 In contrast, camptothecin- and etoposide-induced killing is associate

98 cluding 7-deacetylazadiradione, simvastatin, camptothecin, andrographolide, cinchonine, beta-dihydroa

99 roperties as compared to the clinically used camptothecin anticancer drugs topotecan and irinotecan.

100 s (aclarubicin, ICRF-193, VM26, doxorubicin, camptothecin, aphidicolin, hydroxyurea, cisplatin, mechl

101 protein, DSBs induced by the TOP1 inhibitor camptothecin are resected normally, but the loading of t

102 Camptothecins are potent topoisomerase I inhibitors used

103 +/- 0.05 muM), and it was also equipotent to camptothecin as a Top1 inhibitor.

104 With pyrene and camptothecin as guests, experiments revealed that the gu

105 a next-generation taxoid, 1 (SB-T-1214), and camptothecin as two warheads, self-immolative disulfide

106 ore traditional DNA damaging agents, such as camptothecin, as it was p53-independent.

107 It also is the target for camptothecin-based anticancer drugs that act by increasi

108 observed that the ligand was a derivative of camptothecin binding to phytosphingosine, wich that is i

109 A model "diastereomer" pathway for camptothecin biosynthesis in C. acuminata is proposed th

110 RNA nuclear export, such as leptomycin B and camptothecin, blocked siRNA restriction.

111 ng downy hairs, transporting a derivative of camptothecin bound to phytosphingosine.

112 n identified as a derivative of the alkaloid camptothecin bound to phytosphingosine.

113 t with the DNA-damaging agents, etoposide or camptothecin, BRCA1 is required for the activation of nu

114 G2 arrest and increased the cytotoxicity of camptothecin by 19-fold against SW620 cells.

115 vo, and it regulates cellular sensitivity to camptothecin by interacting with topoisomerase I.

116 tivity of topoisomerase I in the presence of camptothecin by itself through the direct interaction wi

117 More excitingly, our studies of 5q in camptothecin (CCRF-CEM/C2) and mitoxantrone (HL-60/MX2)

118 hemotherapy (vs monotherapy), and receipt of camptothecin chemotherapy.

119 ere assessed before and after treatment with camptothecin, cis-diamminedichloroplatinum(II), hydroxyu

120 operative effect was observed for the taxoid-camptothecin combination when two drugs were delivered t

121 levels by treatment with 7-ethyl-10-hydroxy-camptothecin converted TRAIL signaling in HCT116 cells f

122 l stability compared with the currently used camptothecin (CPT) analogs irinotecan and topotecan.

123 g hydrophobic aromatic molecules including a camptothecin (CPT) analogue, SN38, noncovalently via pi-

124 e report here the robust tubular assembly of camptothecin (CPT) analogues into functional SPs.

125 f-assembling hybrid prodrugs containing both camptothecin (CPT) and a capecitabine (Cap) analogue.

126 ticles were loaded with the chemotherapeutic camptothecin (CPT) and administered to mice bearing intr

127 elopmental defects and are hypersensitive to camptothecin (CPT) and cis-platin.

128 synergistic doses of top I and II inhibitors camptothecin (CPT) and doxorubicin (DOX) to tumors in vi

129 onale for combining veliparib (ABT-888) with camptothecin (CPT) and its clinical derivatives, topotec

130 ), Top1 cleavage complexes can be trapped by camptothecin (CPT) and its derivatives used in cancer tr

131 we show that yKu70 deficiency suppressed the camptothecin (CPT) and methyl methanesulfonate (MMS) sen

132 nsitivity to methyl methanesulphonate (MMS), camptothecin (CPT) and mitomycin C (MMC), agents that hi

133 The natural compound camptothecin (CPT) and the cancer chemotherapeutics deri

134 s, transcription factors and CYPs related to camptothecin (CPT) biosynthesis.

135 uclear enzyme is also the cellular target of camptothecin (CPT) chemotherapeutics.

136 Camptothecin (CPT) derivatives are effective anticancer

137 Moreover, the DNA topoisomerase-1 inhibitor camptothecin (CPT) down-regulated FLIP in pancreatic can

138 Camptothecin (CPT) enhances the interaction between MIB1

139 small molecular hydrophobic anticancer drug camptothecin (CPT) into discrete, stable, well-defined n

140 The anticancer agent camptothecin (CPT) is a DNA topoisomerase I inhibitor th

141 Moreover, camptothecin (CPT) is used as the anticancer drug and mo

142 Exposure of these cells to camptothecin (CPT) or TNF-alpha/ cycloheximide (CHX) fai

143 trategically compiled into a H2O2-responsive camptothecin (CPT) polymer prodrug micelle, which endowe

144 ctive of the present study was to identify a camptothecin (CPT) prodrug with optimal release and cyto

145 urons, treatment with the DNA-damaging agent camptothecin (CPT) resulted in elongated mitochondria, i

146 -S267A mutation is epistatic to mre11-nd for camptothecin (CPT) sensitivity and synergizes with sgs1D

147 The camptothecin (CPT) Top1 (topoisomerase I) inhibitors exe

148 quiescent (serum-starved) human WI-38 cells, camptothecin (CPT) was shown to induce Top1 down-regulat

149 y sensitive to the topoisomerase 1 inhibitor camptothecin (CPT) which breaks DNA replication forks.

150 a is a rich source of potent anticancer drug camptothecin (CPT) whose biosynthetic pathway is unresol

151 e H6-based nanofiber assemblies encapsulated camptothecin (CPT) with up to 60% efficiency, a 7-fold i

152 the structural similarity of KuQuinones with camptothecin (CPT), a largely used anticancer agent, KuQ

153 Camptothecin (CPT), a topoisomerase (Top) I-targeting dr

154 Camptothecin (CPT), a topoisomerase I (TOP1) inhibitor,

155 patient-derived cells exhibit sensitivity to camptothecin (CPT), impaired CPT-induced topoisomerase I

156 In cells treated with camptothecin (CPT), PIAS3 contributes to formation of DN

157 Topoisomerase IB (Top1) inhibitors, such as camptothecin (CPT), stabilize the Top1-DNA cleavage comp

158 totoxicities vs Top1 that surpassed those of camptothecin (CPT), the natural alkaloid that is being u

159 rticle-drug conjugate containing the payload camptothecin (CPT), to improve therapeutic responses as

160 tivation of p53 by genotoxic agents, such as camptothecin (CPT), triggers apoptosis, while non-genoto

161 To overcome chemical limitations of camptothecin (CPT), we report design, synthesis, and val

162 methane sulfonate (MMS), hydroxyurea (HU) or camptothecin (CPT), we show that genotoxic stress during

163 the cellular target of the anti-cancer drug camptothecin (CPT), which reversibly stabilizes a covale

164 ted genes also showed that Top1 poisoning by camptothecin (CPT), which traps Top1 cleavage complexes

165 Camptothecin (CPT)-11 (irinotecan) has been used widely

166 We report here on the development of a camptothecin (CPT)-based self-assembling prodrug (SAPD)

167 nuated their clonogenic potential, abrogated camptothecin (CPT)-induced Chk1 phosphorylation, and pot

168 on as an intermediate step, end resection of camptothecin (Cpt)-induced DNA damage, and RAD51 recruit

169 nd chromosomal aberrations, as well as fewer camptothecin (CPT)-induced RAD51 foci in subject-derived

170 was increased prominently after delivery of camptothecin (CPT)-loaded FA-CLC/SPIO micelles and thera

171 tress involving collision of replisomes with camptothecin (CPT)-stabilized DNA-Topoisomerase I adduct

172 unctional, polymeric nanoparticle containing camptothecin (CPT).

173 lls' dynamic response to an anticancer drug, camptothecin (CPT).

174 tivity to topoisomerase-1 inhibitors such as camptothecin (CPT).

175 of the topoisomerase I poisons topotecan and camptothecin (CPT).

176 with precise ratios of doxorubicin (DOX) and camptothecin (CPT).

177 gnaling pathway by the chemotherapeutic drug camptothecin (CPT).

178 ytotoxicity of the topoisomerase I inhibitor camptothecin (CPT).

179 tors, including a topoisomerase I inhibitor, camptothecin (CPT).

180 and protection against a DNA-damaging drug, camptothecin (CPT).

181 (5-FU), 5-fluoro-2'-deoxyuridine (FUDR), and camptothecin (CPT).

182 xes (Top1mtcc) can be stabilized in vitro by camptothecin (CPT).

183 ycin C (MMC, an interstrand crosslinker) and camptothecin (CPT, a type 1 topoisomerase inhibitor) in

184 l development to circumvent the drawbacks of camptothecins (CPT).

185 either the nanoparticle or its drug payload (camptothecin, CPT) contained within the nanoparticle.

186 are the key DNA lesion induced by anticancer camptothecins (CPTs) (e.g. topotecan and irinotecan) as

187 cificity is different and it is resistant to camptothecins (CPTs) and non-CPT Top1 inhibitors, LMP744

188 a null mutant, including hypersensitivity to camptothecin, defective sporulation, reduced hairpin-ind

189 compromised enzymes and DNA topoisomerase I-camptothecin dependent lethality.

190 wever, despite the clinical successes of the camptothecin derivatives, a significant need for less to

191 ombination with Top1 inhibitors, such as the camptothecin derivatives, topotecan, and irinotecan, whi

192 are the key DNA lesion induced by anticancer camptothecins (e.g. topotecan and irinotecan) as well as

193 d not significantly inhibit the diffusion of camptothecin encapsulated inside the hydrogel matrix.

194 tably, cotreatment of chemotherapeutic agent camptothecin enhanced LSD1 inhibitor-induced senescence

195 ons from p53-dependent cell death induced by camptothecin, etoposide, heterologous p53 expression or

196 ng UV irradiation, 4-nitroquinoline 1-oxide, camptothecin, etoposide, hydroxyurea, and H(2)O(2).

197 tivation of Src at Tyr-416 was detected upon camptothecin exposure.

198 The pharmacological camptothecin feeding experiment and cell death analysis

199 onse to multiple genotoxic agents, including camptothecin, H2O2, and nitric oxide itself, despite the

200 mus81 and mms4 mutants are hypersensitive to camptothecin; however, these mutants are not hypersensit

201 yr-861 was detected upon genotoxic stress by camptothecin in ADAM15-transfected T/C28a4 cells, but no

202 After a short dose of camptothecin in human colon carcinoma HT29 cells, DNA re

203 ional nanoparticle-drug conjugate containing camptothecin, in preclinical mouse models of orthotopic

204 Resistance to camptothecin, indenoisoquinoline, aphidicolin, hydroxyur

205 -DNA covalent complexes after treatment with camptothecins, indenoisoquinolines and cisplatin but not

206 Here, we found that etoposide (VP16) and camptothecin induced increases in intracellular free cal

207 Camptothecin-induced activation of caspase-3 was reduced

208 DDR activation, nitric oxide suppresses only camptothecin-induced apoptosis and not H2O2-induced necr

209 Camptothecin-induced apoptosis markedly increased subseq

210 merase (PARP) cleavage and susceptibility to camptothecin-induced apoptosis.

211 1-methyl-4-phenylpyridinium-, glutamate-, or camptothecin-induced cell death.

212 rogation of the checkpoint markedly enhanced camptothecin-induced DNA damage at replication sites whe

213 We also find that radiation or camptothecin-induced DNA damage promotes RRM2 deacetylat

214 sister chromatid exchange and resistance to camptothecin-induced DNA damage, and mutants lacking bot

215 n the tolerance of crosslinker, UV light and camptothecin-induced DNA damage.

216 ng UV irradiation, the smt3-331 mutation and Camptothecin-induced formation of covalent topoisomerase

217 that defects of p21(CDKN1A) and p53 enhance camptothecin-induced histone H2AX phosphorylation (gamma

218 We also observed increased camptothecin-induced inhibition of DNA replication and h

219 esses HR and promotes cellular resistance to camptothecin-induced replication stress in vivo.

220 sister chromatid exchange, and resistance to camptothecin-induced replication stress.

221 tors abrogate the doxorubicin-induced G2 and camptothecin-induced S checkpoint arrests, confirming th

222 Processing of blocked DNA ends, like camptothecin-induced trapped-topoisomerase I, can be med

223 A topo I) exhibited increased sensitivity to camptothecin-induced trapping on DNA during mitosis.

224 Camptothecin inhibited the Zta transcription activation

225 that do not bind include C-DIM12, celastrol, camptothecin, IP7e, isoalantolactone, ethyl 2-[2,3,4-tri

226 Camptothecin is a monoterpene indole alkaloid (MIA) used

227 Camptothecin is a potent anticancer agent producing well

228 vation by BRCA1 in response to etoposide and camptothecin is demonstrated by the significantly reduce

229 extrin polymer-based nanoparticle containing camptothecin, is in clinical development for the treatme

230 is before finally being resolved to a single camptothecin isomer after deglucosylation, much as a mul

231 Camptothecins kill mammalian cells by stabilizing topois

232 During apoptosis of NSC34 cells induced by camptothecin, levels of Dnmt1 and Dnmt3a increased fivef

233 tes topoisomerase I, an important target for camptothecin-like chemotherapeutic drugs, but the regula

234 molar doses of the Topoisomerase I inhibitor camptothecin, loss of WRN exonuclease stimulates fork in

235 ile overexpression of top1-T(722)A allele, a camptothecin mimetic, identified 190 sensitive gene-disr

236 Trastuzumab-coated camptothecin nanoparticles inhibited cell growth at a do

237 religation in contrast to the inefficacy of camptothecin on Top1mt.

238 In neuronal apoptosis induced by camptothecin or an MDM2 (murine double minute 2) inhibit

239 When tumor cells treated with camptothecin or cisplatin were subsequently exposed to g

240 ts of the Akt inhibitors in combination with camptothecin or etoposide were more complicated.

241 inhibition of Akt signaling synergized with camptothecin or etoposide, but higher A-443654 or MK-220

242 concentration range enhanced the effects of camptothecin or etoposide.

243 l gamma-H2AX induced by doxorubicin, but not camptothecin or hydrogen peroxide, in H9C2 cardiomyocyte

244 on stress, through aphidicolin, gemcitabine, camptothecin or hydroxyurea exposure, activates transcri

245 In the presence of camptothecin or its derivative topotecan, ATP (at up to

246 ly increased cell recovery after exposure to camptothecin or methotrexate.

247 ronic ester-caged anticancer prodrugs (e.g., camptothecin or paclitaxel prodrug) and hydrophilic gluc

248 d exposed to 400 microM ethanol or 20 microM camptothecin or to infection with influenza A virus (mul

249 ecome trapped on DNA by TOP1 poisons such as camptothecin, or by collision with replication or transc

250 se 1 (PDK1) along with cisplatin, melphalan, camptothecin, or etoposide and assayed for colony format

251 UV irradiation or to mitomycin C, cisplatin, camptothecin, or etoposide, without increasing the amoun

252 rt that cellular exposure to UV irradiation, camptothecin, or hydroxyurea induces accumulation of HDH

253 ous than LPA in reducing gamma irradiation-, camptothecin-, or tumor necrosis factor alpha/cyclohexim

254 ng pathway steps and demonstrated nearly all camptothecin pathway intermediates are present as multip

255 t a gamma-glutamyl transpeptidase-responsive camptothecin-polymer conjugate that actively infiltrates

256 on and self-fluorescence, both recognized as camptothecin properties.

257 Treatment with camptothecin reduced both Zta and RecQL1 binding to OriL

258 reover, we show that inhibition of Top1mt by camptothecin reduces the level of formation of the 7S DN

259 By contrast, gammaH2AX increases after camptothecin removal in HCT116 cells deficient for p53 (

260 rcinogenic and endogenous DNA lesions and by camptothecin, resulting in transcription blocks.

261 In addition to known camptothecin-sensitive strains, this set contained mutat

262 that expression of SLFN11 does not increase camptothecin sensitivity by promoting accumulation of to

263 er-based prodrug of a structurally optimized camptothecin (SN22) designed to overcome key chemoresist

264 ting the growth of SUMO-2/3 chains formed on camptothecin-stabilized topoisomerase I-DNA cleavage com

265 difications of topoisomerase I purified from camptothecin-stabilized topoisomerase I-DNA cleavage com

266 Camptothecin-stabilized topoisomerase I-DNA cleavage int

267 uced by a number of chemotherapeutic agents (camptothecin, staurosporine, and doxorubicin).

268 mycin C and Irofulven, but not etoposide and camptothecin, suggesting a role in nucleotide excision r

269 colocalizes with Rad22 in cells treated with camptothecin, suggesting that it has a direct role in re

270 We investigated camptothecin synthesis in Camptotheca acuminata by combi

271 ion stress, came as a top candidate gene for camptothecin synthetic lethality.

272 ovided optimal Top1 inhibitors equipotent to camptothecin that demonstrate low nanomolar cytotoxiciti

273 ER dramatically increased cell resistance to camptothecin that induced damage required ATM to facilit

274 d in tumours, and the chemotherapeutic agent camptothecin) that self-assemble in situ into a supramol

275 ensitivity to DNA damaging agents, including camptothecin, that cause replication fork breakage.

276 Of note, distinct from camptothecin, the Top1cc produced by 4NQO accumulate pro

277 After induction of apoptosis by H. pylori or camptothecin, there was a 5-fold increase in the binding

278 -dimethylbenz[alpha]anthracene (mutagen) and camptothecin (topoisomerase inhibitor), as well as to ag

279 Here, we undertook genome-wide analysis of camptothecin-treated cells at exon resolution.

280 s, we show that the response of H23 cells to camptothecin treatment is unaffected by changes in intra

281 Genotoxic stress induced by camptothecin treatment of NPCs stabilized p53, which for

282 mia cells are exposed to the same dual-pulse camptothecin treatment regimen.

283 Most importantly, cell viability data after camptothecin treatment showed responses that were drug-d

284 NA damage response to uncapped telomeres and camptothecin treatment, in a manner that suggests Exo1 p

285 308 localizes to replication forks following camptothecin treatment.

286 d carcinogenic DNA lesions, base damage, and camptothecin treatment.

287 D silencing reduced: the ssDNA fraction upon camptothecin treatment; AsiSI-induced DSB resection; and

288 hanced in sae2Delta or mre11-3 mutants after camptothecin treatment; both of these mutants are defect

289 Dynamic rheological studies showed that camptothecin was encapsulated within the hydrogel networ

290 ignificantly more stable than those in which camptothecin was incorporated.

291 is the target for the anticancer activity of camptothecins, we assessed TOP1 transcript levels in the

292 to be unrepairable although DSBs induced by camptothecin were efficiently removed in the progeroid c

293 Treatment with camptothecin which transiently stabilized nucleolar R-lo

294 ed sensitivity to UV light, hydroxyurea, and camptothecin, which are known activators of ATR (ataxia-

295 Unlike camptothecin, which binds at the TOP1-DNA interface to f

296 a mechanism distinct from compounds like the camptothecins, which interact at the site of cleavage.

297 elective killing of p53-deficient cells with camptothecin while sparing isogenic p53-positive cells.

298 0(S)-O-propionate hydrate (CZ48) by reacting camptothecin with propionic anhydride using concentrated

299 ces resistance to the topoisomerase 1 poison camptothecin yet hypersensitizes cancer cells to doxorub

300 umerous other drugs that bind tubulin and to camptothecin, yet this mutant was sensitive to nocodazol