ライフサイエンスコーパス: camptothecin

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

2 particles of comparable dimensions made from camptothecin.

3 cells upon treatment with DNA damaging agent camptothecin.

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

5 A crosslinking agents, alkylating agents and camptothecin.

6 itomycin C and the topoisomerase-1 inhibitor camptothecin.

7 rs cellular resistance to DNA crosslinks and camptothecin.

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

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

10 P2 inhibition but also by the TOP1 inhibitor camptothecin.

11 ll resistance to the chemotherapeutic agent, camptothecin.

12 rvival in response to ionizing radiation and camptothecin.

13 notoxic stresses, such as UVC irradiation or camptothecin.

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

15 range of hypersensitivities to the toposide camptothecin.

16 ochondria from human cells were treated with camptothecin.

17 and religation activities in the absence of camptothecin.

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

19 lin was markedly longer than by etoposide or camptothecin.

20 with the specific topoisomerase I inhibitor camptothecin.

21 ctivity relationships for the 11-position of camptothecin.

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

23 of endogenous ARF causes desensitization to camptothecin.

24 NA-damaging antitumor agents doxorubicin and camptothecin.

25 n could contribute to cellular resistance to camptothecin.

26 prolonged G2 arrest, and hypersensitivity to camptothecin.

27 en more dramatic increase in the presence of camptothecin.

28 DNA damage induced by ionizing radiation or camptothecin.

29 after exposure to the S phase specific drug, camptothecin.

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

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

32 se population as compare to positive control camptothecin.

33 apoptosis induced by the DNA-damaging agent camptothecin.

34 but not to hydroxyurea, neocarzinostatin, or camptothecin.

35 hSSB1 being required for survival to HU and camptothecin.

36 le GSK3beta inhibitors and anti-cancer agent camptothecin.

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

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

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

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

41 3d inhibited 47% Topo I (camptothecin, 34%) and 20% Topo II (etoposide 24%) at 20

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

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

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

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

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

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

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

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

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

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

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

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

54 topoisomerase I activity in the presence of camptothecin analogs.

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

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

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

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

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

60 o acid ester prodrugs of the antitumor agent camptothecin and a more potent, lipophilic silatecan ana

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

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

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

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

65 ar S-phase arrest as wt cells in response to camptothecin and aphidicolin does not abrogate the enhan

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

67 e clinically significant DNA damaging agents camptothecin and cisplatin.

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

69 Camptothecin and doxorubicin treatment caused activation

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

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

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

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

74 While camptothecin and H2O2 both induce DDR activation, nitric

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

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

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

78 Camptothecin and its derivatives, topotecan and irinotec

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

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

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

82 Despite its structural resemblance to camptothecin and luotonin A, a biological evaluation of

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

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

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

86 Camptothecin and taxane-based regimens combined with rad

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

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

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

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

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

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

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

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

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

96 DNA topoisomerase I (Top1) is the target of camptothecin, and novel Top1 inhibitors are in developme

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

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

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

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

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

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

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

104 +/- 0.05 muM), and it was also equipotent to camptothecin as a Top1 inhibitor.

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

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

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

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

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

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

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

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

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

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

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

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

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

118 H(2)O(2)), methyl methanesulfonate (MMS), or camptothecin by monitoring NAD(P)H.

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

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

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

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

123 Cells lacking Tdp1 are hypersensitive to camptothecin, consistent with a role for Tdp1 in process

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

169 (5-FU), 5-fluoro-2'-deoxyuridine (FUDR), and camptothecin (CPT).

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

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

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

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

174 lls treated with the topoisomerase inhibitor camptothecin (CPT).

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

176 unctional, polymeric nanoparticle containing camptothecin (CPT).

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

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

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

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

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

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

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

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

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

186 ramolecular nucleophilic amine attack at the camptothecin E-ring carbonyl to generate a lactam (I) fo

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

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

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

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

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

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

193 The pharmacological camptothecin feeding experiment and cell death analysis

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

195 Liposome formulations of camptothecins have been actively pursued because of the

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

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

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

199 omic instability and therapeutic response to camptothecins in colorectal cancers.

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

201 5) Camptothecin increases cellular ATP levels, whereas infl

202 Resistance to camptothecin, indenoisoquinoline, aphidicolin, hydroxyur

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

204 Many agents (e.g. camptothecins, indolocarbazoles, indenoisoquinolines, an

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

206 Camptothecin-induced activation of caspase-3 was reduced

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

208 Camptothecin-induced apoptosis markedly increased subseq

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

210 1-methyl-4-phenylpyridinium-, glutamate-, or camptothecin-induced cell death.

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

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

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

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

215 hydroxystaurosporine (UCN-01) also increases camptothecin-induced gammaH2AX formation and inhibits ca

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

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

218 cin-induced gammaH2AX formation and inhibits camptothecin-induced p21(CDKN1A) upregulation in HCT116

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

223 Similarly, camptothecin-induced upregulation of TAF1-3 and TAF1-4 s

224 Camptothecin inhibited the Zta transcription activation

225 Camptothecin is a monoterpene indole alkaloid (MIA) used

226 Camptothecin is a potent anticancer agent producing well

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

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

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

230 Camptothecins kill mammalian cells by stabilizing topois

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

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

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

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

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

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

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

238 The conversion of prodrugs of camptothecin or DB-67 containing either alpha-NH(2) or a

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

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

241 concentration range enhanced the effects of camptothecin or etoposide.

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

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

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

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

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

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

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

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

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

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

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

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

254 ed experimentally and the timing of a second camptothecin pulse is shown to significantly alter the o

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

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

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

258 wild-type (wt) p53, gammaH2AX reverses after camptothecin removal.

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

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

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

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

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

264 Camptothecin-stabilized topoisomerase I-DNA cleavage int

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

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

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

268 We investigated camptothecin synthesis in Camptotheca acuminata by combi

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

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

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

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

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

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

275 indenoisoquinolines represent a class of non-camptothecin topoisomerase I (Top1) inhibitors that exer

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

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

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

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

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

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

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

283 t DNA-PKcs phosphorylation is increased upon camptothecin treatment, which induces replication stress

284 308 localizes to replication forks following camptothecin treatment.

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

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

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

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

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

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

291 Treatment with camptothecin which transiently stabilized nucleolar R-lo

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

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

294 breaks, we examined checkpoint responses to camptothecin, which induces replication-mediated DNA dou

295 itive than BLM-complemented cells (PNSF5) to camptothecin, which specifically traps topoisomerase I c

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