ライフサイエンスコーパス: DNA fragmentation

1 d dUTP nick-end labeling positive nuclei and DNA fragmentation).

2 caspase-3 activation, Hoechst staining, and DNA fragmentation.

3 y increased caspase 3 activity and increased DNA fragmentation.

4 spase activation and annexin V binding or by DNA fragmentation.

5 EITC-mediated autophagy as well as apoptotic DNA fragmentation.

6 eath, which accompanies ROS accumulation and DNA fragmentation.

7 stalled DNA replication forks, and apoptotic DNA fragmentation.

8 apoptosis, assessed by Hoechst staining and DNA fragmentation.

9 we recorded a drastic increase in cells with DNA fragmentation.

10 ated DMNQ-induced caspase-3/7 activation and DNA fragmentation.

11 amate release, NMDA receptor activation, and DNA fragmentation.

12 hydrogenase release, caspase activation, and DNA fragmentation.

13 ytochrome c release, caspase activation, and DNA fragmentation.

14 denced by caspase activation and nucleosomal DNA fragmentation.

15 linositol-3,4,5-trisphosphate and suppresses DNA fragmentation.

16 by monitoring the cleavage of caspase-3 and DNA fragmentation.

17 dephosphorylation, caspase-3 activation and DNA fragmentation.

18 ering them less vulnerable to stress-induced DNA fragmentation.

19 t with reduction of caspase 3 activation and DNA fragmentation.

20 tochrome c release, caspase-3 activation and DNA fragmentation.

21 fraction and cytoplasmic histone-associated DNA fragmentation.

22 on of JNK and caspase-3 as well as decreased DNA fragmentation.

23 nonical site is required for caspase-induced DNA fragmentation.

24 r, these breaks are not related to apoptotic DNA fragmentation.

25 olved in inducing chromatin condensation and DNA fragmentation.

26 o-2'-deoxyguanosine (8-oxo-dG) formation and DNA fragmentation.

27 art failure, without completion of apoptotic DNA fragmentation.

28 mitochondrial transmembrane potential and by DNA fragmentation.

29 ore constantly binds to DFF/CAD and inhibits DNA fragmentation.

30 hat arrested in G2 and underwent significant DNA fragmentation.

31 ese are followed by caspase-3 activation and DNA fragmentation.

32 doses induced ER stress and caspase-mediated DNA fragmentation.

33 endothelial binding and marked reduction of DNA fragmentation.

34 ion, phosphatidylserine externalization, and DNA fragmentation.

35 (PS) translocation, caspase activation, and DNA fragmentation.

36 wing CsA treatment was accompanied by marked DNA fragmentation.

37 oramphenicol-treated bacteria did not induce DNA fragmentation.

38 hate [ADP]-ribose polymerase), and increased DNA fragmentation.

39 th caspase-3 activity and histone-associated DNA fragmentation.

40 on of caspase-8 and caspase-3, and increased DNA fragmentation.

41 he latter stages of apoptosis in response to DNA fragmentation.

42 idation of proteins, lipid peroxidation, and DNA fragmentation.

43 membrane blebbing, nuclear condensation and DNA fragmentation.

44 on was accompanied by G0/G1 phase arrest and DNA fragmentation.

45 c pathway that is post-Caspase 3, but before DNA fragmentation.

46 was evaluated by activation of caspases and DNA fragmentation.

47 d etoposide- and UV/gamma radiation-mediated DNA fragmentation.

48 hout displaying concomitant internucleosomal DNA fragmentation.

49 membrane blebbing, nuclear condensation, and DNA fragmentation.

50 y increased caspases-9 and -3 activities and DNA fragmentation.

51 protein (CHOP) but did not lead to apoptotic DNA fragmentation.

52 ochrome c release, caspase-3 activation, and DNA fragmentation.

53 induce apoptotic chromatin condensation and DNA fragmentation.

54 nel nuclear staining of cells with apoptotic DNA fragmentation (0-100 mug/mL) with no effects in norm

55 Furthermore, DNA fragmentation (119.9 +/- 1.40 vs. 57.5 +/- 0.80; p <

56 We report here that MV induces myonuclear DNA fragmentation (3-fold increase; P<0.01) and selectiv

57 ase-activated DNase (CAD) is responsible for DNA fragmentation, a hallmark event during apoptosis.

58 activated caspase activity, with consequent DNA fragmentation, accumulation of pro-apoptotic protein

59 enhance TRAIL-induced apoptosis as shown by DNA fragmentation, activation of caspase-8 and Bid, and

60 atically increased caspase-3, annexin V, and DNA fragmentation activity.

61 ate and intracellular calcium, and to induce DNA fragmentation after 24 hours of exposure, in line wi

62 ssay revealed that 70% of THP-1 cells showed DNA fragmentation after 4 h of infection, increasing to

63 iver injury with peroxynitrite formation and DNA fragmentation, all of which was attenuated by both t

64 Arrested stamen cells showed no signs of DNA fragmentation, an absence of CYCLIN B expression, an

65 DNA fragmentation analysis further supports that cell de

66 DNA fragmentation and active caspase-3 were measured by

67 cell proliferation, while increasing sub-G0 DNA fragmentation and Annexin V markers of apoptosis.

68 protein and mRNA expression, and apoptosis (DNA fragmentation and annexin V staining) in vitro using

69 ed in chondrocyte apoptosis, as evidenced by DNA fragmentation and annexin V staining.

70 hondria, activated caspase-3/7, and enhanced DNA fragmentation and apoptosis.

71 However, the StEP method does not require DNA fragmentation and can be carried out in a single tub

72 -induced apoptosis as reflected by increased DNA fragmentation and caspase 3 activation.

73 Apoptosis was evaluated by detecting DNA fragmentation and caspase activation.

74 e of cell death was assessed with assays for DNA fragmentation and caspase activation.

75 those cells, as assessed by internucleosomal DNA fragmentation and caspase-3 cleavage.

76 Histone-associated DNA fragmentation and caspase-3/7 activity were signific

77 DNA fragmentation and caspase-8 and -3 activities were m

78 , which was found to significantly attenuate DNA fragmentation and caspase-9 and -3 activation.

79 herapeutic drug cisplatin is associated with DNA fragmentation and cell death.

80 Evaluation of DNA fragmentation and chromatin condensation revealed th

81 tion, and intrinsic apoptosis as assessed by DNA fragmentation and cleaved caspase-9.

82 ity was assessed in vitro by alkaline comet, DNA fragmentation and DAPI staining assays.

83 from very well preserved samples, where both DNA fragmentation and deamination have been limited.

84 he entire molecular process from post-mortem DNA fragmentation and DNA damage to experimental sequenc

85 DNA fragmentation and ethidium bromide/acridine orange (

86 Apoptosis was confirmed by cell morphology, DNA fragmentation and flow cytometry.

87 Cell lysis, DNA fragmentation and immunoaffinity purification of the

88 t fibronectin inhibits apoptosis by reducing DNA fragmentation and inhibiting the activities of caspa

89 sistent with the involvement of CAD in 50-kb DNA fragmentation and its Ca(2+) independence.

90 d angiogenic network formation, and promoted DNA fragmentation and laddering in U87MG and U118MG cell

91 ction of caspase-3-like activity followed by DNA fragmentation and loss of cell viability.

92 , and caspase-7, and significantly increased DNA fragmentation and M30-positive RPE cells.

93 on P37 displayed a significant reduction in DNA fragmentation and microglial activation in Enriched

94 onist effect at M1 and M3 mAChRs, leading to DNA fragmentation and neuronal death by apoptosis.

95 ough a TRPV1-mediated pathway that increases DNA fragmentation and p53 expression.

96 method (shotgun proteolysis) based on random DNA fragmentation and protease selection of the encoded

97 on of FOXO3a in HIV-1-infected MDM decreased DNA fragmentation and protected macrophages from death i

98 tment also markedly reduced internucleosomal DNA fragmentation and reduced levels of active caspase 3

99 ge model, but we find no correlation between DNA fragmentation and sample age over the timespans anal

100 n increase in cytoplasmic histone-associated DNA fragmentation and sub-G(0)/G(1)-DNA fraction, and cl

101 ity, which is possibly involved in apoptotic DNA fragmentation and the resolution of stalled DNA repl

102 on to elicit HCE cell apoptosis, detected by DNA fragmentation and TUNEL assays.

103 e, (MTT) whereas apoptosis was determined by DNA fragmentation and TUNEL.

104 ble overexpression of RNase H suppressed the DNA-fragmentation and hypermutation phenotypes.

105 ransbilayer migration of phosphatidylserine, DNA fragmentation, and a general increase in lipid order

106 ernalization of membrane phosphatidylserine, DNA fragmentation, and activation of caspase-3.

107 examined the relationship between G2 arrest, DNA fragmentation, and activation of the apoptotic casca

108 Additionally, markers of apoptosis, DNA fragmentation, and active caspase 3 were increased i

109 Furthermore, activation of microglial cells, DNA fragmentation, and apoptosis of infected or uninfect

110 significantly enhanced caspase-3 activation, DNA fragmentation, and apoptosis.

111 ull DNA-PK activation, gamma-H2AX formation, DNA fragmentation, and apoptotic body formation.

112 tatins decreased germling formation, induced DNA fragmentation, and attenuated damage to endothelial

113 sis was quantified by trypan blue exclusion, DNA fragmentation, and caspase 3 activation.

114 ed colony formation, chromatin condensation, DNA fragmentation, and caspase activation but also indep

115 on, cytoplasmic histone-associated apoptotic DNA fragmentation, and caspase-3 activation compared wit

116 factor withdrawal-induced activation of Bax, DNA fragmentation, and cell death.

117 adhesion kinase (FAK) and p130Cas cleavage, DNA fragmentation, and cell survival assays.

118 totic death, including caspase-3 activation, DNA fragmentation, and chromatin condensation within 72

119 ion, HSV-induced cellular alterations, viral DNA fragmentation, and clearance.

120 condensation, cytoplasmic histone-associated DNA fragmentation, and cleavage of poly-(ADP-ribose)-pol

121 to PEITC-mediated ROS generation, apoptotic DNA fragmentation, and collapse of mitochondrial membran

122 9 and caspase-3 activation, internucleosomal DNA fragmentation, and cytochrome c release.

123 trated by activation of caspase-3, increased DNA fragmentation, and decreased cellular viability.

124 ndrial ROS production, caspase-3/7 activity, DNA fragmentation, and decreased mitochondrial transmemb

125 a its effects on the activation of caspases, DNA fragmentation, and downstream cleavage of lamin A.

126 ew studies of apoptotic regulatory proteins, DNA fragmentation, and gene microarrays to highlight the

127 en species, activation of caspases-3 and -9, DNA fragmentation, and leakage of mitochondrial cytochro

128 tion and delayed Bax and caspase activation, DNA fragmentation, and loss of clonogenic survival.

129 er, 11 and 18 caused chromatin condensation, DNA fragmentation, and loss of mitochondrial membrane po

130 demonstrated by caspase-3 and PARP cleavage, DNA fragmentation, and nuclear condensation.

131 knockout mice was characterized with TUNEL, DNA fragmentation, and nuclear staining assays.

132 This results in caspase activation, DNA fragmentation, and phosphatidylserine externalizatio

133 s blocked Cdt-induced apoptosis, Cdt-induced DNA fragmentation, and phosphorylation of the histone H2

134 ced caspase-3 activation, prevented cellular DNA fragmentation, and suppressed the release of cytochr

135 Retinal cell death was analyzed by DNA fragmentation, and surviving ganglion cells were qua

136 vidence that low dose-rate radiation induced DNA fragmentation, and there was no evidence of double s

137 peptide binding were chromatin condensation, DNA fragmentation, annexin V binding, lamin disruption,

138 tors significantly inhibited MIP-133-induced DNA fragmentation approximately 7 to 12 times in HCE cel

139 uggest that mitochondrial damage and nuclear DNA fragmentation are likely to be critical events in AP

140 The drug had modest effects on DNA fragmentation as a single agent at concentrations th

141 EITC-mediated cytoplasmic histone-associated DNA fragmentation as well as production of reactive oxyg

142 with poly(I:C) (12 h) displayed substantial DNA fragmentation, as detected by terminal deoxynucleoti

143 as efficient as wild-type virus in inducing DNA fragmentation, as judged by terminal deoxynucleotidy

144 nation with ASA on tumor cells, we performed DNA fragmentation assay and immunoblot analysis for poly

145 ST-1 assay, and apoptosis was evaluated with DNA fragmentation assay and M30 assay.

146 dition, morphology of DAPI stained cells and DNA fragmentation assay using gel electrophoresis showed

147 ns were collected at different intervals for DNA fragmentation assay, reverse transcription PCR, West

148 helial cells was determined by caspase-3 and DNA fragmentation assays.

149 evaluated by the activation of caspases and DNA fragmentation assays.

150 death as assessed by Annexin V staining and DNA fragmentation assays.

151 logic criteria (tubular necrosis and in situ DNA fragmentation assessed by the terminal deoxynucleoti

152 wn cells treated with TRAIL revealed similar DNA fragmentation but a marked decrease in apoptotic nuc

153 nhibition of caspase 8 activation suppressed DNA fragmentation but failed to protect macrophages agai

154 Silencing p21 expression reduced levels of DNA fragmentation by 50% in cells treated with bortezomi

155 a factor, which contributes to inhibition of DNA fragmentation by CAD.

156 ore, this combination enhances apoptosis and DNA fragmentation by factors of 2-5 compared with cispla

157 tioxidants inhibited both ROS generation and DNA fragmentation by H. pylori.

158 Ebp1 binds nuclear Akt and prevents DNA fragmentation by inhibiting caspase-activated DNase.

159 itor MG132 completely inhibited IBDV-induced DNA fragmentation, caspase 3 activation, and NF-kappaB a

160 cell lines was associated with increases in DNA fragmentation, caspase activation, GFP-fusion protei

161 t mutant virus induces earlier and increased DNA fragmentation, caspase activity, and NF-kappaB activ

162 ells, TAT-Surv-T34A induced cell detachment, DNA fragmentation, caspase-3 activation and mitochondria

163 mice exhibited apoptotic changes, including DNA fragmentation, caspase-3 activation, and caspase-cle

164 creased the levels of malondialdehyde (MDA), DNA fragmentation, caspase-3 and glutathione reductase (

165 iver functions, decreased the levels of MDA, DNA fragmentation, caspase-3 and GSR activities with an

166 DNA fragmentation, caspase-3/7 activity and cytochrome c

167 exposure produced apoptosis demonstrated by DNA fragmentation, caspase-3/7 activity, cytochrome c re

168 lls, which preceded the internucleosomalsize DNA fragmentation characteristic of late-stage apoptosis

169 8, is activated, and its inhibition prevents DNA fragmentation, consistent with involvement of a mito

170 n substrates, leading to caspase activation, DNA fragmentation, cytoskeletal instability, and rapid i

171 These changes were accompanied by increased DNA fragmentation, decreased high molecular weight mitoc

172 DNA fragmentation/degradation is an important step for a

173 CCL11 and CCL24 protected ASM cells against DNA fragmentation dependent upon p42/44 MAPK activity on

174 DNA fragmentation detected by TUNEL staining could be in

175 endent, and DFF40/CAD-mediated double-strand DNA fragmentation does not warrant the distribution of t

176 h nocodazole, paclitaxel, or 17-AAG) induced DNA fragmentation during early mitosis.

177 athway of apoptosis as determined by genomic DNA fragmentation, extensive mitochondrial fission, acti

178 sponsible for internucleosomal DNA cleavage, DNA fragmentation factor (DFF).

179 Inhibition or loss of the DNA fragmentation factor (DFF)/caspase-activated DNase (

180 DNA fragmentation factor (DFF)/caspase-activated DNase (

181 The apoptotic nuclease, DNA fragmentation factor (DFF40/CAD), is primarily respo

182 AR accumulation was observed upon caspase or DNA fragmentation factor 40 (DFF40) inhibition.

183 ase-3, poly ADP-ribose polymerase (PARP), or DNA fragmentation factor 45 was triggered by PS-341 trea

184 Cidea (cell death-inducing DNA fragmentation factor alpha-like effector A), a membe

185 The cell death-inducing DNA fragmentation factor alpha-like effector c (CIDEC; a

186 cleavage of poly-(ADP-ribose) polymerase and DNA fragmentation factor as well as prevent apoptosis.

187 onizing radiation, suggesting that apoptotic DNA fragmentation factor contributes to genomic stabilit

188 human cancer samples, suggest that apoptotic DNA fragmentation factor is required for the maintenance

189 Here, we show that DNA fragmentation factor plays an important role for mai

190 Once activated, DNA fragmentation factor, 40-kDa subunit (DFF40)/caspase

191 Cell death-inducing DNA fragmentation factor, alpha subunit-like effector A

192 n 27) is a member of the cell death-inducing DNA fragmentation factor-alpha-like effector (CIDE) fami

193 on causes cell cycle deviations, cell death, DNA fragmentation, gamma-H2AX accumulation and C-to-T mu

194 the apoptotic nuclear morphology depends on DNA fragmentation has been questioned.

195 The alternative-sampling coincidence from DNA fragmentation-has not been systematically investigat

196 However, DNA contamination and DNA fragmentation heterogeneity produce false positives

197 No evidence of deoxyribonucleic acid (DNA) fragmentation, however, was identified by immunohis

198 ng, nuclear isolation, chromatin extraction, DNA fragmentation, immunoprecipitation, DNA purification

199 ns of variable length were used to study CMV DNA fragmentation in 20 SOTR plasma samples, viral stock

200 eiotrophin promotes caspase-mediated genomic DNA fragmentation in a dose- and time-dependent manner.

201 duced phosphatidylserine externalization and DNA fragmentation in a manner independent of caspase act

202 hat P. gingivalis induces S. mitis death and DNA fragmentation in an in vitro biofilm system.

203 alized cytosolic Ca(2+) levels and prevented DNA fragmentation in cells expressing Q209L.

204 rane integrity, apoptotic body formation and DNA fragmentation in cultured HepG2 cells.

205 ed poly(ADP-ribose)polymerase 1 cleavage and DNA fragmentation in different extrinsic and intrinsic m

206 in kinase C delta proteolytic activation and DNA fragmentation in dopaminergic cells protected agains

207 se and fails to condense properly or undergo DNA fragmentation in dying nurse cells.

208 ent assays were used to measure apoptosis or DNA fragmentation in GCF and active caspase-3, soluble F

209 attenuated caspase-3 activity and subsequent DNA fragmentation in isolated cerebral microvessels, lea

210 NPI-0052 also induces DNA fragmentation in leukemia lines and in mononuclear c

211 ent enhanced the caspase-3-like activity and DNA fragmentation in MCF-7 cells, and significantly inhi

212 anner with corresponding increased levels of DNA fragmentation in proton-irradiated cells compared wi

213 on of birinapant and TNFalpha induced sub-G0 DNA fragmentation in sensitive lines and birinapant alon

214 r progesterone (P) on days 14-28 had reduced DNA fragmentation in serotonin neurons of the dorsal rap

215 ly(ADP-ribose) polymerase (PARP) and induced DNA fragmentation in slices.

216 Peak nuclear DNA fragmentation in the abnormal LT cohort was also inc

217 Smooth muscle cell DNA fragmentation in the airways of patients with stable

218 ed expression of the Bax protein and nuclear DNA fragmentation in the cerebral cortex of newborn pigl

219 of conformation on speed, and the amount of DNA fragmentation in the device.

220 decrease in histological neuronal damage and DNA fragmentation in the hippocampal CA1 subregion after

221 by inhibiting fungal caspase activation and DNA fragmentation in the murine lung.

222 iated with the shrinkage of their nuclei and DNA fragmentation in the peripheral retina.

223 TUNEL labeling illustrated a higher level of DNA fragmentation in the secondary fiber lens cells of D

224 The level of DNA fragmentation in the suprarenal aorta correlated wit

225 phosphatidylserine by annexin V binding, as DNA fragmentation in the TUNEL assay, and as caspase-3 a

226 tation in the phoP regulatory gene abolished DNA fragmentation in the TUNEL assay.

227 isingly, caspase-3 is not activated prior to DNA fragmentation, in contrast to classical intrinsic or

228 Unexpectedly, DNA fragmentation increased when GADD153 expression was

229 on multiple genomic defects in human sperm [DNA fragmentation index (DFI), chromatin integrity, gene

230 es are equally important in internucleosomal DNA fragmentation (INDF), including the PARP-1-regulated

231 nted MPP(+)-induced caspase-3 activation and DNA fragmentation, indicating that Pin1 plays a proapopt

232 -VAD-fmk and form independently of apoptotic DNA fragmentation, indicating that they do not correspon

233 al studies showed that it is associated with DNA fragmentation induced by an unknown endonuclease.

234 A and EndoG, suggesting that EndoG may cause DNA fragmentation induced by cisplatin.

235 eavage, caspase activation and the 30-300 kb DNA fragmentation induced by SN-38 treatment.

236 Hallmarks included DNA fragmentation, induced gene expression of vacuolar p

237 extract demonstrates that B23 contributes to DNA fragmentation inhibitory activity.

238 DNA fragmentation is a hallmark of apoptosis (programmed

239 Although DNA fragmentation is an evolutionarily conserved process

240 After 12h, DNA fragmentation is substantially increased by querceti

241 d the induction of nuclear and mitochondrial DNA fragmentation, leading to trypanosome destruction.

242 Because DNA fragmentation mediated by DFF40 augmented PARP-1 mod

243 s are able to complete palate fusion without DNA fragmentation-mediated programmed cell death, indica

244 hermore, inactivation of ASF/SF2 also blocks DNA fragmentation normally induced by a variety of apopt

245 th SPER/NO induced such apoptotic markers as DNA fragmentation, nuclear condensation, poly(ADP-ribose

246 ar ROS, mitochondrial membrane collapse, and DNA fragmentation observed in control-treated cells upon

247 However, DNA fragmentation occurred only in H2AX wild-type MEFs.

248 Nuclear DNA fragmentation (ODxmm2) was 147+/-15 in Nx; 797+/-84

249 umor activity by promoting growth arrest and DNA fragmentation of CD30(+) tumor cells.

250 tion, nuclear envelope permeabilization, and DNA fragmentation of the nurse cells are impaired when p

251 o11-1 mutant background failed to rescue the DNA fragmentation of xri1 mutants, suggesting that XRI1

252 No DNA fragmentation or active caspase 3 was observed in co

253 rkinje cells in these animals do not display DNA fragmentation or caspase-3 activation.

254 xel-induced apoptosis evidenced by increased DNA fragmentation, poly (ADP-ribose) polymerase (PARP) c

255 Alternative DNA fragmentation processes approximately 10% of the nan

256 d coronary arteries, there were increases in DNA fragmentation rate and caspase 3/7 activity (indicat

257 owever, the biological function of apoptotic DNA fragmentation remains unclear.

258 Inhibition of apoptotic DNA fragmentation resulted in increased clonogenic survi

259 The cytoplasmic histone-associated DNA fragmentation resulting from WA exposure was signifi

260 gel electrophoresis revealed that 9 induced DNA fragmentation resulting in cell apoptosis.

261 se of apoptosis inducing factor, and nuclear DNA fragmentation resulting in centrilobular necrosis in

262 optotic mitochondrial membrane proteins, and DNA fragmentation, resulting in cell death in part throu

263 ads to mitochondrial dysfunction and nuclear DNA fragmentation, resulting in necrotic cell death.

264 The percent DNA fragmentation results from the paper-based ICP devic

265 , tumors established from cells deficient in DNA fragmentation showed enhanced growth in nude mice.

266 th without activating the caspase cascade or DNA fragmentation, showing that the death pathway is non

267 was found that the major problems are in the DNA fragmentation step and the use of the manifold appar

268 cell death is caspase dependent and displays DNA fragmentation, suggesting that autophagy represents

269 R. oryzae germination, DNA fragmentation, susceptibility to oxidative stress, a

270 with cleaved caspase-3 (CC3) activation and DNA fragmentation (TdT-mediated dUTP nick-end labeling [

271 earrangements in mammals, but not during the DNA fragmentation that accompanies breakdown of the pare

272 The JAM Test is a method that measures the DNA fragmentation that accompanies cell suicide.

273 ephrotoxicity, but it is unknown whether the DNA fragmentation that occurs is produced by DNase I or

274 an increase in 8-hydroxyguanine lesions and DNA fragmentation that signaled PARP-1 activation eviden

275 , externalization of phosphatidylserine, and DNA fragmentation, that ultimately resulted in the progr

276 brary preparation protocol exploits acoustic DNA fragmentation to reduce bias inherent to widely used

277 or antiapoptotic mechanisms was verified by DNA fragmentation (TUNEL) analysis.

278 death as evidenced by annexin V staining and DNA fragmentation (TUNEL) assays.

279 in the left ventricle, as indicated by lower DNA fragmentation, TUNEL-positive staining, and caspase-

280 DNA fragmentation was abolished and the number of TUNEL-

281 DNA fragmentation was demonstrated by LM-PCR in type 1 d

282 and Bcl-2 were analyzed by Western blot and DNA fragmentation was determined by agarose gel electrop

283 of apoptosis are apparent, internucleosomal DNA fragmentation was not detected.

284 ose-dependent effect of Cd on hatching rate, DNA fragmentation was observed in embryos that were expo

285 DNA fragmentation was positively correlated with PD and

286 The PEITC-mediated apoptotic DNA fragmentation was significantly attenuated in the pr

287 DNA fragmentation was used to label apoptotic cells.

288 The appearance of DNA-fragmentation was detected by terminal deoxynucleoti

289 on, and phosphatidylserine translocation and DNA fragmentation were also detected at 48 and 72 hours.

290 BAK (Bcl-2 homologous antagonist/killer) and DNA fragmentation were decreased in gp96-deficient B cel

291 exposure, mitochondrial depolarization, and DNA fragmentation were dramatically reduced in magnitude

292 Caspase-3 activity and DNA fragmentation were measured by enzyme-linked immunos

293 Histone H2AX phosphorylation and DNA fragmentation were suppressed in MST1 knockdown Jurk

294 appaB binding activity, FADD, caspase-8, and DNA fragmentation) were investigated in soleus (predomin

295 erine exposure, chromosome condensation, and DNA fragmentation-when faced with cell death-triggering

296 rylated by PKC, barely binds Akt or inhibits DNA fragmentation, whereas Ebp1 S360D, which mimics phos

297 Additionally, DNA fragmentation, which was evident in cells with reduc

298 sion of MKP-1 reduced caspase activation and DNA fragmentation while enhancing viability in the face

299 of a constitutively active FOXO3a increased DNA fragmentation with decreased cell viability in MDM,

300 Here DNA fragmentation would accelerate extraction and isolat