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 tivated B cells (NF-kappaB), caspase 3/9 and DNA fragmentation.

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

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

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

6 ric TUNEL System was used to observe nuclear DNA fragmentation.

7 induce apoptotic chromatin condensation and DNA fragmentation.

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

9 y increased caspase 3 activity and increased DNA fragmentation.

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

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

12 eath, which accompanies ROS accumulation and DNA fragmentation.

13 stalled DNA replication forks, and apoptotic DNA fragmentation.

14 apoptosis, assessed by Hoechst staining and DNA fragmentation.

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

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

17 hydrogenase release, caspase activation, and DNA fragmentation.

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

19 denced by caspase activation and nucleosomal DNA fragmentation.

20 rase chain reaction assays, and reproducible DNA fragmentation.

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

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

23 dephosphorylation, caspase-3 activation and DNA fragmentation.

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

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

26 fraction and cytoplasmic histone-associated DNA fragmentation.

27 e, which also accounts for increase in sperm DNA fragmentation.

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

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

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

31 olved in inducing chromatin condensation and DNA fragmentation.

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

33 art failure, without completion of apoptotic DNA fragmentation.

34 mitochondrial transmembrane potential and by DNA fragmentation.

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

36 hat arrested in G2 and underwent significant DNA fragmentation.

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

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

39 endothelial binding and marked reduction of DNA fragmentation.

40 ion, phosphatidylserine externalization, and DNA fragmentation.

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

42 membrane blebbing, nuclear condensation, and DNA fragmentation.

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

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

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

46 membrane blebbing, nuclear condensation and DNA fragmentation.

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

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

49 was evaluated by activation of caspases and DNA fragmentation.

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

51 hout displaying concomitant internucleosomal DNA fragmentation.

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

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

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

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

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

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

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

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

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

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

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

63 the actin cytoskeleton of the gut cells and DNA fragmentation analyses by agarose gel electrophoresi

64 DNA fragmentation analysis further supports that cell de

65 DNA fragmentation and active caspase-3 were measured by

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

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

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

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

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

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

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

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

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

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

76 Evaluation of DNA fragmentation and chromatin condensation revealed th

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

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

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

80 posure to DEHP and/or PCB153 alone increased DNA fragmentation and decreased motility, the scale of d

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

82 DNA fragmentation and ethidium bromide/acridine orange (

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

84 Cell lysis, DNA fragmentation and immunoaffinity purification of the

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

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

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

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

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

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

91 and polychlorinated biphenyl 153 (PCB153) on DNA fragmentation and motility in human and dog sperm.

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

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

94 Increased DNA fragmentation and potential modulation of caspase-3,

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

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

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

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

99 existing approaches, limited by reliance on DNA fragmentation and short-read sequencing, cannot prov

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

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

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

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

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

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

120 9 and caspase-3 activation, internucleosomal DNA fragmentation, and cytochrome c release.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

135 concentration, motility, morphology, volume, DNA fragmentation, and total motile sperm count) at 6 mo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 cell shrinkage, cytoplasm condensation, and DNA fragmentation, can be detected by temporal diffusion

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

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

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

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

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

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

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

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

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

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

167 ed cell death (PCD) that is characterized by DNA fragmentation, chromatin condensation, cellular swel

168 8, is activated, and its inhibition prevents DNA fragmentation, consistent with involvement of a mito

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

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

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

172 DNA fragmentation detected by TUNEL staining could be in

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

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

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

176 assay utilizing the unique properties of the DNA fragmentation factor (DFF) coupled with sequencing o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 Biological and chemical DNA fragmentation generates DNA molecules with a variety

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

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

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

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

196 of each chemical (DEHP.PCB interaction for: DNA fragmentation; human p < 0.001, dog p < 0.001; Motil

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

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

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

200 e cellular uptake, cytochrome c release, and DNA fragmentation in a label-free 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 lementation (mean of 29.7% for percentage of DNA fragmentation in the folic acid and zinc group and 2

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

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

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

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

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

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

227 s the extent to which measurement of a sperm DNA fragmentation index (DFI) can predict sperm quality

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

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

230 only 1 day incubation, while the absence of DNA fragmentation indicates a low level of nonselective

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

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

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

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

235 DNA fragmentation is a hallmark of apoptosis (programmed

236 Although DNA fragmentation is an evolutionarily conserved process

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

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

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

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

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

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

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

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

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

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

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

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

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

250 ssibility of TF binding sites from cell-free DNA fragmentation patterns.

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

252 Alternative DNA fragmentation processes approximately 10% of the nan

253 re significantly lower, while means of sperm DNA fragmentation, protamine deficiency, and lipid perox

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

255 gressive motility negatively correlated with DNA fragmentation regardless of chemical presence (Human

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

257 Inhibition of apoptotic DNA fragmentation resulted in increased clonogenic survi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

278 DNA fragmentation, TUNEL-positive neurons, cleaved caspa

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

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

283 A statistically significant increase in DNA fragmentation was observed with folic acid and zinc

284 DNA fragmentation was positively correlated with PD and

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

286 DNA fragmentation was significantly increased at 24 hour

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