ライフサイエンスコーパス: PARP cleavage

1 on of caspases, and IETD similarly prevented PARP cleavage.

2 activation of procaspase-9, procaspase-3 and PARP cleavage.

3 ytochrome c release, caspase-3 activity, and PARP cleavage.

4 l lines resulted in apoptosis as measured by PARP cleavage.

5 ition of Ac-YVAD-cho to the cultures blocked PARP cleavage.

6 D437 did not induce caspase-3 activation and PARP cleavage.

7 l the activation of caspases as indicated by PARP cleavage.

8 k activity and markedly increased TG-induced PARP cleavage.

9 or cells; and activated caspase-3 leading to PARP cleavage.

10 is-Asp(O-methyl)-fluoromethylketone prevents PARP cleavage.

11 methacrylate) stimulates TPT-induced PCD and PARP cleavage.

12 duced apoptosis, activation of SAPK/JNK, and PARP cleavage.

13 sistant cells to AZD6244 by inducing BIM and PARP cleavage.

14 This cleavage occurs shortly after PARP cleavage.

15 stages of apoptosis in this system and after PARP cleavage.

16 ble-strand breaks, caspase-8 activation, and PARP cleavage.

17 optosis were identified by TUNEL labeling or PARP cleavage.

18 from mitochondria, caspase-3 activation and PARP cleavage.

19 pontaneous and fludarabine-induced Mcl-1 and PARP cleavage.

20 stic induction of caspases-3, -8, and -9 and PARP cleavage.

21 totic phenotype as revealed by caspase-3 and PARP cleavage.

22 e coupled with increased Bax/Bcl-2 ratio and PARP cleavage.

23 tion of caspase-3, caspase-8, caspase-9, and PARP cleavage.

24 xin-V/PI staining, caspase-3 activation, and PARP cleavage.

25 by pycnotic nuclei, annexin V staining, and PARP cleavage.

26 nfection led to a reduction in the amount of PARP cleavage.

27 ges in mitochondrial membrane potential, and PARP cleavage.

28 X suppressed ERK and p38 phosphorylation and PARP cleavage.

29 ase-8, caspase-9, and caspase-3, followed by PARP cleavage.

30 Annexin-V staining, caspase-3 activation and PARP cleavage.

31 t transactivation and induction of TRAIL and PARP cleavage.

32 ed with enhanced procaspase (3, 8 and 9) and PARP cleavage.

33 spase-3 activity, cleavage of caspase-3, and PARP cleavage.

34 optosis, cell surface Annexin V staining and PARP cleavage.

35 membrane potential, caspase activation, and PARP cleavage.

36 is by DNA damage, resulting in caspase-3 and PARP cleavage.

37 AD, the pancaspase inhibitor, suppressed the PARP cleavage.

38 ctivation of terminal caspases, resulting in PARP-cleavage.

39 f caspases, and poly(ADP-ribose) polymerase (PARP) cleavage.

40 activation, and poly(ADP-ribose) polymerase (PARP) cleavage.

41 yadenosine-5'-diphosphate-ribose polymerase (PARP) cleavage.

42 tress based on poly (ADP-ribose) polymerase (PARP) cleavage.

43 laddering and poly (ADP-ribose) polymersae (PARP) cleavage.

44 of Fas- induced poly-ADP ribose polymerase (PARP) cleavage.

45 rmed by assay of poly ADP-ribose polymerase (PARP) cleavage.

46 as well as with poly(ADP)ribose polymerase (PARP) cleavage.

47 se activity and poly(ADP-ribose) polymerase (PARP) cleavage.

48 activation and poly-(ADP-ribose) polymerase (PARP) cleavage.

49 and (TRAIL) and poly(ADP-ribose) polymerase (PARP) cleavage.

50 d detection of poly (ADP-ribose) polymerase (PARP) cleavage.

51 d poly (adenosine diphosphate [ADP]) ribose (PARP) cleavage.

52 substrates and poly (ADP ribose) polymerase (PARP) cleavage.

53 and Dex induce poly (ADP ribose) polymerase (PARP) cleavage, a signature event of apoptosis.

54 hibitor blocked ATM phosphorylation, induced PARP cleavage, abrogated cell cycle checkpoint activatio

55 ce of dopamine-stimulated apoptosis included PARP cleavage, activation of mitochondrial-derived caspa

56 unoblotting for poly(ADP-ribose) polymerase [PARP] cleavage; activation of caspases-3, -8, and -9; ex

57 po B- or Apo-2L/TRAIL-induced processing and PARP cleavage activity of caspase-3.

58 greater cytosolic accumulation of cyt c and PARP cleavage activity of caspase-3.

59 Marked caspase-3-like PARP cleavage activity, proteolytic processing of CPP32

60 ted significant poly(ADP-ribose) polymerase (PARP) cleavage after exposure to Stx1 or Stx2.

61 ath receptor DR5 led to complete ablation of PARP cleavage and apoptosis, indicating the essential ro

62 avage of procaspase 3, 8, and 9 and enhances PARP cleavage and apoptosis.

63 siRNA) in C4-2 cells significantly prevented PARP cleavage and apoptosis.

64 RA synovial fibroblasts to TNFalpha-induced PARP cleavage and apoptotic cell death.

65 Furthermore, PARP cleavage and caspase activation were confined exclu

66 sed ratio of cells in the subG1 phase and by PARP cleavage and caspase activation.

67 lls also generated apoptosis as reflected by PARP cleavage and DNA fragmentation indicating a cell su

68 e of cytochrome c, caspase-3 activation with PARP cleavage and DNA fragmentation.

69 static human mammary tumor, was resistant to PARP cleavage and loss of viability in response to actin

70 formed cells, as evidenced by an increase in PARP cleavage and partial inhibition of this effect by t

71 ERK activity potentiated paclitaxel-induced PARP cleavage and phosphatidylserine externalization, su

72 ition of JNK, p38 MAPK, or MEK did not alter PARP cleavage and the cell death induced by paclitaxel.

73 fragmentation, poly (ADP-ribose) polymerase (PARP) cleavage and activation of caspase-3 and -8.

74 ed caspase-3 and poly(ADP)ribose polymerase (PARP) cleavage and apoptosis (>50% 2 micromol/L, 48 h).

75 nduce elevated poly (ADP-ribose) polymerase (PARP) cleavage and apoptosis.

76 ly(adenosine diphosphate-ribose) polymerase (PARP) cleavage and cleavage of caspase-3 substrates, sug

77 with increased poly(ADP-ribose) polymerase (PARP) cleavage and cytochrome c release was observed in

78 splayed elevated poly ADP-ribose polymerase (PARP) cleavage and susceptibility to camptothecin-induce

79 injury, activation of procaspases-3 and -8, PARP cleavage, and apoptosis.

80 s, as indicated by histology, DNA laddering, PARP cleavage, and caspase-3 activation.

81 as evidenced by induction of DNA laddering, PARP cleavage, and caspase-3/9 activities.

82 G2 arrest, leading to caspase-3 activation, PARP cleavage, and cell apoptosis.

83 by increases in Annexin V binding activity, PARP cleavage, and chromatin disorganization.

84 c, but it did prevent caspase-3 activation, PARP cleavage, and DNA fragmentation.

85 ase of cytochrome c, caspase activation with PARP cleavage, and DNA fragmentation.

86 rome c but did prevent caspase-3 activation, PARP cleavage, and DNA fragmentation.

87 r UV treatment, as measured by caspase-7 and PARP cleavage, and IGF-I co-treatment protected against

88 CH2F prevented caspase activation, inhibited PARP cleavage, and inhibited cell death.

89 uces apoptosis by activating caspase 3/7 and PARP cleavage, and its longer exposure causes increase i

90 fied which involved procaspase-7 activation, PARP cleavage, and nuclear condensation.

91 n caused significantly greater caspase-3 and PARP cleavage, and the combined toxicity also was inhibi

92 ced DNA fragmentation, cytochrome c release, PARP cleavage, and the formation of active caspase 3.

93 w pI) release), poly(ADP-ribose) polymerase (PARP) cleavage, and apoptosis.

94 denosine 5'-diphosphate]-ribose) polymerase (PARP) cleavage, and apoptotic cell death.

95 ochrome c (CC), poly(ADP-ribose) polymerase (PARP) cleavage, and DNA fragmentation.

96 on of caspase-3, poly(ADP-ribose)polymerase (PARP) cleavage, and DNA fragmentation.

97 h caspase-3 and poly(ADP-ribose) polymerase (PARP) cleavage, and inhibited constitutive activation of

98 procaspase-3 and poly(ADP-ribose)polymerase (PARP) cleavage, and reduced p53 and p21 levels.

99 ansferase dUTP nick-end labeling positivity, PARP cleavage, Annexin V positivity, and drug-induced ce

100 5 inhibited 2-ME-induced caspase activation, PARP cleavage, apoptosis and reversed mitochondrial memb

101 nt effects on Akt phosphorylation, caspase-3/PARP cleavage, apoptotic phenotype, and cell viability,

102 caspases activity increase and caspases and PARP cleavage as well as a lack in cytochrome c release

103 In contrast, zVAD-FMK blocked PARP cleavage as well as loss of delta psi(m) and cell d

104 sub-G(1) phase cells; caspase-3 and -9, and PARP cleavage as well as morphological signs of apoptosi

105 on and enhanced poly(ADP-ribose) polymerase (PARP) cleavage as a result of bortezomib, in the presenc

106 as found to induce nuclear fragmentation and PARP cleavage, as well as to arrest cells at the G(2)/M

107 signaling-p53 increase, AMPK activation, and PARP cleavage-as well as autophagy induction were also i

108 f oligomer induced apoptosis, according to a PARP-cleavage assay.

109 oly-adenosine diphosphate ribose polymerase (PARP) cleavage at low concentrations of EGCG (3 microg/m

110 In contrast, caspase inhibitors prevented PARP cleavage but not cytochrome c release, suggesting t

111 these events (e.g. caspase-3 activation and PARP cleavage) but did not block cytochrome c release or

112 Z-VAD-FMK inhibits PARP cleavage, but does not alter the AGN193198-dependen

113 The 24-kDa product of PARP cleavage by caspase-3 may contribute to the irrever

114 TM small-molecule inhibitors that attenuated PARP cleavage by inhibiting gamma-H2AX, which in turn in

115 The prevention of PARP cleavage by inhibition of caspase-3 resulted in a 1

116 deprivation for 4 h increased cell death and PARP cleavage by promoting activation of caspase-8 and c

117 , methotrexate) caused minimal caspase-3 and PARP cleavage by themselves, and their toxicity was not

118 se of measuring poly(ADP-ribose) polymerase (PARP) cleavage by Western blot, as an index of apoptosis

119 roteins, cdc6, MCM2, cdc25A, nor increase in PARP cleavage, caspase activation and the 30-300 kb DNA

120 1 and Gli2 expression and induced gammaH2AX, PARP cleavage, caspase-3 activation, and cell death.

121 ilization, cytochrome c release, caspase and PARP cleavage, consistent with the hypothesis that p38(M

122 Whereas PARP cleavage defined cell death in most other cell type

123 lls with zAPFcmk alone led to characteristic PARP cleavage, depletion of the precursor forms of two I

124 d apoptosis as demonstrated by caspase-3 and PARP cleavage, DNA fragmentation, and nuclear condensati

125 Asp-fluoromethylketone (Z-VAD-fmk) inhibited PARP cleavage, DNA fragmentation, calpain activation, an

126 ivation and Bax cleavage but did not inhibit PARP cleavage, DNA fragmentation, or 9-amino-20(S)-campt

127 tely prevented poly (ADP-ribose) polymerase (PARP) cleavage, E(2)-inhibited growth, and apoptotic mor

128 spase-3/CPP32 and caspase-7/Mch3 followed by PARP cleavage, effects that can be blocked either by SPP

129 poptosis as determined by DNA fragmentation, PARP cleavage, fluorescence microscopy and flow cytometr

130 PARP cleavage followed caspase activation and reached ma

131 trophy was also confirmed by the presence of PARP cleavage (H: 74+/-7 versus T: 41+/-4 arbitrary dens

132 optosis was determined by TUNEL staining and PARP cleavage (immunoblotting of nuclear extracts) and c

133 caspase-3 activation, and partially reduced PARP cleavage in a concentration-dependent manner.

134 The role of PARP cleavage in apoptosis has now been investigated in

135 targeted Bak leads to enhanced caspase 7 and PARP cleavage in comparison with the ER-targeted Bak.

136 viral MET RNA interference construct induces PARP cleavage in MM.1S cells.

137 ulation of sub-G(1) population and block the PARP cleavage in response to etoposide.

138 nM, and triggers activation of caspases and PARP cleavage in the MDA-MB-231 breast cancer cell line.

139 Patients having caspase-3 activation and PARP cleavage in vivo had a significantly lower blood le

140 caspase-3, and poly(ADP-ribose) polymerase (PARP) cleavage in blood leukemia cells immediately follo

141 Bid and protein poly(ADP-ribose) polymerase (PARP) cleavage in HeLa cells lacking MTS-hOGG1.

142 agmentation and poly(ADP-ribose) polymerase (PARP) cleavage in LA-treated MCF10A cells indicated prog

143 did not induce poly(ADP-ribose) polymerase (PARP) cleavage in virus-negative BJAB cells.

144 ulation of MAP and p70S6K growth kinases and PARP cleavage; in contrast, IL-6 does not inhibit IR-ind

145 JNK activation and PARP cleavage induced by 30 nM Taxotere at 48 h were rev

146 elation between both assays, indicating that PARP cleavage is an accurate method to examine PCD.

147 B3(Fv)-PE38-induced PARP cleavage is inhibited by several protease inhibitor

148 after nsPEF and poly-ADP ribose polymerase (PARP) cleavage is detected in 2 hr.

149 CPV gave no PARP-cleaving activity, and all PARP cleavage mediated by SPI-2 and CrmA mutants of RPV

150 These data demonstrate that PARP cleavage occurs during glucocorticoid-induced apopt

151 Like PARP, cleavage of these substrates in apoptotic cell ext

152 Bax cleavage and calpain activation, but not PARP cleavage or cell death.

153 ng and lysis of DHL-4 cells, without caspase/PARP cleavage or TUNEL-positivity, suggesting a necrotic

154 Conversely, propidium iodide staining, PARP cleavage patterns, and random DNA fragmentation rev

155 with increased poly(ADP-ribose) polymerase (PARP) cleavage, phosphatidylserine externalization, and

156 ated prior to the detection of caspase 3 and PARP cleavage, primary indicators of cell death, whereas

157 nstrated by an obvious increase of the 89-kD PARP cleavage product, which was observed at almost the

158 and cyclin D1, whereas caspase activity and PARP cleavage products were increased in tumors of drug-

159 id not recognize the Mr approximately 90,000 PARP cleavage products, in contrast to the parent enzyme

160 h DEVD inhibited the chromatin condensation, PARP cleavage, release of apoptotic bodies, and release

161 creased and prolonged caspase 3 activity and PARP cleavage, suggesting that the sensitization to TRAI

162 anoikis involved caspase-3- and -7-mediated PARP cleavage that was initiated by caspase-8 and probab

163 pase-8, caspase-9, and caspase-3 activation, PARP cleavage, upregulation of Fas-L, Fas, FADD and DR4,

164 Reduced PARP cleavage was also observed in cells treated with tu

165 PARP cleavage was not delayed in XPD LCLs in response to

166 st, a slight, but significant enhancement of PARP cleavage was observed in dephosphorylated extracts,

167 The timing and intensity of PARP cleavage was similar to that of JNK activation.

168 poly(ADP-ribose) polymerase (PARP) cleavage was noted in all Kit mutant lines after i

169 into the cytosol, caspase 3 activation, and PARP cleavage were also detected in these cells.

170 Activation of multiple caspases and PARP cleavage were also observed in the C4-2 tumors trea

171 thamphetamine-induced caspase-3 activity and PARP cleavage were also reduced in c-Jun heterozygous kn

172 induced apoptosis, caspase-8 activation, and PARP cleavage were inhibited by knocking down DR5 using

173 Furthermore, DNA ladder formation and PARP cleavage were observed after treatment for 24 h, in

174 DNA ladder formation, CPP32 activation, and PARP cleavage were observed after treatment with geniste

175 s, in which increased caspase-3 activity and PARP cleavage were observed, but not in PC-3 cells, in w

176 ivity as well as poly-ADP ribose polymerase (PARP) cleavage were increased.

177 the induction of poly-ADP-ribose polymerase (PARP) cleavage were more pronounced and evident 12 h ear

178 er formation and poly-ADP ribose polymerase (PARP) cleavage were performed to measure the induction o

179 , decrease of Bax expression and increase of PARP cleavage) were blocked by the purinergic P2X(7) rec

180 ese drugs also did not increase caspase-3 or PARP cleavage when combined with TRAIL.

181 sub-G(0)/G(1) phase, caspase activation, and PARP cleavage), whereas cells harboring wild-type (wt)-F

182 r with AZD6244 induced expression of BIM and PARP cleavage, whereas activation of the STAT3 pathway i

183 lketone, inhibited PDT-induced apoptosis and PARP cleavage, whereas the inactive peptide analogue, be

184 1 h and induced activation of caspase 3 and PARP cleavage within 24 h.