ライフサイエンスコーパス: procaspase 3

1 otic mechanisms, and decreased activation of procaspase 3).

2 eased expression of the proapoptotic protein procaspase 3.

3 vage of procaspase 8, BID, procaspase 9, and procaspase 3.

4 ly associates with procaspase-7 but not with procaspase-3.

5 H121 and C163, are shifted to higher pH for procaspase-3.

6 t studies demonstrated that these cells lack procaspase-3.

7 s well as the processing of procaspase-9 and procaspase-3.

8 mitochondria induced proteolytic cleavage of procaspase-3.

9 apoptotic protease cascade by activation of procaspase-3.

10 cells when each variable region is fused to procaspase-3.

11 e 2 (TG2), which cross-links and inactivates procaspase-3.

12 r se contributed little to the activation of procaspase-3.

13 n of the active caspase-3 from its precursor procaspase-3.

14 heterodimer that more efficiently activated procaspase-3.

15 than C9Holo for the physiological substrate procaspase-3.

16 fied despite the cytoplasmic localization of procaspase-3.

17 of p21(WAF1/CIP1) coimmunoprecipitating with procaspase-3.

18 by chelation of labile inhibitory zinc from procaspase-3.

19 and ATP (or dATP) resulted in activation of procaspases-3, -6, and -7 but not -2 and -8.

20 n this line, we observed early activation of procaspase-3, -7, and -8, but not -1, -9, and -10.

21 mary CLL cells express high levels of latent procaspases (3, -7, and -9).

22 In addition, the processing of procaspases-3, -7, and -8 into their active forms was ob

23 ll proliferation is associated with enhanced procaspase (3, 8 and 9) and PARP cleavage.

24 raphane treatment also increases cleavage of procaspase 3, 8, and 9 and enhances PARP cleavage and ap

25 Activation of procaspases 3, 8, 9, and 10, as well as Bid and poly(ADP

26 s-inducing ligand (TRAIL), and activation of procaspase-3, -8, -9, and -10.

27 m demonstrate a reduction in the cleavage of procaspase-3, -8, and -9 and the caspase substrate, poly

28 352 and UCN-01 resulted in the activation of procaspase-3, -9, and -8 as well as Bid cleavage.

29 sembly of a catalytically inactive mutant of procaspase-3, a homodimeric protein that belongs to the

30 uce autoprocessing and enzymatic activity of procaspase-3, a pro-apoptotic protein.

31 ractions.We screened for binding partners of procaspase-3, a protein implicated in apoptotic signalin

32 Treatment of cardiomyocytes with procaspase 3 activating compound 1, a small-molecule act

33 the design and discovery of next-generation procaspase-3 activating compounds, and sheds light on th

34 ls a strong correlation between the in vitro procaspase-3 activating effect and their ability to indu

35 rmeability transition, cytochrome c release, procaspase 3 activation, and apoptosis.

36 Smac prevented cIAP1 from inhibiting procaspase-3 activation and reversed the inhibition by p

37 ity for procaspase-3, which is important for procaspase-3 activation at the physiological concentrati

38 Inhibition of procaspase-3 activation depended on BIR2 and BIR3 of cIA

39 ide derived from the amino terminus promotes procaspase-3 activation in vitro.

40 we interrogate the biochemical mechanism of procaspase-3 activation on 1541 fibrils in addition to p

41 Procaspase-3 activation required co-expression of procas

42 rocessing and was a more potent inhibitor of procaspase-3 activation than of already activated caspas

43 f Bcl-2), the inhibition of procaspase-9 and procaspase-3 activation, and the elevated level of Mn-SO

44 osolic cytochrome c release) associated with procaspase-3 activation, poly(ADP-ribose) polymerase cle

45 embrane potential, cytochrome c release, and procaspase-3 activation.

46 ht junction protein expression, and reducing procaspase-3 activation.

47 essed caspase-9 in the apoptosome and blocks procaspase-3 activation.

48 Combinations of procaspase-3 activators PAC-1 and 1541B show considerabl

49 ing for further evaluation of small-molecule procaspase-3 activators, including S-PAC-1, a compound t

50 scovery of a compound, PAC-1, which enhances procaspase-3 activity in vitro and induces apoptotic dea

51 mutant survivin T34A (Ad Survivin T34A) and procaspase 3 (Ad Caspase 3) in ovarian carcinoma cell li

52 ctivity while also delivering high levels of procaspase 3 allow proteolytic cleavage and activation o

53 o previous reports, we find no evidence that procaspase-3 alone is capable of self-activation, consis

54 AG490 abrogated GM-CSF-induced expression of procaspase 3 and activation of caspase 3.

55 ondrial cytochrome c (cyt c) and cleavage of procaspase 3 and caspase substrates were determined by w

56 exhibited significant increases in synaptic procaspase- 3 and active caspase-3 expression levels tha

57 from apoptosis induced by overexpression of procaspase-3 and -7 and inhibited the processing of thes

58 ly(ADP-ribose) polymerase, and processing of procaspase-3 and -7.

59 Notably, we show that the proenzymes procaspase-3 and -9 are basally persulfidated in resting

60 Procaspase-3 and -9 were present as separate and smaller

61 ve investigated the oligomeric properties of procaspase-3 and a mutant that lacks the pro-domain (cal

62 At each age studied, procaspase-3 and caspase-3 were decreased in CBs of Tg m

63 pase-9 in PAI-1-/- EC led to lower levels of procaspase-3 and cleaved caspase-3, thereby promoting su

64 ctivated procaspase-9, but failed to recruit procaspase-3 and induce apoptosis.

65 Similar to PAC-1, S-PAC-1 activated procaspase-3 and induced cancer cell apoptosis.

66 tosol leading to activation of procaspase-9, procaspase-3 and PARP cleavage.

67 reduced cell viability, increased necrosis, procaspase-3 and PARP processing, caspase-3 activity, an

68 densation of chromatin, and cleavage of both procaspase-3 and PARP.

69 prevents apoptosis through interaction with procaspase-3 and partially processed procaspase-3 to pre

70 ng, membrane blebbing, cytochrome c release, procaspase-3 and poly(ADP-ribose)polymerase (PARP) cleav

71 on of Bcl-2 and Bcl-xL and the activation of procaspase-3 and procaspase-8.

72 571 and Taxol also induced the activation of procaspase-3 and significant apoptosis.

73 ng sequential activation of procaspase-9 and procaspase-3 and subsequent proteolysis of caspase subst

74 that zinc inhibits the enzymatic activity of procaspase-3 and that PAC-1 strongly activates procaspas

75 a specific transnitrosation reaction between procaspase-3 and thioredoxin-1 (Trx) occurs in cultured

76 alphaBC is known to bind to procaspase-3 and to decrease caspase-3 activation.

77 directly activate proenzymes, the apoptotic procaspases-3 and -6.

78 rease in mitochondrial injury, activation of procaspases-3 and -8, Bid cleavage, and PARP degradation

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

80 avage of poly(ADP-ribose) polymerase (PARP), procaspase 3, and procaspase 9; benzyloxycarbonyl-VAD, t

81 tosis in renal tissue cells by activation of procaspase-3, and aggravated disease pathology.

82 rial ROS production, proteolytic cleavage of procaspase-3, and apoptosis.

83 h purified recombinant Apaf-1, procaspase-9, procaspase-3, and cytochrome c from horse heart.

84 Soluble factor(s) attenuated procaspase-8, procaspase-3, and poly(ADP-ribose) polymerase cleavage a

85 TNF-alpha)-induced cleavage of procaspase-9, procaspase-3, and poly-(ADP-ribose) polymerase, as well

86 ty have been examined, comparable studies on procaspase-3 are lacking.

87 Taken together, our data establish procaspase-3 as a differentiating oligodendrocyte marker

88 Moreover, using procaspase-3 as a marker, we show that oligodendrocyte d

89 with histidine abolished the activity of the procaspase-3 as well as that of the mature caspase.

90 Specifically, PR3 cleaved procaspase-3 at a site upstream of the canonical caspase

91 ition of catalytic activity upon cleavage of procaspase-3 at Asp(175).

92 amino acid precursors into newly synthesized procaspase 3 but, during the chase (for up to 9 h), had

93 motes not only the proteolytic activation of procaspase-3 but also the enzymatic activity of mature c

94 Hence, cIAP1 prevented the activation of procaspase-3 but had no effect on the processing of proc

95 o demonstrate that ara-C induces cleavage of procaspase-3 by a caspase-8-dependent mechanism and that

96 Because the activation of procaspase-3 by caspase-9 requires the release of cytoch

97 CED4 homolog) and thereby the activation of procaspase-3 (cas-3) and procaspase-9 (cas-9).

98 Processing of procaspase-3, caspase-3 enzyme activities, and immunohis

99 on of dominant negative procaspase 9 blocked procaspase 3 cleavage and the potentiation of DCA-induce

100 However, procaspase 3 cleavage was undetectable, suggesting that

101 DCA-induced apoptosis weakly correlated with procaspase 3 cleavage, yet this effect was also blocked

102 membrane permeabilization (LMP), leading to procaspase-3 cleavage and apoptosis.

103 rocaspase-9 processing as well as downstream procaspase-3 cleavage in several cell types and under mu

104 Moreover, we detected p18 in cells before procaspase-3 cleavage product (p20), suggesting sequenti

105 in with low pI), caspase-3 activity (but not procaspase-3 cleavage), p75NTR induction, and DNA fragme

106 l hallmarks of apoptosis, such as PARP-1 and procaspase-3 cleavage.

107 otein, cytochrome c release, and predominant procaspase-3 cleavage.

108 ctive caspase 3 from the transfected zymogen procaspase 3, concomitant with inhibition of apoptosis.

109 treated cells, and purified tTGase catalyzes procaspase 3 cross-linking in vitro.

110 ing oligomerization of caspase-3; and (d) in procaspase-3-deficient cells a mitochondrial-independent

111 observed in targets after GrB delivery: (a) procaspase-3-deficient cells fail to display a reduced D

112 lex (and thus loses its capacity to activate procaspase-3) dictates how fast the timer 'ticks' over.

113 valine 266, the residue at the center of the procaspase-3 dimer interface, with glutamate resulted in

114 The interface of the procaspase-3 dimer plays a critical role in zymogen matu

115 ts, we propose a model for maturation of the procaspase-3 dimer.

116 ic folding intermediates, demonstrating that procaspase-3 dimerization is a folding event.

117 caspase-3 or other initiator proteases with procaspase-3 dramatically stimulates maturation of the p

118 f caspase-3 in Jurkat cells, we predict that procaspase-3 exists as a dimer in vivo.

119 ibrils can serve as platforms to concentrate procaspase-3 for trans-activation by upstream proteases.

120 nalization, and proteolysis of procaspase-9, procaspase-3, gelsolin, and protein kinase C-delta.

121 ancer cells through the direct activation of procaspase-3, has implications for the design and discov

122 y using purified ProT, Apaf-1, procaspase-9, procaspase-3, Hsp70, cytochrome c, PHAPI, CAS, and regul

123 ctive GST-US3(K220N) protein, phosphorylated procaspase 3 in vitro.

124 ndrocytes transiently upregulate the zymogen procaspase-3 in both female and male mice, equipping the

125 ocaspase-3 and that PAC-1 strongly activates procaspase-3 in buffers that contain zinc.

126 , stimulate rapid and dramatic maturation of procaspase-3 in multiple cancer cell lines, and powerful

127 d macrophage infiltration and GzmB activated procaspase-3 in renal tissue cells, thereby increasing k

128 ) was reported that enhances the activity of procaspase-3 in vitro and induces apoptotic death in can

129 combined data indicate that PAC-1 activates procaspase-3 in vitro by sequestering inhibitory zinc io

130 ntal evidence indicates that PAC-1 activates procaspase-3 in vitro through chelation of inhibitory zi

131 541B show considerable synergy in activating procaspase-3 in vitro, stimulate rapid and dramatic matu

132 in is the mechanism by which PAC-1 activates procaspase-3 in vitro.

133 The levels of procaspase-3 increase at 4 days postlesion, and caspase-

134 NIP3 and the ratio of activated caspase 3 to procaspase 3 increased after LVAD support, Bcl-2 and TUN

135 hain Fv antibody fragment, fused to inactive procaspase-3, induced auto-activation of caspase-3 after

136 capable of processing both procaspase-8 and procaspase-3 into active subunit forms, resistant cell e

137 ns an RGD motif, which potentially activates procaspase-3 intracellular and or binds to integrins.

138 During maturation, procaspase-3 is cleaved at D175, which resides in a link

139 However, the measured Km of C9Holo for procaspase-3 is much lower than that of LZ-C9.

140 ithout effecting a concomitant change in p32 procaspase 3 levels.

141 Interestingly, procaspase-3 levels are often elevated in cancer cells,

142 Procaspase-3 levels remained unaltered if superinfected

143 re caspase-3 is >10(7)-fold more active than procaspase-3, making this proenzyme a remarkably inactiv

144 ion of the denitrosylation of S-nitrosylated procaspase-3 mediated by the redox protein Trx2 is a par

145 and mouse granzyme B cleave species-specific procaspase-3 more efficiently than the unmatched substra

146 ned the enzymatic activity of an uncleavable procaspase-3 mutant (D9A/D28A/D175A), which contains the

147 First, dimerization of procaspase-3 occurs as a result of the association of tw

148 y at pH 7.4, whereas the maximum activity of procaspase-3 occurs at pH 8.3.

149 We confirmed the cleavage of procaspase-3, one of the key substrates of this enzyme,

150 e either transfected with a plasmid encoding procaspase 3 or superinfected with a proapoptotic mutant

151 s, possibly by preventing the formation of a procaspase-3/p21(WAF1/CIP1) complex.

152 Procaspase-3 (P3) and procaspase-7 (P7) are activated th

153 Procaspase-3 (p32) is processed by upstream caspases to

154 Transfection of MCF-7 cells with wild type procaspase-3 partially restored cleavage of these polype

155 eling; phosphatidylserine (PS) exposure; and procaspase 3, poly(ADP-ribose)polymerase, lamin, and tub

156 Apoptosis was associated with processing of procaspase-3, procaspase-7, procaspase-8, and procaspase

157 ement mechanism, so that unlike the effector procaspase-3, procaspase-9 cannot be processed by the ap

158 but not control agents, induced cleavage of procaspase-3, procaspase-9, and procaspase-8, along with

159 Procaspase 3 processing was enhanced by the proteasome i

160 ression is maintained and that inhibition of procaspase-3 processing occurs in A. phagocytophilum-inf

161 GM-CSF also increased procaspase 3 protein levels in OCI/AML3 and Mo7e cells,

162 with levels of Apaf-1 (R(s) = 0.52, P <.02), procaspase-3 (R(s) = 0.56, P <.006) and procaspase-8 (R(

163 ats may be involved in procaspase-9-mediated procaspase-3 recruitment.

164 mutant infection, but significant amounts of procaspase-3 remained in cells superinfected with Bac-Us

165 Once released, mature caspase-9 can process procaspase-3, setting into motion the caspase cascade.

166 nitrated cytochrome c and interaction with a procaspase-3 subunit was assayed.

167 ns of caspase-3 and an uncleavable mutant of procaspase-3 that is enzymatically active.

168 nalyses identified a cluster of mutations in procaspase-3 that resist small-molecule activation both

169 -responsive cells prevents the processing of procaspase-3; thus, STS-induced apoptosis in cells resis

170 (i) Bac-U(S)3 blocks processing of procaspase-3 to active caspase.

171 spase-3 by the identification of cleavage of procaspase-3 to active forms by immunoblots and by cleav

172 estering inhibitory zinc ions, thus allowing procaspase-3 to autoactivate itself to caspase-3.

173 d that directly stimulates the activation of procaspase-3 to caspase-3 could selectively induce apopt

174 o apoptosis is the activation of the zymogen procaspase-3 to caspase-3.

175 on with procaspase-3 and partially processed procaspase-3 to prevent caspase-3 activation.

176 Caspase-9 and -8 cleave procaspase-3 to produce a p24 processing intermediate (c

177 We also show that procaspase-9 can recruit procaspase-3 to the Apaf-1-procaspase-9 complex.

178 embles into nanofibrils, and localization of procaspase-3 to the fibrils promotes activation.

179 ) that stimulates activation of a proenzyme, procaspase-3, to generate mature caspase-3.

180 ally promotes the maturation of the zymogen, procaspase-3, to its mature form, caspase-3.

181 ses oligodendrocyte density, indicating that procaspase-3 upregulation is linked to successful oligod

182 recombinant caspase-11 cleaves and activates procaspase-3 very efficiently.

183 unique biocatalytic material that activates procaspase-3 via induced proximity.

184 Procaspase-3 was detected in monocyte extracts, but its

185 Proteolytic degradation of procaspase-3 was observed in both the CP70 and C30 cells

186 cell differentiation from bone marrow cells, procaspase-3 was present in cells of all stages of matur

187 EK1/2 inhibitors correlated with cleavage of procaspase 3, which was blocked by inhibitors of caspase

188 ates caspase-9 by enhancing its affinity for procaspase-3, which is important for procaspase-3 activa

189 n intracellular, membrane-associated form of procaspase-3 whose activation is controlled by Bcl-2.

190 calpain cleaved recombinant procaspase-9 and procaspase-3 without activating either caspase, confirmi