ライフサイエンスコーパス: effector caspase

1 of the initiator caspase but upstream of the effector caspase.

2 e as to whether caspase-2 is an initiator or effector caspase.

3 gans CED-3, suggesting that DCP-1 is a death effector caspase.

4 es demonstrated that caspase-3 was the major effector caspase.

5 a novel mechanism for the regulation of this effector caspase.

6 to block activation of caspase 3, a critical effector caspase.

7 eam signals lead to activation of downstream effector caspases.

8 K signaling acts upstream of both Reaper and effector caspases.

9 on of a mitochondrial amplification loop via effector caspases.

10 nitiator caspase followed by autocleavage of effector caspases.

11 ess one another, mature caspases only cleave effector caspases.

12 g cells in addition to activating downstream effector caspases.

13 min degradation in the presence of activated effector caspases.

14 eins on the processing and activities of the effector caspases.

15 cessing and activation of both initiator and effector caspases.

16 elease and caspase 9-dependent activation of effector caspases.

17 ts of ionic strength and processes/activates effector caspases.

18 ease of cytochrome c as well as a target for effector caspases.

19 ked these events, indicating dependence upon effector caspases.

20 of both the Apaf-1-caspase-9 apoptosome and effector caspases.

21 2 of XIAP and to promote the activity of the effector caspases.

22 ctioning as a direct inhibitor of downstream effector caspases.

23 B1 to fragments that indicate activation of effector caspases.

24 nucleases and suppressing the activation of effector caspases.

25 o increase survivin expression and activated effector caspases.

26 stimulated with HCMV secretome and activated effector caspases.

27 ptotic stimuli and mediate the activation of effector caspases.

28 neurally driven apoptosis of oocytes through effector caspases.

29 trol of the initiator caspase Dronc, but not effector caspases.

30 ac are not able to reverse inhibition of the effector caspases.

31 e signals by cleaving and thereby activating effector caspases.

32 es, and then cleave and activate downstream 'effector' caspases.

33 -1beta) secretion by macrophage requires the effector caspases 1 and 11, the adapter ASC, and NLRP1,

34 cking the NLR protein Ipaf or its downstream effector caspase-1 are permissive to intracellular Legio

35 mice deficient for Nlrp3 or the inflammasome effector caspase-1 were highly susceptible to azoxymetha

36 mes consist of a sensor, an adapter, and the effector caspase-1, which interact through homotypic int

37 ll-like receptor 4 (Tlr4) and its downstream effector, caspase-1.

38 ic mediator, caspase-8, and the inflammasome effector, caspase-1.

39 pression of various NALPs and its downstream effectors caspase-1, ASC (Apoptosis-associated speck-lik

40 The absence of AIM2 or its downstream effectors, caspase-1 and interleukin-1beta, erases the a

41 signaling pathway, including its downstream effectors caspase-12 and the transcription factor C/EBP

42 ed proliferation and decreased activation of effector caspase 3 in postconfluent EOMA cell cultures.

43 ation of both initiator caspases 8 and 9 and effector caspase 3 was noted 4 h later when full-blown D

44 r capsases 9 and 8 followed by activation of effector caspase 3.

45 (extrinsic pathway) initiating caspase 8 and effector caspase 3.

46 initiator caspases 8 and 9, and their common effector caspase 3.

47 eavage of caspase 9 but not caspase 8 or the effector caspase 3.

48 y cleavage of poly(ADP-ribose) polymerase by effector caspases 3 and 7 was similar in neo and mIkappa

49 and showed no evidence of activation of the effector caspases 3 and 7, although the initiator caspas

50 e mitochondrial death pathway and downstream effector caspases 3 and 7, which resulted from reduced c

51 creased cleavage of PARP, a substrate of the effector caspases 3 and 7.

52 and selective non-peptide inhibitors of the effector caspases 3 and 7.

53 cide programme mediated by activation of the effector caspases 3, 6 and 7.

54 With both effectors, caspase 3 activity appears subsequent to that

55 We generated mice deficient in the two effectors, caspase 3 and caspase 7, which died immediate

56 both initiator (caspases-2, -8 and -10) and effector (caspases-3, -6 and -7) caspases.

57 Mirroring this specific effect on effector caspase-3 activation, alphaB-crystallin selecti

58 caspase-8 or caspase-9 abolished downstream effector caspase-3 activation.

59 nhibition of the initiator caspase-9 and the effector caspase-3 and -7.

60 hondrial apoptosis signaling by neutralizing effector caspase-3 and caspase-7 maturation.

61 otic protein Bid, resulting in activation of effector caspase-3 and cleavage of its cellular target p

62 und to elicit not only the activation of the effector caspase-3 but also the initiators caspase-8 and

63 was found to not only activate the apoptosis effector caspase-3 but also to cause a large and prolong

64 brane permeabilization and processing of the effector caspase-3 in a benzyloxycarbonyl-VAD-fluorometh

65 ts a novel scaffold protein that directs the effector caspase-3 to certain substrates facilitating th

66 hondrial-derived caspase-9, and the terminal effector caspase-3.

67 ification circuit that includes the critical effector caspase-3.

68 otherapeutic drugs by downregulating the key effector caspase-3.

69 ted the activation of the apoptosis-inducing effector caspase-3.

70 f initiator caspases-8 and -9 and downstream effector caspase-3.

71 Effector caspases-3 and -6, but not -7, were cleaved wit

72 The effector caspases-3 and -7 play a central role in progra

73 and dramatically higher levels of apoptotic effector, caspase-3.

74 s apoptosis by binding to and inhibiting the effectors caspase-3/-7 and an initiator caspase-9 throug

75 The effector caspases-6 and -7, and to a lesser extent caspa

76 rophages lacking the downstream inflammasome effector caspase-7 were partially protected.

77 iator capase-8 followed by activation of the effector caspase-9, independent of cytochrome c, and sub

78 Effector caspase activation and apoptosis following RNA

79 inhibitor of apoptosis efficiently increased effector caspase activation and apoptosis of NSCLC cells

80 as responsible for the significantly delayed effector caspase activation and hepatocyte injury upon e

81 Intrinsic or extrinsic routes to effector caspase activation are frequently the most rapi

82 n of JNK by vinblastine occurred upstream of effector caspase activation because treatment with a pan

83 nal prodomain plays a regulatory role during effector caspase activation or enzyme activity in insect

84 The mechanism of effector caspase activation primarily involves reorganiz

85 resence of actinomycin D in concordance with effector caspase activation, but addition of proteasome

86 Cell death involved effector caspase activation, cytochrome c release and Ba

87 ytokine concentrations (1 ng/ml) also led to effector caspase activation, increased paracellular flux

88 e externalization, cytochrome c release, and effector caspase activation.

89 odels, and in vivo via MCL1 reduction and by effector caspase activation.

90 s the initiator caspase, and its loss blocks effector caspase activation.

91 l outer membrane permeabilization (MOMP) and effector caspase activation.

92 hondrial apoptosis signaling at the level of effector caspase activation.

93 c release from mitochondria, and subsequent effector caspases activation leading to a decreased sens

94 tress response can then become terminal with effector caspase activity mediated in part by the transc

95 was delayed, cytochrome c was not released, effector caspase activity was reduced and the cleavage o

96 apoptosis at a step before the induction of effector caspase activity, and the directed silencing of

97 TcapQ to image single-cell apoptosis through effector caspase activity.

98 They do not require Dcp1, although this effector caspase also can cleave dSREBP in vitro.

99 on; and subsequently inhibited activation of effector caspases and apoptosis.

100 rly requisite features for the activation of effector caspases and apoptotic nucleases in Fas recepto

101 also induced epithelial apoptosis, activated effector caspases and stimulated proteases and chemokine

102 interaction seen both between initiator and effector caspases and within IAP-antagonist family membe

103 ads to proteolytic activation of downstream (effector) caspases and cleavage of a number of vital pro

104 activity and levels of cleaved caspase 3, an effector caspase, and could only detect increased levels

105 n are enzymatically modified, most likely by effector caspases, and have a direct or indirect effect

106 hindrance that prevents XIAP from inhibiting effector caspases, and therefore small molecule mimics o

107 permeabilization, switch-like activation of effector caspases, and variability in the timing and pro

108 , and a postmitochondrial phase during which effector caspases are activated and APR(6) is destroyed.

109 XIAP and proteasome-dependent degradation of effector caspases are important in restraining activity

110 When effector caspases are inhibited, mitochondria become unc

111 relatively slow, however, and key downstream effector caspases are not activated.

112 onstrated that active forms of initiator and effector caspases are selectively localized at the NMJ i

113 uently P49 blocked proteolytic activation of effector caspases at a unique step upstream from that af

114 phology and with documented activation of an effector caspase, but there are also many exceptions.

115 MALT1 diminishes the activation of apoptotic effector caspases, but it does not alter the activity of

116 hila Inhibitor of Apoptosis 1, DIAP1, blocks effector caspases by targeting them for polyubiquitylati

117 his initiates the postmitochondrial-mediated effector caspase cascade.

118 The effector caspases caspase 3 and caspase 6 are responsibl

119 (F4/80, MCP-1, TLR4, TLR2 and IL-1beta) and effector caspase (caspase 3 and 7) activation compared t

120 The presence of the activated form of the effector caspase (caspase-3) was observed 24 h after LPS

121 lei of apoptotic cells, no activation of the effector caspases (caspase 3, 6, 7, or 12) or the initia

122 IAPs and assists the initiator caspase-9 and effector caspases (caspase-3, caspase-6, and caspase-7)

123 While activation of the effector caspase, caspase-3, has indeed been observed as

124 duced apoptosis was largely dependent on the effector caspase, caspase-3, which was activated through

125 hibits the activity of caspase-9 but not the effector caspase, caspase-3.

126 o significantly reduce activation of the key effector caspase, caspase-3.

127 ndrial apoptotic pathway, and the downstream effector caspases, caspase-3 and caspase-7.

128 echanistically, PANX1 itself was a target of effector caspases (caspases 3 and 7), and a specific cas

129 While the set of effector caspases (caspases-3/7 and caspase-6) in sea ur

130 have addressed the order in which apical and effector caspases, caspases-9 and -3, respectively, are

131 late oogenesis, we examined whether another effector caspase, Dcp-1, could drive the unique morpholo

132 We found that premature activation of the effector caspase, Dcp-1, resulted in a disappearance of

133 cted upon PTEN expression, and inhibitors of effector caspases did not restore proliferative capacity

134 s of caspases, with inhibitors of downstream effector caspases displaying more effective suppression

135 The Drosophila effector caspase Drice cleaves dSREBP, and cleavage requ

136 ote apoptosis, as dOmi fails to displace the effector caspase DrICE from the BIR1 domain in DIAP1.

137 In this report, we show that the effector caspase Drice is activated during cell death in

138 Here we report that the principal effector caspase DrICE is required for baculovirus-induc

139 ediated ablation of the principal Drosophila effector caspase DrICE or its upstream initiator caspase

140 We find that DIAP2 regulates the effector caspase drICE through a mechanism that resemble

141 utants have elevated levels of the apoptotic effector caspase Drice, suggesting one potential site of

142 ed following aspartate residue Asp-20 by the effector caspase DrICE.

143 Drosophila cells and labelled the activated effector caspase Drice.

144 for the involvement of both an initiator and effector caspase, Dronc and Dcp-1, and mitochondrial-dep

145 In this paper, we show that the Drosophila effector caspase, Drosophila caspase 1 (Dcp-1), localize

146 initiator caspase(s) (e.g. caspase-8) to the effector caspases (e.g. caspase-3), which ensures the ge

147 DR5 agonist antibody to induce activation of effector caspases efficiently without the need for mitoc

148 Smac/DIABLO to function at the level of the effector caspases, expression of a cytosolic Smac/DIABLO

149 of the NEDD8 conjugation pathway, targeting effector caspases for neddylation and inactivation.

150 P with caspase-9, whereas how Smac liberates effector caspases from XIAP inhibition is not clear.

151 pase and supports a model wherein apical and effector caspases function through a proteolytic cascade

152 not be cleaved by caspase-3, -7, or -6, the "effector" caspases generally believed to carry out the c

153 Two remaining effector caspase genes, decay and damm, found no apparen

154 profound insight into the inhibition of the effector caspases has been gained in recent years, the m

155 ular fluorescence quenching and activated by effector caspases, has been previously described and val

156 (caspase-9) initiating caspase and caspase-3 effector caspase; however, expression of the antiapoptot

157 ng the ubiquitination and turnover of active effector caspases in cells.

158 rfere with activation of caspase-3 and other effector caspases in cytosolic extracts where caspase ac

159 omparing the activity levels of the two main effector caspases in Drosophila melanogaster, Drice and

160 thway appeared to be upstream to that of the effector caspases in nucleoside analogue-induced apoptos

161 Interestingly, effector caspases in photoreceptor neurons stimulate Hh

162 hat PIP2 is a direct regulator of apical and effector caspases in the death receptor and mitochondria

163 l role in neutralizing IAP inhibition of the effector caspases in the death receptor pathway of Type

164 ownward arrowG processing sites among insect effector caspases, including Drosophila drICE and DCP-1,

165 t-lived plasma cells in vitro and in vivo is effector caspase-independent.

166 we describe the consequence of caspase-9 and effector caspase inhibition on mitochondrial physiology

167 ty via adenoviral expression of the biologic effector caspase inhibitor p35 blunted cardiomyocyte hyp

168 pulation-based fluorescent cell assays in an effector caspase inhibitor-specific manner.

169 The effector caspase is recruited through PYD, whose overexp

170 Ancaspase-7, an Anopheles effector caspase, is proteolytically activated during Pl

171 apoptotic process, and caspase 3, one of the effector caspases, is proposed to play essential roles i

172 aspase-8, which in turn activates downstream effector caspases leading to programmed cell death.

173 l caspase-9 (C9), and in turn its downstream effector caspases, leading to apoptosis.

174 release and activation of caspase-9 and the effector caspases, leading to macrophage apoptosis.

175 ion wherein matrix metalloproteases activate effector caspases, leading to remodeling of basal lamina

176 Thus, effector caspases may cleave and activate another cytoso

177 duction of reactive oxygen species, and that effector caspases may depolarize mitochondria to termina

178 ggesting that a cytoplasmic substrate of the effector caspases may mediate in the mechanism of Bax in

179 The ability to modulate the activity of effector caspases may therefore represent an unexploited

180 Interestingly, the effector caspase-mediated depolarization of the mitochon

181 ic processing of Sf-caspase-1, the principal effector caspase of the host insect Spodoptera frugiperd

182 ucture of active Sf-caspase-1, the principal effector caspase of the insect Spodoptera frugiperda, is

183 cantly inhibit the proteolytic activities of effector caspases on fluorogenic or endogenous substrate

184 or-alpha (TNF) activates caspase-8 to cleave effector caspases or Bid, resulting in type-1 or type-2

185 tween functionally distinct domains, whereas effector caspases processed clathrin's heavy chain.

186 Corresponding delays were detected for effector caspase processing and cell death.

187 B ((I/L/V)EXD) resembles activation sites in effector caspase proenzymes, consistent with a role for

188 In nonlymphoid cells that cannot activate effector caspases, programmed cell death is delayed in r

189 erexpression of endogenous inhibitors of the effector-caspases, rather than decreased levels of these

190 eptide-based permeation peptide sequence, an effector caspase recognition sequence, DEVD, and a flank

191 Loss of the dectin-1 downstream effector caspase recruitment domain 9 (CARD9) blocks CRE

192 spase activation, Apaf-1, caspase-9, and the effector caspases redistributed and formed the aposome.

193 aken together, our findings demonstrate that effector caspases regulate their own inhibition through

194 h related, P49 and P35 inhibit initiator and effector caspases, respectively, during infection of per

195 on of regulatory links between initiator and effector caspases reveals that XIAP and proteasome-depen

196 teases is whether selective inhibition of an effector caspase(s) will prevent cell death.

197 The principal effector caspase, Sf-caspase-1, is proteolytically activ

198 termediates, the activation of initiator and effector caspases shares the features of interdimer clea

199 Thus, TcapQ647 represents a sensitive, effector caspase-specific far-red "smart" probe to nonin

200 In contrast, the effector caspase specificity of P35 was unaltered when P

201 and release of caspase-8, thereby enhancing effector-caspase stimulation and apoptosis.

202 This leads in turn to the inhibition of effector caspases such as caspase 3.

203 ng in cytochrome c release and activation of effector caspases such as Caspase-3 (Casp3).

204 ains three BIR domains and directly inhibits effector caspases such as caspase-7 via a linker_BIR2 fr

205 cluding an initiator caspase, caspase 8, and effector caspases, such as caspase 6.

206 Caspase-3 is an important effector caspase that mediates many of the terminal prot

207 initiator caspases, which then activate the effector caspases that dismantle cells and cause death.

208 nd exposure and the sudden activation of the effector caspases that kill cells.

209 p35 protein, which inhibits the activity of effector caspases that mediate apoptosis.

210 be processed and activated by the downstream effector caspases, thereby completing an amplifying feed

211 l death pathways and activates initiator and effector caspases through Ang2-dependent pathways in viv

212 t of an anti-apoptotic complex that presents effector caspases to Bcl-2, enabling Bcl-2 to inhibit ca

213 ascade by proteolytic cleavage/activation of effector caspases to form active approximately 60-kDa he

214 sis resistance by using chemically inducible effector caspases to trigger apoptosis in prostate cance

215 As for effector caspases, vCrz PCD requires both ice and dcp-1

216 bles Bcl2L12 to block the activation of both effector caspases via distinct mechanisms, thereby contr

217 Specific cleavage of TcapQ647 by effector caspases was demonstrated using a panel of puri

218 FC loading, and activation of caspase-9 and effector caspases was observed at 6 h.

219 endogenous Sf-caspase-1, an insect group II effector caspase, we show that Op-IAP blocked the first

220 h upstream initiator caspases and downstream effector caspases, we conclude that P49 is a broad-spect

221 This mechanism is dependent on effector caspases which trigger the activation of Hedgeh

222 This resulted in the processing of the effector caspases, which were then released, possibly bo

223 antagonists block interaction of downstream effector caspases with XIAP, thus inducing apoptosis of

224 -1 is most comparable with that of the human effector caspases, with which it shares highest sequence

225 the DISC cannot directly activate downstream effector caspases without mitochondrial help.