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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
39 pression of various NALPs and its downstream effectors caspase-1, ASC (Apoptosis-associated speck-lik
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
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
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
74 s apoptosis by binding to and inhibiting the effectors caspase-3/-7 and an initiator caspase-9 throug
77 iator capase-8 followed by activation of the effector caspase-9, independent of cytochrome c, and sub
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
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
85 resence of actinomycin D in concordance with effector caspase activation, but addition of proteasome
87 ytokine concentrations (1 ng/ml) also led to effector caspase activation, increased paracellular flux
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
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
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
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)
124 duced apoptosis was largely dependent on the effector caspase, caspase-3, which was activated through
128 echanistically, PANX1 itself was a target of effector caspases (caspases 3 and 7), and a specific cas
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
136 ote apoptosis, as dOmi fails to displace the effector caspase DrICE from the BIR1 domain in DIAP1.
139 ediated ablation of the principal Drosophila effector caspase DrICE or its upstream initiator caspase
141 utants have elevated levels of the apoptotic effector caspase Drice, suggesting one potential site of
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
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
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
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
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,
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
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.
175 ion wherein matrix metalloproteases activate effector caspases, leading to remodeling of basal lamina
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
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.
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
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
198 termediates, the activation of initiator and effector caspases shares the features of interdimer clea
204 ains three BIR domains and directly inhibits effector caspases such as caspase-7 via a linker_BIR2 fr
207 initiator caspases, which then activate the effector caspases that dismantle cells and cause death.
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
216 bles Bcl2L12 to block the activation of both effector caspases via distinct mechanisms, thereby contr
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
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
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