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1 proposed, which suggests caspase-2 to be an initiator caspase.
2 strating its capacity to affect a vertebrate initiator caspase.
3 polyubiquitination and aggregation of a key initiator caspase.
4 domains is required for their processing by initiator caspases.
5 tive suppression than inhibitors of upstream initiator caspases.
6 daptor protein bridging death receptors with initiator caspases.
7 ause it induces apoptosis independent of the initiator caspases.
8 le of selectively binding to large prodomain initiator caspases.
9 are sufficient to cleave and activate other initiator caspases.
10 activity that resides in the zymogens of the initiator caspases.
11 requires a novel pathway in addition to the initiator caspases.
12 be achieved through restricted activation of initiator caspases.
13 d by mature executioner caspases rather than initiator caspases.
14 sts diverse mechanisms for the activation of initiator caspases.
15 d near complete loss of the p10 subunit from initiator caspases 1 and 8 but not from the executioner
17 death was associated with activation of both initiator (caspases-2, -8 and -10) and effector (caspase
23 These bile acids differentially activate initiator caspases-2 and -8 and induce cleavage of full-
29 bisphosphate (PIP2) is a direct inhibitor of initiator caspases 8 and 9, and their common effector ca
30 (i) rapid formation of covalent complex with initiator caspases 8 or 1, (ii) very slow deacylation, a
32 erexpression of TIMP-3 induced activation of initiator caspase-8 and -9 and promoted caspase-mediated
33 gnals from death receptors to the downstream initiator caspase-8 and connects to the mitochondrial in
34 aspases and, surprisingly, activation of the initiator caspase-8 and processing of its substrate Bid.
35 ken together these data demonstrate that the initiator caspase-8 can directly activate pro-caspase-3
37 lustering with subsequent recruitment of the initiator caspase-8, and ultimately cellular demise.
38 We show here that in a purified system, the initiator caspases-8 and -10 directly process the execut
39 only modulated by either VES or MSA included initiator caspases-8 and -10, as well as executioner cas
40 rinsic apoptotic pathways with activation of initiator caspases-8 and -9 and downstream effector casp
41 ation of the effector caspase-3 but also the initiators caspase-8 and caspase-9, mitochondrial cytoch
43 d (1.5- and 1.4-fold, respectively), whereas initiator caspase-9 and death caspase-3 transcripts were
44 mac antagonizes several IAPs and assists the initiator caspase-9 and effector caspases (caspase-3, ca
47 sis largely through direct inhibition of the initiator caspase-9 and the effector caspase-3 and -7.
48 the executioner caspase-3 and the intrinsic initiator caspase-9 in primary cerebellar granule neuron
51 ed in recent years, the mechanism of how the initiator caspase-9 is regulated by IAPs remains enigmat
52 D specifically cleaved caspase-8 but not the initiator caspase-9 or -10 and significantly increased c
53 inhibiting the effectors caspase-3/-7 and an initiator caspase-9 through its BIR2 and BIR3 domains, r
54 are exemplified by XIAP, which regulates the initiator caspase-9, and the executioner caspases-3 and
55 data suggest that caspase-9 is the critical initiator caspase activated during heat-induced apoptosi
57 ctive caspase, we identified caspase-2 as an initiator caspase activated in rotenone-treated primary
58 Although widely regarded as an inhibitor of initiator caspase activation and cell death, c-FLIP(L) i
59 nducing signaling complex (DISC) to regulate initiator caspase activation and launch the apoptotic pr
61 at TNF death signals are blocked proximal to initiator caspase activation, at the level of TNF recept
63 mitochondrial dysfunction, we determined the initiator caspase and its role in cell death in primary
65 9 has the potential to inhibit both upstream initiator caspases and downstream effector caspases, we
66 ins assemble into the DISC to fully activate initiator caspases and execute cell death, and finally w
69 reted to be proximity-driven dimerization of initiator caspases, and consequently their activation.
73 cytometry, and immunoblotting, we find that initiator caspases are active during the long and variab
76 activated by the cleavage of caspase-8, the initiator caspase associated with the death receptor pat
78 and execution phases of cell death, with the initiator caspases being recruited to multicomponent sig
79 the decline in SK1 occurs downstream of the initiator caspase but upstream of the effector caspase.
81 o that any free p20 formed by deacylation of initiator caspases cannot reassociate to active heterote
82 tor caspases (caspase 3, 6, 7, or 12) or the initiator caspases (caspase 8 or 9) could be detected in
83 de biochemical evidence that other apoptosis initiator caspases (caspase-2 and -10) as well as a proc
84 related activities of caspases, including an initiator caspase, caspase 8, and effector caspases, suc
85 he activity of the death receptor-associated initiator caspase, caspase 8, and is inhibited by the pe
89 ved to have a low potency for inhibiting the initiator caspases, caspase-1 and caspase-8, and caspase
90 DP-ribose) polymerase, and activation of the initiator caspases, caspase-8 and -9, earlier in infecti
91 stern blots, indicated that each of the main initiator caspases, caspase-8, caspase-9, and caspase-12
92 ccompanied by activation of a combination of initiator caspases (caspases-2, -8, and -9) and executed
94 provide evidence that ceramide generation is initiator caspase-dependent and occurs prior to commitme
97 CRINKLED (CK) selectively interacts with the initiator caspase DRONC and regulates some of its non-ap
102 phila effector caspase DrICE or its upstream initiator caspase DRONC prevented FHV-induced apoptosis
103 wing that cellular NADPH levels modulate the initiator caspase Dronc through its phosphorylation at S
106 nfirming that P49 targeted DrICE and not the initiator caspase DRONC, depletion of DrICE by RNA silen
107 bitor p35 or a dominant-negative form of the initiator caspase Dronc, is sufficient to inhibit saliva
111 as distal to activation of several different initiator caspases, evidence for a further downstream pr
113 ctivation is started by trans-cleavage by an initiator caspase followed by autocleavage of effector c
117 Specific adaptors regulate the activation of initiator caspases; for example, FADD and Apaf-1 engage
118 ap1 silencing was rescued by cosilencing the initiator caspase gene Aedronc, indicating that the mort
119 inally proposed to explain the activation of initiator caspases, has recently been reinterpreted to b
120 lly, b-VAD-fmk failed to label any activated initiator caspase in Apaf-1-deficient cells exposed to h
121 rthermore, we determined that caspase-10, an initiator caspase in death receptor signaling, is the mo
123 utocatalytic cleavage of Dronc, an important initiator caspase in Drosophila, results in a drastic en
124 ase inhibitor, we identified caspase-2 as an initiator caspase in EtOH-treated corneal fibroblasts.
125 previously unknown role for caspase-2 as an initiator caspase in lipoapoptosis and suggest that casp
127 and reduced activations of both effector and initiator caspases in high cell density, postconfluent C
128 n neuronal injury, direct evidence of active initiator caspases in stroke and the functional relevanc
129 evidence for the differential involvement of initiator caspases in the apoptotic volume decrease duri
132 ignificantly reduced the expression level of initiator caspases, increased the ratio of XIAP to Smac/
140 etected in dying cells, and neither of these initiator caspases nor the endoplasmic reticulum stress-
143 e examine the role of caspase-9 (Casp9), the initiator caspase of the intrinsic apoptotic cascade, in
144 quitous IAP, can inhibit both caspase-9, the initiator caspase of the mitochondrial apoptotic pathway
145 heat shock does not require any of the known initiator caspases or their activating complexes to prom
148 NOS) inhibitors regulate S-nitrosation of an initiator caspase, procaspase-9, in a human colon adenoc
149 eptors include the adaptor protein FADD, the initiator caspases procaspases-8 and -10 and the regulat
152 esults suggest that caspase-11 is a critical initiator caspase responsible for the activation of casp
154 uring apoptosis occurs in a cascade from the initiator caspase(s) (e.g. caspase-8) to the effector ca
155 other basal deuterostomes, signal-responsive initiator caspase subfamilies (caspases-8/10 and 9, whic
156 as caspase-7 via a linker_BIR2 fragment and initiator caspases such as caspase-9 via the BIR3 domain
158 otif, P49 was impaired for inhibition of the initiator caspase that cleaves and activates pro-Sf-casp
159 el in vivo specificity for a P35-insensitive initiator caspase that functions at an evolutionarily co
161 e consistent with the involvement of a novel initiator caspase that is resistant to P35, but directly
162 sulted in isolation of caspase-8 (Casp8), an initiator caspase that mediates death-receptor-induced a
166 e to TRAIL or TNF requires the activation of initiator caspases, which then activate the effector cas
167 nc mutation, indicating that dronc is a main initiator caspase, while strica plays a minor role that
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