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1 SMA in SSc dermal fibroblasts treated with a caspase 1 inhibitor.
2 aride-induced endotoxemia, and injected with caspase 1 inhibitor.
3 inhibited by a caspase-2 inhibitor but not a caspase-1 inhibitor.
4 , TNFalpha, and IL-6) that were blocked by a caspase-1 inhibitor.
5 not inhibited by IL-1 receptor antagonist or caspase-1 inhibitor.
6  Rip2 is a caspase-1 activator, and Cop is a caspase-1 inhibitor.
7 nse to CO, and cell death was inhibited by a caspase-1 inhibitor.
8 ciency, but are unaffected by cathepsin B or caspase-1 inhibitors.
9 pression of siRNA directed against IRF-1 and caspase-1 inhibitors.
10 FN-gamma-induced cell death was inhibited by caspase-1 inhibitors.
11 r antagonist (IL-1RA), and in mice given the caspase 1 inhibitor Ac-YVAD-CMK.
12 ective NLRP3 inhibitor, MCC950; the specific caspase-1 inhibitor Ac-YVAD-cho; and neutralizing anti-I
13 e intracerebroventricularly administered the caspase-1 inhibitor ac-YVAD-CMK (ac-Tyr-Val-Asp-2,6-dime
14 itor Z-DEVD-FMK but were not affected by the caspase-1 inhibitor AC-YVAD-CMK.
15                             The tetrapeptide caspase 1 inhibitor (Ac-YVAD-CMK) prevents 3-aminopropan
16 f caspase 3, Ac-DEVD-CHO but not by the ICE (caspase 1) inhibitor, Ac-YVAD-CHO.
17 aspase-3 inhibitor, Ac-DEVD-CHO, but not the caspase-1 inhibitor, Ac-YVAD-CHO, also selectively inhib
18 The pan-caspase inhibitor, ZVAD-fmk, and the caspase-1 inhibitor, Ac-YVAD-cho, both inhibited NO-indu
19 ike activity in Arabidopsis cells, while the caspase-1 inhibitor, Ac-YVAD-CMK, blocked NO-induced cel
20 rther substantiated by the use of a specific caspase-1 inhibitor, Ac-YVAD-CMK.
21 stimulus-coupled response revealed that some caspase-1 inhibitors allow pro-IL-1beta secretion, where
22  as pyroptosis by the protective effect of a caspase 1 inhibitor and a pyroptosis inhibitor.
23 indings identify SHARPIN as a potent in vivo caspase 1 inhibitor and propose the caspase 1-SHARPIN in
24                                              Caspase 1 inhibitor and the combination of caspase 3 and
25 uced activation of NK cells was prevented by caspase-1 inhibitors and by natural antagonists to IL-1
26                                     In fact, caspase-1 inhibitors are the first orally active agents
27                                              Caspase-1 inhibitors blocked all of these responses.
28  caspase 3/7 inhibitor (but not glycine or a caspase 1 inhibitor) blocked morphological damage and DN
29 X-765, an orally active IL-converting enzyme/caspase-1 inhibitor, blocked IL-1beta secretion with equ
30                                  A selective caspase-1 inhibitor blocks both lipopolysaccharide-induc
31                                          The caspase-1 inhibitor Boc-D-cmk blocked caspase-1 activity
32 ne release was inhibited by a small molecule caspase-1 inhibitor but not by high levels of exogenous
33 aspase-1 activator Rip2 and reduction of the caspase-1 inhibitor Cop.
34 1a, Il1b, and Nlrp3, and pretreatment with a caspase 1 inhibitor decreased IL-1beta secretion in resp
35 at of cytokine response modifier A, a potent caspase-1 inhibitor from the cowpox virus.
36 )-berkeleyamide A (1), a naturally occurring caspase-1 inhibitor, has been achieved by employing Evan
37 upporting a potential role of the endogenous caspase-1 inhibitor in this chronic inflammatory disease
38 tals were shown to be IL-1-dependent using a caspase-1 inhibitor (inhibits IL-1 maturation) and IL-1R
39                                              Caspase-1 inhibitor not only attenuated podocyte express
40           Furthermore, the administration of caspase-1 inhibitors or the infusion of bone marrow-deri
41      Inflammasome inhibition with a specific caspase-1 inhibitor, or blocking of IL-1 signaling by IL
42       Tyr-Val-Ala-Asp-chloromethyl ketone, a caspase-1 inhibitor, prevented ATP-induced release of pr
43  vivo proof of concept of the ability of the caspase-1 inhibitor prodrug VX-765 to mitigate alpha-syn
44                         Late addition of the caspase-1 inhibitor reversed the losses of plasma membra
45                  This cycle can be broken by caspase 1 inhibitors shown to be safe in humans, raising
46 ivation, and support the clinical testing of caspase-1 inhibitors such as VX-765 in autoinflammatory
47 suggest that Flightless-I may be a bona fide caspase-1 inhibitor that acts through a mechanism simila
48 new treatment strategies, such as the use of caspase-1 inhibitors that inhibit pyroptosis, may mainta
49  inflammatory response if a LF was used or a caspase-1 inhibitor was administered during EVLP.
50 ts either saline or a centrally administered caspase-1 inhibitor, which specifically prevents the syn
51                                     Specific caspase-1 inhibitors would provide a new class of anti-i
52 -)Casp11(-/-) BMDC, WT BMDC treated with the caspase-1 inhibitor YVAD, and BMDC lacking the inflammas
53 tion of IL-1beta production using a specific caspase-1 inhibitor (YVAD-fmk; 100 microM) significantly
54 neral caspase inhibitor Z-VAD-Fmk and by the caspase 1 inhibitor Z-YVAD-Fmk.
55 ant cells was significantly protected by the caspase-1 inhibitor (zVAD-fmk) in a dose-dependent manne

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