ライフサイエンスコーパス: caspase-1 inhibitor

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 Cell death was also blocked by a caspase-1 inhibitor, a key enzyme promoting pyroptosis,

12 r antagonist (IL-1RA), and in mice given the caspase 1 inhibitor Ac-YVAD-CMK.

13 ective NLRP3 inhibitor, MCC950; the specific caspase-1 inhibitor Ac-YVAD-cho; and neutralizing anti-I

14 e intracerebroventricularly administered the caspase-1 inhibitor ac-YVAD-CMK (ac-Tyr-Val-Asp-2,6-dime

15 itor Z-DEVD-FMK but were not affected by the caspase-1 inhibitor AC-YVAD-CMK.

16 The tetrapeptide caspase 1 inhibitor (Ac-YVAD-CMK) prevents 3-aminopropan

17 Tau-induced neuronal loss was blocked by caspase-1 inhibitors (Ac-YVAD-CHO and VX-765) as well as

18 f caspase 3, Ac-DEVD-CHO but not by the ICE (caspase 1) inhibitor, Ac-YVAD-CHO.

19 aspase-3 inhibitor, Ac-DEVD-CHO, but not the caspase-1 inhibitor, Ac-YVAD-CHO, also selectively inhib

20 The pan-caspase inhibitor, ZVAD-fmk, and the caspase-1 inhibitor, Ac-YVAD-cho, both inhibited NO-indu

21 ike activity in Arabidopsis cells, while the caspase-1 inhibitor, Ac-YVAD-CMK, blocked NO-induced cel

22 rther substantiated by the use of a specific caspase-1 inhibitor, Ac-YVAD-CMK.

23 stimulus-coupled response revealed that some caspase-1 inhibitors allow pro-IL-1beta secretion, where

24 as pyroptosis by the protective effect of a caspase 1 inhibitor and a pyroptosis inhibitor.

25 indings identify SHARPIN as a potent in vivo caspase 1 inhibitor and propose the caspase 1-SHARPIN in

26 Caspase 1 inhibitor and the combination of caspase 3 and

27 uced activation of NK cells was prevented by caspase-1 inhibitors and by natural antagonists to IL-1

28 In fact, caspase-1 inhibitors are the first orally active agents

29 Caspase-1 inhibitors blocked all of these responses.

30 caspase 3/7 inhibitor (but not glycine or a caspase 1 inhibitor) blocked morphological damage and DN

31 X-765, an orally active IL-converting enzyme/caspase-1 inhibitor, blocked IL-1beta secretion with equ

32 A selective caspase-1 inhibitor blocks both lipopolysaccharide-induc

33 The caspase-1 inhibitor Boc-D-cmk blocked caspase-1 activity

34 ne release was inhibited by a small molecule caspase-1 inhibitor but not by high levels of exogenous

35 aspase-1 activator Rip2 and reduction of the caspase-1 inhibitor Cop.

36 1a, Il1b, and Nlrp3, and pretreatment with a caspase 1 inhibitor decreased IL-1beta secretion in resp

37 at of cytokine response modifier A, a potent caspase-1 inhibitor from the cowpox virus.

38 )-berkeleyamide A (1), a naturally occurring caspase-1 inhibitor, has been achieved by employing Evan

39 upporting a potential role of the endogenous caspase-1 inhibitor in this chronic inflammatory disease

40 tals were shown to be IL-1-dependent using a caspase-1 inhibitor (inhibits IL-1 maturation) and IL-1R

41 was completely suppressed by AC-YVAD-CMK (a caspase-1 inhibitor), MCC-950 (an NLRP3 inflammasome inh

42 Caspase-1 inhibitor not only attenuated podocyte express

43 beta secretion was blocked by treatment with caspase-1 inhibitors or knockdown of NLRP1 or caspase-1

44 Furthermore, the administration of caspase-1 inhibitors or the infusion of bone marrow-deri

45 Inflammasome inhibition with a specific caspase-1 inhibitor, or blocking of IL-1 signaling by IL

46 Tyr-Val-Ala-Asp-chloromethyl ketone, a caspase-1 inhibitor, prevented ATP-induced release of pr

47 vivo proof of concept of the ability of the caspase-1 inhibitor prodrug VX-765 to mitigate alpha-syn

48 Late addition of the caspase-1 inhibitor reversed the losses of plasma membra

49 of two non-antiviral therapeutic agents, the caspase-1 inhibitor SDZ 224015 and Tarloxotinib that tar

50 The caspase-1 inhibitor SDZ 224015, was found to be a potent

51 This cycle can be broken by caspase 1 inhibitors shown to be safe in humans, raising

52 ivation, and support the clinical testing of caspase-1 inhibitors such as VX-765 in autoinflammatory

53 suggest that Flightless-I may be a bona fide caspase-1 inhibitor that acts through a mechanism simila

54 new treatment strategies, such as the use of caspase-1 inhibitors that inhibit pyroptosis, may mainta

55 rved hyperinflammation, which decreased upon caspase-1 inhibitor treatment of K. pneumoniae-infected

56 CH-rats were treated with the Caspase-1 inhibitor VX-765 (15 mg/kg/d, 10 doses, n=11/g

57 We evaluated the effects of the caspase-1 inhibitor VX-765 on HIV-1 infection in humaniz

58 Pretreatment of Vpr-exposed neurons with the caspase-1 inhibitor, VX-765, reduced cleavage of both ca

59 inflammatory response if a LF was used or a caspase-1 inhibitor was administered during EVLP.

60 CARD18, a caspase-1 inhibitor, was the most upregulated protein by

61 ts either saline or a centrally administered caspase-1 inhibitor, which specifically prevents the syn

62 Specific caspase-1 inhibitors would provide a new class of anti-i

63 -)Casp11(-/-) BMDC, WT BMDC treated with the caspase-1 inhibitor YVAD, and BMDC lacking the inflammas

64 tion of IL-1beta production using a specific caspase-1 inhibitor (YVAD-fmk; 100 microM) significantly

65 neral caspase inhibitor Z-VAD-Fmk and by the caspase 1 inhibitor Z-YVAD-Fmk.

66 ant cells was significantly protected by the caspase-1 inhibitor (zVAD-fmk) in a dose-dependent manne