ライフサイエンスコーパス: TLCK

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1 TLCK and MG 132 inhibited both IL-1beta-induced activati

2 TLCK treatment had no effect on Fas expression levels on

3 These effects were seen with both active and TLCK-inactivated protease, confirming that they were not

4 We find that TPCK and TLCK are not general signaling inhibitors since the acti

5 ety of physiological processes that TPCK and TLCK have been shown to effect.

6 Both TLCK and MG 132 also inhibited iNOS gene expression at t

7 zation of cells to Fas-mediated apoptosis by TLCK or other agents (cycloheximide, protein kinase C in

8 Purified GGT was inactivated by TLCK (Nalpha-p-tosyl-L-lysine chloromethyl ketone) and p

9 ant to these inhibitors but was inhibited by TLCK (Nalpha-p-tosyl-L-lysine chloromethyl ketone) and i

10 ion with HPV 18 DNA demonstrated that either TLCK (5--10 microM) or TPCK (0.25 microM) could inhibit

11 rations with the cysteine protease inhibitor TLCK.

12 as not inhibited by the proteinase inhibitor TLCK (N alpha-p-tosyl-L-lysine chloromethyl ketone), pro

13 The NFkappaB inhibitor (TLCK and PTD-p65), or a specific CaMKII inhibitor (m-AIP

14 ffect was blocked by the protease inhibitor, TLCK (P = 0.05 and P = 0.024, respectively), and was blo

15 eatment of CP30 with the protease inhibitors TLCK (Nalpha-p-tosyl-l-lysine chloromethyl ketone) and E

16 -alpha-p-tosyl-l-lysine chloromethyl ketone (TLCK) (85.4%), benzamidine (80.2%), and soybean trypsin

17 nhibitor tosyl-l-lysine chloromethyl ketone (TLCK) (P < 0.05).

18 alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK) and dithiothreitol was performed.

19 Nalpha-p-tosyl-L-lysine chloromethyl ketone (TLCK) and, to a lesser extent, H-D-Tyr-L-Pro-L-arginyl c

20 Nalpha-p-tosyl-L-lysine chloromethyl ketone (TLCK) blocked its effects on cultured cells, indicating

21 Nalpha-p-tosyl-l-lysine chloromethyl ketone (TLCK) exhibited dose-dependent inhibitory effects on a G

22 PCK) and tosyl-L-lysine chloromethyl ketone (TLCK) modified the HPV type 18 E7 protein in cell extrac

23 Nalpha-p-tosyl-L-lysine chloromethyl ketone (TLCK) or by infection with rAd-IkappaB, an rAd-encoding

24 hereas N-tosyl-L-lysine chloromethyl ketone (TLCK), Ac-Leu-Leu-L-norleucinal, Ac-Leu-Leu-L-methional,

25 Nalpha-P-tosyl-L-lysine chloromethyl ketone (TLCK), and a proteasome complex (26S) inhibitor, MG 132,

26 but N-p-tosyl-L-lysine chloromethyl ketone (TLCK), another serine protease inhibitor, was without ef

27 bitor, N-tosyl-L-lysine chloromethyl ketone (TLCK), dramatically enhances Fas-mediated apoptosis in t

28 Nalpha-p-tosyl-L-lysine chloromethyl ketone (TLCK)-inactivated HRgpA, indicating it was independent o

29 alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK).

30 (TPCK) and tosyllysine chloromethyl ketone (TLCK).

31 In an analogous manner, TLCK (100 micromol/l) and MG 132 (10 micromol/l) inhibit

32 ndings suggest that the inhibitory action of TLCK and MG 132 on iNOS and COX-2 expression precedes tr

33 Application of TLCK or PTD-p65 inhibited the glutamate-induced BDNF exp

34 The enhancing effect of TLCK is specific to Fas-induced cell death, with no effe

35 the present study we evaluated the effect of TLCK or TPCK treatment on the immortalization of primary

36 cleavage of collagens and susceptibility to TLCK.

37 pe I and IV collagens and was susceptible to TLCK inhibition.

38 edium of primary foreskin keratinocytes with TLCK or TPCK during their immortalization with HPV 18 DN

39 n cells exposed to proteases pretreated with TLCK to inactivate the catalytic component.

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