ライフサイエンスコーパス: triacsin

1 Inhibition by triacsins and troglitazone of long chain fatty acid inco

2 Pretreatment with 2 mumol/L triacsin C (an inhibitor of acyl coenzyme A synthases) i

3 60-1) (BMS) (inhibits only MTP activity), or triacsin C (TC) (inhibits only TG synthesis).

4 armacological targets but also indicate that triacsin C and analogues can be explored as potential ne

5 n E. coli, activity of AasC was sensitive to triacsin C and rosiglitazone G.

6 ts, together with previous data showing that triacsin C and troglitazone strongly inhibit triacylglyc

7 xamine the effect on productive infection of triacsin C and YIC-C8-434, which inhibit synthesis of TA

8 Triacsin C blocked esterification, thereby rendering the

9 In uptake studies, triacsin C blocked the incorporation of [3H]glycerol int

10 ATP1, FATP4 was insensitive to inhibition by triacsin C but was sensitive to feedback inhibition by a

11 Triacsin C caused a loss of about 60% of the TG mass fro

12 Instead, our results suggest that triacsin C causes global alterations in the cellular lip

13 We confirmed that triacsin C competes directly with atRE by incubating mem

14 The long-chain acyl-CoA synthetase inhibitor triacsin C completely reversed fatty acid-induced ABCA1

15 lack of inhibition of a metabolic pathway by triacsin C does not prove lack of acyl-CoA involvement.

16 Most importantly, triacsin C effectively reduced parasite oocyst productio

17 The ACS inhibitor triacsin C strongly inhibited ACS1 and ACS4, but not ACS

18 We found triacsin C to be a competitive inhibitor of RPE65 (IC50

19 h for perturbing lipid metabolism was to use triacsin C to inhibit long-chain acyl-CoA synthetase.

20 Prolonged triacsin C treatment activates both the IRE1 and PERK br

21 Triacsin C was highly effective against C. parvum growth

22 ptosporidial efficacies of the ACS inhibitor triacsin C were evaluated both in vitro and in vivo.

23 site ACSs could be specifically inhibited by triacsin C with the inhibition constant Ki in the nanomo

24 bolic reactions, PMNs (37 or 4 degreesC; +/- triacsin C) could not be shown to receptor bind either r

25 could be partially blocked by an inhibitor (triacsin C) of long chain acyl-CoA synthetase.

26 Triacsin C, a competitive inhibitor of both ACS1 and ACS

27 in colon cancer and other cell lines, as did triacsin C, a FACL inhibitor.

28 tion of long-chain acyl-CoA synthetases with triacsin C, a fatty acid analogue, impairs lipid droplet

29 Triacsin C, an inhibitor of ACSL1 and ACSL4, also inhibi

30 ACSL-mediated inhibition, we discovered that triacsin C, an inhibitor of ACSLs, also potently inhibit

31 l triglyceride transfer protein inhibitor or triacsin C, an inhibitor of acyl-CoA synthase, completel

32 expose TG hydrolysis in NLSD cells by using triacsin C, an inhibitor of acyl-CoA synthetase that blo

33 Triacsin C, an inhibitor of fatty acyl-CoA synthetase, a

34 Triacsin C, an inhibitor of fatty acyl-CoA synthetase, p

35 Both effects were reversed by triacsin C, an inhibitor of fatty acyl-CoA synthetase, t

36 t of 832/13 cells with AdCMV-MCD Delta 5 and triacsin C, an inhibitor of long chain acyl-CoA syntheta

37 drolysis with RHC80267 or its acylation with triacsin C, enhanced recruitment of perilipin 3 to the E

38 by the fatty acyl-CoA synthetase inhibitor, triacsin C, evidence of its mediation by fatty acyl-CoA.

39 blocked by the acyl-CoA synthetase inhibitor triacsin C, implicating that mLDs are synthesized de nov

40 The acyl:CoA synthetase blocker, triacsin C, inhibited esterification but also led to an

41 In the case of triacsin C, reduced stability of the viral core protein,

42 acids to fatty acyl-CoA, was inhibited with triacsin C, the increases in both AMPK activity and AMP:

43 ngly, FATP1 was insensitive to inhibition by triacsin C, whereas ACS1 was inhibited by micromolar con

44 Moreover, triacsin C, which blocks both triglyceride and cholester

45 Triacsin C, which inhibits the conversion of FFAs to lon

46 Triacsin C, with an alkenyl chain resembling but not ide

47 The absence of a triacsin C-insensitive pathway and the increased inhibit

48 owered and PFK Vmax was increased, both in a triacsin C-reversible fashion.

49 Indeed, triacsin C-treated membranes bound (Kd = 3.8 nM) 5-[3H]o

50 ecenal and the acyl-CoA synthetase inhibitor triacsin C.

51 n cells were pretreated with sodium azide or Triacsin C.

52 be partially rescued by the ACSL inhibitor, Triacsin C.

53 ly enhanced the apoptosis-inducing effect of triacsin C.

54 glycerol synthesis was blocked with 6 microm triacsin C.

55 r [3H]glycerol and chased in the presence of triacsin C.

56 Addition of Triacsin-C, an inhibitor of long-chain acyl-CoA syntheta

57 Triacsin-C, which blocks palmitoyl-CoA synthesis, and L-

58 Inhibition of TG synthesis by Triacsin D, on the other hand, significantly decreased t

59 ria, suggesting that a hitherto unidentified triacsin-sensitive ACS is present in mitochondria.