ライフサイエンスコーパス: triacsin C

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

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

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

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

5 glycerol synthesis was blocked with 6 microm triacsin C.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

24 Triacsin C blocked esterification, thereby rendering the

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

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

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

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

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

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

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

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

33 Most importantly, triacsin C effectively reduced parasite oocyst productio

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

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

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

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

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

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

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

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

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

43 60-1) (BMS) (inhibits only MTP activity), or triacsin C (TC) (inhibits only TG synthesis).

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

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

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

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

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

49 Triacsin C was highly effective against C. parvum growth

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

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

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

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

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

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

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