1 stall the N-hydroxytriazene pharmacophore of
triacsins.
2 Inhibition by
triacsins and troglitazone of long chain fatty acid inco
3 Triacsins are an intriguing class of specialized metabol
4 Triacsins are notable as potent acyl-CoA synthetase inhi
5 Pretreatment with 2 mumol/L
triacsin C (an inhibitor of acyl coenzyme A synthases) i
6 60-1) (BMS) (inhibits only MTP activity), or
triacsin C (TC) (inhibits only TG synthesis).
7 armacological targets but also indicate that
triacsin C and analogues can be explored as potential ne
8 n E. coli, activity of AasC was sensitive to
triacsin C and rosiglitazone G.
9 ts, together with previous data showing that
triacsin C and troglitazone strongly inhibit triacylglyc
10 xamine the effect on productive infection of
triacsin C and YIC-C8-434, which inhibit synthesis of TA
11 Triacsin C blocked esterification, thereby rendering the
12 In uptake studies,
triacsin C blocked the incorporation of [3H]glycerol int
13 ATP1, FATP4 was insensitive to inhibition by
triacsin C but was sensitive to feedback inhibition by a
14 Triacsin C caused a loss of about 60% of the TG mass fro
15 Instead, our results suggest that
triacsin C causes global alterations in the cellular lip
16 We confirmed that
triacsin C competes directly with atRE by incubating mem
17 The long-chain acyl-CoA synthetase inhibitor
triacsin C completely reversed fatty acid-induced ABCA1
18 lack of inhibition of a metabolic pathway by
triacsin C does not prove lack of acyl-CoA involvement.
19 Most importantly,
triacsin C effectively reduced parasite oocyst productio
20 The ACS inhibitor
triacsin C strongly inhibited ACS1 and ACS4, but not ACS
21 We found
triacsin C to be a competitive inhibitor of RPE65 (IC50
22 h for perturbing lipid metabolism was to use
triacsin C to inhibit long-chain acyl-CoA synthetase.
23 Prolonged
triacsin C treatment activates both the IRE1 and PERK br
24 Triacsin C was highly effective against C. parvum growth
25 ptosporidial efficacies of the ACS inhibitor
triacsin C were evaluated both in vitro and in vivo.
26 site ACSs could be specifically inhibited by
triacsin C with the inhibition constant Ki in the nanomo
27 bolic reactions, PMNs (37 or 4 degreesC; +/-
triacsin C) could not be shown to receptor bind either r
28 could be partially blocked by an inhibitor (
triacsin C) of long chain acyl-CoA synthetase.
29 Triacsin C, a competitive inhibitor of both ACS1 and ACS
30 in colon cancer and other cell lines, as did
triacsin C, a FACL inhibitor.
31 tion of long-chain acyl-CoA synthetases with
triacsin C, a fatty acid analogue, impairs lipid droplet
32 Triacsin C, an inhibitor of ACSL1 and ACSL4, also inhibi
33 ACSL-mediated inhibition, we discovered that
triacsin C, an inhibitor of ACSLs, also potently inhibit
34 l triglyceride transfer protein inhibitor or
triacsin C, an inhibitor of acyl-CoA synthase, completel
35 expose TG hydrolysis in NLSD cells by using
triacsin C, an inhibitor of acyl-CoA synthetase that blo
36 Triacsin C, an inhibitor of fatty acyl-CoA synthetase, a
37 Triacsin C, an inhibitor of fatty acyl-CoA synthetase, p
38 Both effects were reversed by
triacsin C, an inhibitor of fatty acyl-CoA synthetase, t
39 t of 832/13 cells with AdCMV-MCD Delta 5 and
triacsin C, an inhibitor of long chain acyl-CoA syntheta
40 drolysis with RHC80267 or its acylation with
triacsin C, enhanced recruitment of perilipin 3 to the E
41 by the fatty acyl-CoA synthetase inhibitor,
triacsin C, evidence of its mediation by fatty acyl-CoA.
42 blocked by the acyl-CoA synthetase inhibitor
triacsin C, implicating that mLDs are synthesized de nov
43 The acyl:CoA synthetase blocker,
triacsin C, inhibited esterification but also led to an
44 In the case of
triacsin C, reduced stability of the viral core protein,
45 acids to fatty acyl-CoA, was inhibited with
triacsin C, the increases in both AMPK activity and AMP:
46 ngly, FATP1 was insensitive to inhibition by
triacsin C, whereas ACS1 was inhibited by micromolar con
47 Moreover,
triacsin C, which blocks both triglyceride and cholester
48 Triacsin C, which inhibits the conversion of FFAs to lon
49 Triacsin C, with an alkenyl chain resembling but not ide
50 The absence of a
triacsin C-insensitive pathway and the increased inhibit
51 owered and PFK Vmax was increased, both in a
triacsin C-reversible fashion.
52 Indeed,
triacsin C-treated membranes bound (Kd = 3.8 nM) 5-[3H]o
53 ecenal and the acyl-CoA synthetase inhibitor
triacsin C.
54 n cells were pretreated with sodium azide or
Triacsin C.
55 be partially rescued by the ACSL inhibitor,
Triacsin C.
56 ly enhanced the apoptosis-inducing effect of
triacsin C.
57 glycerol synthesis was blocked with 6 microm
triacsin C.
58 r [3H]glycerol and chased in the presence of
triacsin C.
59 Addition of
Triacsin-
C, an inhibitor of long-chain acyl-CoA syntheta
60 Triacsin-
C, which blocks palmitoyl-CoA synthesis, and L-
61 Inhibition of TG synthesis by
Triacsin D, on the other hand, significantly decreased t
62 ria, suggesting that a hitherto unidentified
triacsin-
sensitive ACS is present in mitochondria.