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1 e when its endogenous FAS was inhibited with cerulenin.
2 e superfamily, and the site of alkylation by cerulenin.
3 LDs, a phenomenon not exhibited by 2-FPA and cerulenin.
4 (2-BP), 2-fluoro palmitic acid (2-FPA), and cerulenin.
5 s on viral replication compared to 2-FPA and cerulenin.
6 esence of the fatty acid synthesis inhibitor cerulenin.
7 and fasted wild-type mice, were treated with cerulenin.
8 ity of elongation reactions to inhibition by cerulenin.
9 he addition of the FA biosynthesis inhibitor cerulenin.
10 o natural products, thiolactomycin (TLM) and cerulenin.
11 ed condensation reaction, was insensitive to cerulenin (100 microM) and cross-reacted with spinach KA
12 e have demonstrated that the natural product cerulenin ([2R,3S]-2,3-epoxy-4-oxo-7,10-trans,trans-dode
13 We examined the effects of the mycotoxin cerulenin (a covalent FAS inactivator), and the novel sm
15 and carcinoma lines are growth inhibited by cerulenin, a noncompetitive inhibitor of fatty acid synt
19 FASN as the inhibitor of its activity, named cerulenin, abolished the growth response to both ligands
23 stration of a fatty acid synthase inhibitor, cerulenin, also alleviated the pathology of psoriasis.
25 tures are also smaller in cells treated with cerulenin, an inhibitor of de novo fatty acid synthesis
28 te elongation was 85% inhibited by 50 microm cerulenin, an inhibitor of ketoacyl-acyl carrier protein
29 Expression of each marker is inhibited by cerulenin, an inhibitor of polyketide synthesis, and can
31 side other palmitoylation inhibitors such as cerulenin and 2-fluoro palmitic acid (2-FPA), as well as
35 ed growth in YPD medium containing 25 microM cerulenin and 500 microM fatty acid (myristate (C14:0),
37 e with fatty acid synthase (FAS) inhibitors (cerulenin and a synthetic compound C75) led to inhibitio
44 tment with the fatty acid synthase inhibitor cerulenin and is rescued by addition of exogenous unsatu
47 ynthase (FAS), including the natural product cerulenin and the novel compound c75, are selectively cy
48 ynthase (FAS), including the natural product cerulenin and the novel synthetic compound c75, are sele
49 75 based on the known mechanism of action of cerulenin and the theoretical reaction intermediates of
52 gar metabolism (2-DG), fatty acid synthesis (cerulenin), and N-linked glycosylation (tunicamycin) com
58 al rearrangement upon covalent inhibition of cerulenin at the active cysteine residue in E. coli type
63 lished ascites tumor; and (e) treatment with cerulenin causes reduction in ascites incidence, delay i
64 etworks and differential network analyses on cerulenin, chlorpromazine, ethionamide, ofloxacin, thiol
66 e, the major product of FAS, indicating that cerulenin cytotoxicity is mediated through fatty acid st
68 about 30% (P<0.05), further suggesting that cerulenin does not non-specifically activate wide variet
71 ts selective and potent inhibitory activity, cerulenin has found significant utility in multidiscipli
76 y acid synthase was inhibited with 45 microm cerulenin in the presence of 100 microm oleate (C(18:1))
82 The mechanism of DNA synthesis inhibition by cerulenin is indirect, because expression of certain vir
83 t studies have shown that the FAS inhibitor, cerulenin, is selectively cytotoxic to cell lines derive
86 the specific fatty acid synthase inhibitor, cerulenin, markedly reduces tumor cell fatty acid biosyn
88 Conjugates of mycothiol with the antibiotic cerulenin, N-ethylmaleimide, 3-(N-maleimidopropionyl)-bi
89 contrast, the fatty-acid synthase inhibitor cerulenin nearly completely blocked sphingoid base produ
90 age was taken of this to study the effect of cerulenin on the K(ATP) channel-independent pathway of g
92 entiated apoptosis induced by FAS inhibitors cerulenin or C75 only in cells with constitutively activ
93 Furthermore, inhibition of FAS activity by cerulenin or C75 resulted in downregulation of phospho-A
95 -altering inhibitor of fatty acid synthesis (cerulenin), or an inhibitor of intracellular membrane tr
96 s a correlation between growth on fatty acid/cerulenin plates, the levels of fatty acid accumulation,
98 increased metabolic rate in ob/ob mice, and cerulenin produced the same effects in wild-type mice, w
102 ilis resting cells whereas a strain having a cerulenin-resistant FabF mutant produced more biotin.
103 alent inhibition profile has been confirmed, cerulenin's mechanism has not been fully determined at a
104 nsitive to the fatty acid synthase inhibitor cerulenin, showed aberrant expression of fatty acid bios
105 esis with 5-(tetradecyloxy)-2-furoic acid or cerulenin significantly attenuates the enhancement of HC
106 ferences between the FabB-cerulenin and FabF-cerulenin structures explain the differences in the sens
107 Tsc13p-GFP into NV junctions is perturbed by cerulenin, suggesting that its binding to Nvj1p depends
108 eatment with the chemical inhibitors C75 and cerulenin suppressed NLRP3-mediated caspase-1 activation
110 on of the fatty acid biosynthesis inhibitor, cerulenin, that possesses an alkyl chain length in the r
111 inhibit fatty acid oxidation is affected by cerulenin, these data suggest that protein acylation is
114 tty acid biosynthesis (FAB), since following cerulenin treatment, wild-type and relA strains expresse
116 for growth under hypoxic conditions and when cerulenin was included in the culture media in the prese
117 ected with the fatty acid synthase inhibitor cerulenin were examined for Fos (a marker for neuronal a
119 d mass/cell) but retain their sensitivity to cerulenin, which is reversed by 3-fold excess oleate sup
120 medium show a dose-dependent sensitivity to cerulenin, which is reversed by palmitate, the major pro
121 inishes, and the cells become insensitive to cerulenin while acquiring a differentiated, macrophage-l