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1 ol regulatory element-binding protein 1c and fatty acid synthase.
2 s of lipogenesis, acetyl CoA carboxylase and fatty acid synthase.
3 and highly selective inhibitor of mammalian fatty acid synthase.
4 id synthesis genes acetyl CoA carboxylase or fatty acid synthase.
5 combinant form of the thioesterase domain of fatty acid synthase.
6 demonstrated with acetyl-CoA carboxylase and fatty acid synthase.
7 ruvate kinase, acetyl-CoA carboxylase 1, and fatty acid synthase.
8 hydroxy-3-methylglutaryl CoA reductase), and fatty acid synthase.
9 oacyl synthase domain of the human cytosolic fatty acid synthase.
10 radation, thiamin biosynthesis and cytosolic fatty acid synthase.
11 y-terminal thioesterase domain of the animal fatty acid synthase.
12 f both hepatic stearoyl CoA desaturase-1 and fatty acid synthase.
13 nt fatty acid product derived from mammalian fatty acid synthase.
14 the expression of acetyl-CoA carboxylase and fatty acid synthase.
15 protein, acetyl coenzyme A carboxylase, and fatty acid synthase.
16 tease serine 2, FK506-binding protein 51 and fatty acid synthase.
17 compared to the homologous dimeric mammalian fatty acid synthase.
18 ibits up-regulation of ATP citrate lyase and fatty-acid synthase.
19 acids are synthesized by type I and type II fatty acid synthases.
20 ta-ketoacyl-ACP synthase activity of type II fatty acid synthases.
21 acyl thioesters generating novel short-chain fatty acid synthases.
22 ective inhibitors of bacterial and mammalian fatty acid synthases.
23 products that target bacterial and mammalian fatty acid synthases.
24 atory element-binding protein 1c target gene fatty-acid synthase (3.0-fold), early growth response-1
25 and 18-carbon fatty acids is carried out by fatty acid synthase, a 2.6 megadalton molecular-weight m
26 acid synthetic genes, including Srebp-1 and fatty acid synthase, a pathway previously shown to be in
27 r, to the acyl carrier protein domain of the fatty acid synthase, a thioesterase active toward shorte
29 macologic inhibition of Rho, glutaminase, or fatty acid synthase abrogated the increased lipid conten
30 ory element-binding transcription factor 1c, fatty acid synthase, acetyl coenzyme A carboxylase 2, an
31 of the key enzymes involved in lipogenesis: fatty acid synthase, acetyl-CoA carboxylase 1, and glyce
32 cells, the mRNA levels of SREBP1-c, SREBP2, fatty-acid synthase, acetyl-CoA carboxylase, ATP citrate
33 ction of apoptosis in VarK-infected MCC with fatty acid synthase-activating antibody significantly en
34 thioesterase domain and resulted in reduced fatty acid synthase activity and an increase in product
35 We traced this defect to the uncoupling of fatty acid synthase activity from stearoyl-CoA desaturas
36 romotes insulin clearance and down-regulates fatty acid synthase activity in the liver upon its phosp
39 leptin resistance and elevated hypothalamic fatty-acid synthase activity could underlie altered ener
42 with type I polyketide synthases and related fatty-acid synthases also extends to the interdomain con
43 de-1-beta-D-ribofuranoside) enhanced and the fatty acid synthase-AMPK inhibitor C75 (3-carboxy-4-octy
44 ovel inhibitor of the thioesterase domain of fatty acid synthase, an enzyme strongly linked to tumor
45 s, which correlates with increased levels of Fatty Acid Synthase and Acetyl CoA Carboxylase mRNAs, en
47 ly increased the hepatic protein contents of fatty acid synthase and acetyl-coenzyme A carboxylase (A
48 ocess by application to the Escherichia coli fatty acid synthase and apply it to probe protein-protei
49 wnregulation of stearoyl CoA desaturase-1 or fatty acid synthase and by upregulation of hepatic chole
51 l activation of lipogenic enzymes, including fatty acid synthase and glycerol-3-phosphate acyltransfe
52 ious enzymes in lipogenic pathway, including fatty acid synthase and glycerol-3-phosphate acyltransfe
53 lipogenic genes, acetyl CoA carboxylase, and fatty acid synthase and increasing the expression of bet
54 of utilization and degradation catalyzed by fatty acid synthase and malonyl-CoA decarboxylase, respe
55 ces secretion of several proteins, including fatty acid synthase and metastasis-associated laminins.
57 the catalytic domains of multidomain type I fatty acid synthase and polyketide synthase (PKS) system
58 everal proadipogenic genes, adiponectin, and fatty acid synthase and reduced the expression of inflam
60 enes involved in lipid metabolism, including fatty acid synthase and steroyl coenzyme-A desaturase, t
61 ective inhibitors of bacterial and mammalian fatty acid synthases and have emerged as promising drug
64 arboxylase), elevation in expression of FAS (fatty acid synthase), and lipid accumulation in human He
68 member 2, solute carrier family 27 member 4, fatty acid synthase, and long-chain acyl-CoA synthetase
69 n the acyltransferase (AT) domains of DynE8, fatty acid synthase, and modular polyketide synthases, w
72 y role between malonyl-CoA, the substrate of fatty acid synthase, and the neural circuitry regulating
73 or 3-hydroxy-3-methylglutaryl-CoA reductase, fatty-acid synthase, and squalene synthase in livers of
74 y lipogenic enzymes, acetyl-CoA carboxylase, fatty-acid synthase, and stearoyl-CoA desaturase-1 were
76 regulation of lipogenic enzymes SREBP-1c and fatty acid synthase, as well as increased hepatic lipid
78 ifunctional enzymes that resemble eukaryotic fatty acid synthases but can make highly functionalized
79 ular administration of a potent inhibitor of fatty acid synthase, C75, increases the level of its sub
80 trol encoding, for example, the cyclopropane fatty acid synthase, Cfa, the glycogen synthesis protein
83 issue indicated that nuclear localization of fatty acid synthase correlates with Gleason grade, impli
84 MFN1, MFN2 or inhibiting lipid synthesis via fatty acid synthase deficiency in AEC2 cells exacerbates
85 ketide synthase that uniquely incorporates a fatty acid synthase-derived dichloropyrrolyl extender un
86 biochemical regulators of bacterial type II fatty acid synthases due to their ability to feedback-in
88 ma gondii enoyl reductase (TgENR), a type II fatty acid synthase enzyme essential in parasites but no
90 that fatty acid oxidation was increased and fatty acid synthase expression associated with lipogenes
92 9), (11)C-acetate uptake was independent of fatty acid synthase expression using immunohistochemistr
95 eptococcus pneumoniae, the expression of the fatty acid synthase (fab) genes is controlled by a helix
96 III (KSIII) AsuC3/C4 as well as the cellular fatty acid synthase FabH to produce the asukamycin conge
97 els in E1 and E4-mice were linked to reduced fatty acid synthase (FAS) activity and hepatic expressio
98 f nicotine increased lipolysis and inhibited fatty acid synthase (FAS) activity in a time- and dose-d
99 ly by overexpression and/or hyperactivity of fatty acid synthase (FAS) and acetyl-CoA carboxylase (AC
100 sis as reflected by increased mRNA levels of fatty acid synthase (Fas) and acetyl-CoA carboxylase (Ac
101 arrier proteins (ACPs) are essential to both fatty acid synthase (FAS) and polyketide synthase (PKS)
102 Activation of AKT and overexpression of fatty acid synthase (FAS) are frequently observed in hum
106 chanisms in the fetal liver, reduces hepatic fatty acid synthase (Fas) expression and improves glucos
108 related with its inability to increase liver fatty acid synthase (FAS) gene expression, which was up-
110 el of intrauterine growth restriction due to fatty acid synthase (FAS) haploinsufficiency (FAS deleti
120 tent inhibitor of the thioesterase domain of fatty acid synthase (FAS) led us to develop a concise an
122 feeding-dependent regulation of SREBP-1c and fatty acid synthase (FAS) mRNA expression in the transit
123 We developed a detailed kinetic model of the fatty acid synthase (FAS) of Escherichia coli and paired
128 tween autophagy-related protein 8 (Atg8) and fatty acid synthase (FAS), a pivotal enzymatic complex r
129 Endogenous fatty acid synthesis, mediated by fatty acid synthase (FAS), affects membrane composition.
131 or of lipid metabolism by inducing SREBP-1c, fatty acid synthase (FAS), and acetyl-CoA carboxylase (A
132 ncluding choline kinase alpha (ChoK(alpha)), fatty acid synthase (FAS), and phosphorylated ATP-citrat
134 ing protein (aP2), lipoprotein lipase (LPL), fatty acid synthase (FAS), hormone sensitive lipase (HSL
135 nistration of C75, a potent inhibitor of the fatty acid synthase (FAS), increases malonyl-CoA concent
137 es involved in fatty acid synthesis, such as fatty acid synthase (FAS), sterol receptor element bindi
138 ional activators of lipogenic genes, such as fatty acid synthase (FAS), sterol regulatory element-bin
139 expression is impaired with inactivation of fatty acid synthase (FAS), suggesting that FAS is involv
142 nd SREBP-2 proteins as well as expression of fatty acid synthase (FAS), the key regulatory enzyme in
144 er cells respond to inhibition of the enzyme fatty acid synthase (FAS), we focused on NF-kappaB-media
153 produced via a combination of type I and II fatty acid synthases (FAS) with FAS-I products being elo
157 e elongation systems, the type I and type II fatty acid synthases (FAS-I and FAS-II respectively).
158 primary lipogenic target enzymes, including fatty-acid synthase (FAS) and acetyl-CoA carboxylase 1 (
159 esis affects atherosclerosis, we inactivated fatty-acid synthase (FAS) in macrophages of apoE-deficie
161 process driven by the multifunctional enzyme fatty-acid synthase (FAS), maintains endothelial functio
162 sms underlying transcriptional activation of fatty-acid synthase (FAS), we examined the relationship
163 We show there is a widespread branch of fatty acid synthase- (FAS)-like polyketide synthase (PKS
164 by competing with the enzymes of the type II fatty acid synthase (FASII) cycle for the beta-hydroxyac
165 mal stress-responsive factors, including the fatty acid synthase FASN-1, anti-microbial peptides, and
166 n-regulating their targeted genes, including fatty acid synthase (FASN) and 3-hydroxy-3-methylglutary
167 hibited CCL2-induced increases in hepatocyte fatty acid synthase (Fasn) and adipose differentiation-r
169 onist CL316,243 (CL) increased expression of fatty acid synthase (FASN) and medium chain acyl-CoA deh
174 noma cell growth; this required simultaneous fatty acid synthase (FASN) inhibition when FASN expressi
189 al genetic and pharmacological inhibition of fatty acid synthase (FASN) suppresses toxicity induced b
190 on of lipid metabolism via overexpression of fatty acid synthase (FASN), a key enzyme in de novo fatt
192 ynthesis resulted from the downregulation of fatty acid synthase (FASN), a key regulator of fatty aci
193 ng up-regulation of lipid synthesis enzymes [fatty acid synthase (FASN), acetyl-CoA carboxylase (ACC)
194 luding fatty acid binding protein 5 (FABP5), fatty acid synthase (FASN), and monoacylglycerol lipase
195 ic enzymes [acetyl CoA carboxylase 1 (ACC1), fatty acid synthase (FASN), and stearoyl CoA desaturase
196 nkage disequilibrium in 17q25.3, which spans fatty acid synthase (FASN), coiled-coil-domain-containin
197 ulatory element-binding protein 1 (SREBP-1), fatty acid synthase (FASN), hormone-sensitive lipase (HS
198 revealed that a key enzyme in this pathway, fatty acid synthase (FASN), is relocalized to sites of D
199 (ChREBP, a master lipogenic regulator), and fatty acid synthase (FASN), its effector lipogenic gene.
202 c model of myocardium-specific expression of fatty acid synthase (FASN), the major palmitate-synthesi
203 he HCV genotype 2a (JFH1) virus, among which fatty acid synthase (FASN), the multifunctional enzyme c
205 ein 1c (SREBP-1c) and its downstream target, fatty acid synthase (FASN), which are key proteins invol
207 bryonic stem cells (hESCs) expressing mutant fatty acid synthase (FASN; R1819W), a metabolic regulato
208 ynthesis, one in the cytoplasm (catalyzed by fatty acid synthase, FASN) and one in the mitochondria (
210 ichment, and identification of DH enzymes in fatty acid synthases (FASs) and polyketide synthases (PK
211 and polyketide biosynthesis, and most of the fatty acid synthases (FASs) and polyketide synthases (PK
212 de synthases (PKSs) use chemistry similar to fatty acid synthases (FASs), although building block var
213 e I polyketide synthases (PKSs), and related fatty acid synthases (FASs), represent a large group of
215 armacological proof of concept of inhibiting fatty acid synthase for the treatment of diabetes and re
216 site serine residue, or functionality of the fatty acid synthase; further shortening of the linker li
219 indicates that the lipogenic "overshoot" for fatty-acid synthase gene expression known to occur durin
222 que carboxyl terminal thioesterase domain of fatty acid synthase hydrolyzes the growing fatty acid ch
223 ulatory element-binding protein-1 (SREBP-1), fatty acid synthase, hydroxy-3-methylglutaryl coenzyme A
224 locks for de novo fatty acid biosynthesis by fatty acid synthase I (FAS I) and for the elongation of
225 ly, EchA6 interacts with selected enzymes of fatty acid synthase II (FAS-II) in bacterial two-hybrid
228 PKD1L2 primarily associates with endogenous fatty acid synthase in normal skeletal muscle, and these
230 xylase content and higher gene expression of fatty acid synthase in the liver indicated reduced fatty
231 t binding protein-1, acetyl-CoA carboxylase, fatty acid synthase) in the group with high VAT/(VAT+SAT
232 ciated enzymes, acetyl-CoA carboxylase-1 and fatty acid synthase, in the liver and hypothalamus.
233 and 18 carbon fatty acids is carried out by fatty acid synthase: in yeast Saccharomyces cerevisiae,
235 efect is recapitulated by treatment with the fatty acid synthase inhibitor cerulenin and is rescued b
236 ulnificus disease, was hypersensitive to the fatty acid synthase inhibitor cerulenin, showed aberrant
237 intake caused by i.c.v.-administered C75, a fatty acid synthase inhibitor that increases hypothalami
238 Correlating with this, administration of a fatty acid synthase inhibitor, cerulenin, also alleviate
239 h a surrogate of TVB-2640, a pharmacological fatty acid synthase inhibitor, has been shown to reduce
240 data support the therapeutic potential of a fatty acid synthase inhibitor, TVB-2640 in particular, i
242 the glycolytic inhibitor, 2-deoxyglucose, or fatty acid synthase inhibitors to perturb the metabolic
243 es with KasA, a key component of the type II Fatty Acid Synthase involved in mycolic acid synthesis.
247 the acyl chain, the overall integrity of the fatty acid synthase is quite tolerant to moderate change
249 y acid biosynthesis by a type II dissociated fatty acid synthases is catalyzed by 3-ketoacyl-acyl car
250 yzed by both polyketide synthases (PKSs) and fatty acid synthases is most often carried out by a thio
252 lecular features including cyclooxygenase 2, fatty acid synthase, KRAS, BRAF, PIK3CA, p53, p21, beta-
258 the upstream acetyl coenzyme A formation and fatty acid synthase modules enabled further production i
260 nic enzymes, including a >2-fold increase in fatty acid synthase mRNA, protein, and activity, there w
262 n of the E1-SUMO intermediate; inhibition of fatty acid synthase; non-specific SIRT inhibition; and a
264 ion of genes coding for a putative cytosolic fatty acid synthase of type 1 (FAS1) and polyketide synt
267 mponents of a putative type II mitochondrial fatty acid synthase pathway have been identified in huma
269 ylcholine, which is blocked by inhibitors of fatty-acid synthase, PI 3-kinase, mTORC, or an antibody
270 t are widely used as inhibitors of mammalian fatty acid synthase, platensimycin specifically inhibits
271 rol regulatory element-binding protein 1 and fatty acid synthase protein levels in epididymal WAT of
273 sruption of the apicoplast-localized type II fatty-acid synthase resulted in greatly reduced synthesi
274 ta-oxidation, augmentation of translation of fatty acid synthase resulting in de novo lipogenesis, an
278 ession of genes involved in lipid synthesis (fatty acid synthase, squalene epoxidase, hydroxy-methylg
279 hesis genes, namely, acetyl-CoA carboxylase, fatty acid synthase, SREBP1c, chREBP, glucokinase, and p
280 g to several crucial lipid metabolism genes (fatty acid synthase, stearoyl-coenzyme A desaturase 1, a
281 involved in the de novo lipogenesis, such as fatty-acid synthase, stearoyl-CoA desaturase (SCD)-1, an
282 rted lower resolution, 4.5-Angstrom model of fatty acid synthase structure, and emphasizes the close
283 iated with a deficiency in the mitochondrial fatty acid synthase system, namely depleted lipoylation
284 he approach is broadly applicable to type II fatty acid synthase systems found in plants and bacteria
285 of the bacterial and eukaryotic multienzyme fatty acid synthase systems offer the prospect of inhibi
286 the conserved reaction chemistry of various fatty acid synthase systems, the individual isozymes tha
287 on of fas, which encodes the multifunctional fatty acid synthase that supports phospholipid and trigl
288 with the DH of the highly related animalian fatty acid synthase, the DH monomer possesses a double-h
289 ses have been studied, including the soluble fatty acid synthases, those involved in polyketide synth
290 n 1c (SREBP-1c), acetyl-CoA carboxylase, and fatty-acid synthase, three key functions in the lipogeni
291 CPS is sufficiently different from the human fatty acid synthase to justify the development of novel
292 tudies presented here show that cyclopropane fatty acid synthase transcription induced by neutral ace
293 of carcinogen-treated versus untreated mice: fatty acid synthase, transketolase, pulmonary surfactant
296 suppressing the expression (and activity) of fatty acid synthase via a nonclassical pathway dependent
297 EBP1 target genes acetyl-CoA carboxylase and fatty-acid synthase was suppressed, along with suppresse
298 ol regulatory element-binding protein 1c and fatty acid synthase, were detected in the livers of Adip
299 bitor of the condensing reactions of type II fatty acid synthase, were synthesized and evaluated for
300 oblast growth factor 21, interleukin-10, and fatty acid synthase, which are all regulated by nuclear