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1 LCAT), which rapidly converts cholesterol to cholesteryl ester.
2 ne, phosphatidylserine, triacylglycerol, and cholesteryl ester.
3 ncrease in the synthesis of phospholipid and cholesteryl ester.
4 d from other condensed structures, including cholesteryl esters.
5 two enzymes that convert free cholesterol to cholesteryl esters.
6 for neutral lipids such as triglycerides and cholesteryl esters.
7 in the duodenal hydrolysis and absorption of cholesteryl esters.
8 ase, leading to a subsequent accumulation of cholesteryl esters.
9 gh arachidonic acid and low linoleic acid in cholesteryl esters.
10 haviors are purines, substituted phenols, or cholesteryl esters.
12 h as in atherosclerosis, excessive levels of cholesteryl ester accumulate in lysosomes for reasons th
13 ell formation assessed by lipid staining and cholesteryl ester accumulation compared with control cel
14 therosclerosis in LDLR(-/-) mice by reducing cholesteryl ester accumulation in atherosclerotic sites.
15 asis and provide a potential explanation for cholesteryl ester accumulation in lysosomes of atheroscl
16 ged with acetylated low density lipoprotein, cholesteryl ester accumulation was 2.5-fold higher in ma
17 When fed a Western-type diet, hepatic TG and cholesteryl ester accumulation was significantly higher
20 tected against hepatic neutral lipid (TG and cholesteryl ester) accumulation, with the greatest diffe
22 in, markedly raises high-density lipoprotein-cholesteryl ester and has no effect on fecal cholesterol
23 R-mitochondrial communication-as measured by cholesteryl ester and phospholipid synthesis, respective
24 ing in quantifying two major neutral lipids: cholesteryl ester and triacylglycerol in cells and tissu
26 L gene-knockout (lal(-/-)) mice, blockage of cholesteryl ester and triglyceride metabolism led to abn
27 that mediate the liver to reduce the hepatic cholesteryl ester and triglyceride release, possibly lea
28 P) is a serum component responsible for both cholesteryl ester and triglyceride trafficking between h
29 s essential for the clearance of endocytosed cholesteryl ester and triglyceride-rich chylomicron remn
30 r protein (CETP) facilitates the transfer of cholesteryl ester and triglycerides between plasma lipop
32 ipoprotein (HDL) that mediates the uptake of cholesteryl esters and delivers them to a metabolically
33 Conditional genetic ablation of MTP reduces cholesteryl esters and enhances free cholesterol in the
34 e 1 (Acat1) converts cellular cholesterol to cholesteryl esters and is considered a drug target for t
36 (ARIC) Study analyzed plasma fatty acids in cholesteryl esters and phospholipids in whites residing
37 onal macrophages with resultant decreases in cholesteryl esters and triglyceride in the lysosomes of
38 ent LAL activity accumulate large amounts of cholesteryl esters and triglycerides in multiple tissues
39 ase (LAL) is essential for the hydrolysis of cholesteryl esters and triglycerides to generate cholest
41 id lipase (LAL) is a key enzyme that cleaves cholesteryl esters and triglycerides to generate free fa
44 id accumulation and storage of oxidized LDL, cholesteryl esters and triglycerides were abolished in H
46 e LAL inhibitor increased the levels of TAG, cholesteryl ester, and RE in both rat and mouse HSCs.
48 copy for the quantitative analysis of waxes, cholesteryl esters, and glycerides in meibum lipid (ML).
49 lipids (including lyso- and ether- species), cholesteryl esters, and glycerolipids were associated wi
50 cylglycerols, 1,2-diol diesters, wax esters, cholesteryl esters, and hydrocarbons, from TLC and high-
51 such as oxidized phospholipids and oxidized cholesteryl esters, and mediate a variety of immune resp
54 hosphatidylcholine-lipid species and gaining cholesteryl esters, and proteomic changes, with losses i
55 ated mice also have reduced levels of plasma cholesteryl esters, and reduced levels of hepatic choles
57 ing di- and triacylglycerols, phospholipids, cholesteryl esters, and wax esters in OG-treated sebocyt
59 GD3 and GD1a), cardiolipin, cholesterol and cholesteryl esters are elevated in autophagic vacuole fr
62 terol (FC)-labeled pre-beta(1)-HDL generated cholesteryl esters at a rate much greater than the rest
63 rate stimulated the synthesis of unsaturated cholesteryl esters at the expense of saturated esters.
64 refore, MTP plays a novel role in regulating cholesteryl ester biosynthesis in cells that produce lip
66 or longer does not impair the hydrolysis of cholesteryl esters but partially impairs the transport o
68 e and metabolism of high density lipoprotein cholesteryl esters by direct and indirect interactions w
69 l metabolism-associated lipids [arachidonoyl cholesteryl ester, C8-dihydroceramide, N-stearoyl-d-sphi
70 intima, contributes to massive intracellular cholesteryl ester (CE) accumulation in human vascular sm
72 eryl ester transfer protein (CETP) transfers cholesteryl ester (CE) and triglyceride (TG) between lip
73 ed O-stained foam cells and showed increased cholesteryl ester (CE) content when cocultured with LDL.
74 ticles or via selective uptake (SU), wherein cholesteryl ester (CE) enters cells without concomitant
75 cal activities of mmLDL were associated with cholesteryl ester (CE) hydroperoxides and were diminishe
77 l-CoA and cholesterol are two substrates for cholesteryl ester (CE) synthesis via the ACAT reaction.
78 tent CETP inhibitor that maximally inhibited cholesteryl ester (CE) transfer activity at an oral dose
79 pment of protocols for the direct measure of cholesteryl ester (CE) transfer activity resident in hum
80 ked selective high-density lipoprotein (HDL) cholesteryl ester (CE) transport and steroidogenesis.
81 by selective high density lipoprotein (HDL)-cholesteryl ester (CE) uptake, mediated by scavenger rec
85 e different CD1c conformations and suggested cholesteryl esters (CE) and acylated steryl glycosides (
87 otein liquid chromatography profiles, aortic cholesteryl esters (CE), and plaque sizes were determine
89 hydrolysis of high-density lipoprotein (HDL) cholesteryl esters (CEs) after selective uptake by hepat
90 rvention on plasma fatty acid composition of cholesteryl esters (CEs) and phospholipids and estimated
91 lyzes the hydrolysis of intracellular stored cholesteryl esters (CEs) and thereby enhances free chole
92 sfer protein (CETP) mediates the transfer of cholesteryl esters (CEs) and triglycerides between diffe
95 is a proatherogenic enzyme that contributes cholesteryl esters (CEs) to apoB-containing lipoproteins
96 binds HDL and mediates selective delivery of cholesteryl esters (CEs) to the liver, adrenals, and gon
97 of lipid species, that is, wax esters (WEs), cholesteryl esters (CEs), and diesters (DEs) were correc
98 major compounds, triacylglycerols (TAGs) and cholesteryl esters (CEs), inside lipid droplets (LDs).
100 el wherein after lysosomal hydrolysis of LDL-cholesteryl esters, cholesterol binds NPC2, which transf
102 (by enzymatic colorimetry and fluorometry); cholesteryl ester composition (by electrospray ionizatio
103 ehyde-preserved eyes (20 eyes of 20 donors), cholesteryl ester composition of BrM/Ch, cornea, and scl
104 (x2.3) and cholesterol (x1.8) levels, while cholesteryl ester concentrations were not significantly
109 l ester transfer protein mediates direct HDL cholesteryl ester delivery to the liver cells; adipose t
110 demonstrate the presence of cholesterol and cholesteryl ester deposits beneath the retinal pigment e
111 h as keto, hydroperoxide, hydroxy, and epoxy cholesteryl ester derivatives from cholesteryl linoleate
112 thase had little or no ability to synthesize cholesteryl esters, diacylglycerols, or triacylglycerols
113 rption by the intestine and the secretion of cholesteryl ester-enriched very low density lipoproteins
115 RD4 has been shown to increase intracellular cholesteryl ester formation and is controlled at the tra
116 CRLPs without probucol, but phospholipid and cholesteryl ester formation from [(3)H]oleate was unaffe
120 ze HDL particles and prevent the transfer of cholesteryl ester from HDL to atherogenic lipoproteins.
122 fer protein (CETP) catalyzes the transfer of cholesteryl ester from high-density lipoprotein (HDL) to
123 r protein inhibitors prevent the transfer of cholesteryl ester from high-density lipoprotein to trigl
124 ester transfer protein-mediated transfer of cholesteryl ester from LDL+HDL to TRLs in vitro without
125 ryl ester transfer protein (CETP) transports cholesteryl ester from the antiatherogenic high-density
126 otein (CETP), which mediates the transfer of cholesteryl esters from HDL to apolipoprotein B-containi
127 eryl ester transfer protein (CETP) transfers cholesteryl esters from high-density lipoproteins to apo
129 lular cholesterol esterification by removing cholesteryl esters from their site of synthesis and depo
132 olesterol acyltransferase, ACAT, the neutral cholesteryl ester hydrolase (nCEH) that catalyzes the re
133 es cholesteryl ester is hydrolyzed by acidic cholesteryl ester hydrolase producing cholesterol and fa
136 us nCEH that can account for the majority of cholesteryl ester hydrolysis in transformed rat hepatic
139 ts with chronic inflammatory conditions, and cholesteryl ester hydroperoxides are present in plasma,
140 report that mmLDL and its active components, cholesteryl ester hydroperoxides, induce TLR4-dependent
141 up to 70-fold increases in specific oxidized cholesteryl esters, identical to those present in human
142 oscopy, we found an aberrant accumulation of cholesteryl ester in human pancreatic cancer specimens a
143 though esterification of free cholesterol to cholesteryl ester in the liver is known to be catalyzed
144 eeply within the protein, shifting the bound cholesteryl ester in the N-terminal pocket of the long h
147 wed excellent inhibition of the oxidation of cholesteryl esters in human low-density lipoprotein and
151 or-mediated uptake of LDL, hydrolysis of LDL-cholesteryl esters in lysosomes, and transfer of the lib
153 ive lipase (HSL) catalyzes the hydrolysis of cholesteryl esters in steroidogenic tissues and, thus, f
155 ficient animals synthesize lesser amounts of cholesteryl esters in vitro, but addition of purified MT
156 olecules with apoA-I residues indicates that cholesteryl esters interact with protein residues mainly
158 accumulation of oxidized LDL (OxLDL)-derived cholesteryl ester is considered to be a critical step in
161 ice had larger plasma HDLs enriched in apoM, cholesteryl ester, lecithin:cholesterol acyltransferase,
162 nous HSL, with siRNAs, resulted in increased cholesteryl ester levels and decreased cholesterol conte
163 had significantly lower free cholesterol and cholesteryl ester levels in the brachiocephalic artery t
166 e numbers and diminished the cholesterol and cholesteryl ester load without causing detectable apopto
168 ere, we have studied endosomal and lysosomal cholesteryl ester metabolism in cultured mouse macrophag
170 esterol, which creates a hydrophobic core of cholesteryl ester molecules in the middle of the discoid
171 itionally, the average number of contacts of cholesteryl ester molecules with apoA-I residues indicat
172 f oxidized phospholipids (OxPL) and oxidized cholesteryl esters (OxCE) was evaluated in 24 filters us
174 ated with ezetimibe showed a 173% higher LDL-cholesteryl ester plasma disappearance rate (P < 0.001 v
175 ase (LCAT) catalyzes the formation of plasma cholesteryl ester, plays a key role in high-density lipo
176 roups from triglycerides, phospholipids, and cholesteryl esters plus total cholesterol (i.e., both es
177 The objective was to study whether the serum cholesteryl ester proportion of palmitoleic acid [16:1n-
178 significantly altered lipoprotein lipase and cholesteryl ester protein mass or measures of insulin re
180 high density lipoprotein (HDL) to spheroidal cholesteryl ester-rich HDL is a central step in reverse
182 the partial disproportionation of HDL into a cholesteryl ester-rich microemulsion (CERM) and a new HD
183 D approximately 8.5 nm) into a single, large cholesteryl ester-rich microemulsion (CERM; D > 100 nm),
188 existing literature on Wolman's disease and cholesteryl ester storage disease, and discuss available
190 plasmic reticulum, where it was converted to cholesteryl esters stored in lipid droplets when ORP1L w
191 ny organs, resulting in a marked increase in cholesteryl esters, suppression of C but not fatty acid
195 mixture of phospholipids, triglycerides, and cholesteryl esters that plays a major role in lipoprotei
196 es enzymes of this family to readily oxidize cholesteryl esters, thus providing an additional source
197 e G420H mutant was unable to deliver the HDL cholesteryl ester to a metabolically active membrane com
198 eding an HCD supplemented with a fluorescent cholesteryl ester to optically transparent fli1:EGFP zeb
202 o converted to o-quinone 28, which inhibited cholesteryl ester transfer protein (CETP) activity and L
208 ockout mice, and human apolipoprotein (apo)B/cholesteryl ester transfer protein (CETP) double transge
212 is study was to identify associations of the cholesteryl ester transfer protein (CETP) gene with coro
213 xplore two HDL-C raising target modulations, Cholesteryl Ester Transfer Protein (CETP) inhibition and
214 ofuroquinoline derivatives exhibiting potent cholesteryl ester transfer protein (CETP) inhibition at
215 ne is consistent with a protective effect of cholesteryl ester transfer protein (CETP) inhibition on
217 te the efficacy and safety of torcetrapib, a cholesteryl ester transfer protein (CETP) inhibitor, in
224 cuses on the studies with niacin and the new cholesteryl ester transfer protein (CETP) inhibitors tor
225 mine the recent advances in our knowledge of cholesteryl ester transfer protein (CETP) inhibitors, he
238 terol acyltransferase (LCAT) and transfer by cholesteryl ester transfer protein (CETP) were measured
239 ls can be increased by >50% by inhibition of cholesteryl ester transfer protein (CETP), a molecule th
243 Asp), apolipoprotein E (Apo E2, E3, and E4), cholesteryl ester transfer protein (TaqIB), and leptin r
244 , apolipoprotein E (Apo E2, E3, and E4), and cholesteryl ester transfer protein (TaqIB)] and equol pr
246 ty, HDL ability to esterify cholesterol, and cholesteryl ester transfer protein activity), HDL antiox
247 ding expression of the emerging drug targets cholesteryl ester transfer protein and apolipoprotein (a
248 protein E and change in LDL cholesterol, and cholesteryl ester transfer protein and change in HDL cho
249 tigate the mechanisms of action, we measured cholesteryl ester transfer protein and indexes of plasma
251 oproteinemia seems associated with a related cholesteryl ester transfer protein genotype difference.
254 s; adipose tissue-specific overexpression of cholesteryl ester transfer protein in mice reduces the p
255 carry cholesterol accepted from LDL+HDL via cholesteryl ester transfer protein in vivo, may contribu
256 Initial studies addressing the effect of cholesteryl ester transfer protein inhibition on cardiov
258 and low-density lipoprotein cholesterol, the cholesteryl ester transfer protein inhibitor torcetrapib
260 s after ACS to treatment with dalcetrapib (a cholesteryl ester transfer protein inhibitor) or placebo
261 te the safety and efficacy of anacetrapib, a cholesteryl ester transfer protein inhibitor, in patient
262 , 0.94-1.09) vs 0.90 (95% CI, 0.89-0.91) for cholesteryl ester transfer protein inhibitors (P = .002)
266 apeutic agents such as fibrates, niacin, and cholesteryl ester transfer protein inhibitors that are k
267 t should be possible to develop more optimal cholesteryl ester transfer protein inhibitors that do no
268 less, drugs that raise HDL-C concentrations, cholesteryl ester transfer protein inhibitors, are in la
270 specific and, since the crystal structure of cholesteryl ester transfer protein is now known, it shou
273 hat do not form a nonproductive complex with cholesteryl ester transfer protein on the high-density l
274 zed in the presence of PLA2 by the action of cholesteryl ester transfer protein or by guanidine hydro
275 holesterol concentration and adipocyte size; cholesteryl ester transfer protein TaqIB polymorphism is
276 for hepatic lipase, endothelial lipase, and cholesteryl ester transfer protein were analyzed, patien
277 RATIONALE: Therapies that inhibit CETP (cholesteryl ester transfer protein) have failed to demon
279 of coexpression of scavenger receptor BI or cholesteryl ester transfer protein, both of which promot
280 frequency for the TaqI B1/B2 polymorphism in cholesteryl ester transfer protein, consistent with the
281 lipoprotein-cholesterol, i.e. inhibition of cholesteryl ester transfer protein, is markedly effectiv
282 -cholesterol fractional esterification rate, cholesteryl ester transfer protein, phospholipid transfe
283 of postprandial TRLs in plasma increased the cholesteryl ester transfer protein-mediated transfer of
284 translocated through caveolae were detected (cholesteryl ester, triacylglycerol) and/or enriched (cho
285 se of nonpolar lipids, including wax esters, cholesteryl esters, triacylglycerols, and diesters, wher
286 is a lipolytic enzyme capable of hydrolyzing cholesteryl esters, triacylglycerols, and phospholipids
287 ation-of-function between SR-BI-mediated HDL cholesteryl ester uptake and cholesterol efflux to HDL,
288 cholesterol (HDL-C) metabolism in selective cholesteryl ester uptake and in free cholesterol cellula
292 ion by increasing the rate of HDL-associated cholesteryl ester uptake, possibly by optimizing SR-BI l
297 cetrapib markedly decreases clearance of HDL cholesteryl ester via an indirect pathway, but has no ef
298 ansferase (LCAT), a key enzyme that produces cholesteryl esters via transfer of acyl groups from phos
299 learance of HDL particles and HDL-associated cholesteryl esters was also similar between hLrp1(+/+) a
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