ライフサイエンスコーパス: cholesterol

1 index, smoking, diabetes mellitus and total cholesterol).

2 he ER, also called the ER regulatory pool of cholesterol.

3 No differences were seen for HDL, LDL and cholesterol.

4 ficiency and ability of T1317-sHDL to efflux cholesterol.

5 rosclerosis by being the first to accumulate cholesterol.

6 ated levels of low-density lipoprotein (LDL) cholesterol.

7 evated concentrations of free and esterified cholesterol.

8 iber and has low levels of saturated fat and cholesterol.

9 nsumption was positively associated with HDL cholesterol.

10 of saturated lipids, unsaturated lipids, and cholesterol.

11 holesterol and for the ratio of total to HDL cholesterol.

12 in HbA1c, 5 mm Hg in SBP, or 10 mg/dL in LDL cholesterol.

13 that catalyzes conversion of desmosterol to cholesterol.

14 LAMP-1-positive vesicles in association with cholesterol.

15 scularisation) per 1 mmol/L reduction in LDL cholesterol.

16 posite leaflet containing unsaturated PC and cholesterol.

17 2.38-2.95]), or low high-density lipoprotein cholesterol (2.63 [95% CI, 2.33-2.94]), but was not sign

18 ssure (3.78 [95% CI, 2.76-4.81]), high total cholesterol (2.85 [95% CI, 2.38-3.32]), or family histor

19 studies demonstrating that SFAs increase LDL cholesterol, a major causal factor in the development of

20 Cholesterol, a necessary component of animal cell membra

21 olesterol profile or surrogate biomarkers of cholesterol absorption and endogenous synthesis.

22 ORP2 knock-down modifies the distribution of cholesterol accessible to a D4H probe, between late endo

23 reduce cholesterol uptake, preventing toxic cholesterol accumulation.

24 In the ER, excess cholesterol acts to reduce cholesterol uptake, preventin

25 cyltransferase 1 (also named acyl-coenzyme A:cholesterol acyltransferase, ACAT1) transfers a long-cha

26 ese effects, such as a 50% decrease in serum cholesterol after 4 weeks of post-treatment with lipoMSN

27 ther, these findings suggest, independent of cholesterol, an association between circulating PCSK9 an

28 nclude reduced bioavailability of intestinal cholesterol and alterations in endogenous cholesterol sy

29 -liver signaling axis that regulates hepatic cholesterol and bile acid homeostasis.

30 Blood-based biomarkers were HbA1c, total cholesterol and C-reactive protein.

31 link between high-density lipoprotein (HDL) cholesterol and cardiovascular disease, leading to the h

32 dies for metabolic conditions including high cholesterol and diabetes.

33 ANSS general psychopathology subscale, total cholesterol and education (all p < 0.05) were the influe

34 d that the loading-conditioned urine reduced cholesterol and elevated dopamine and melatonin.

35 impairment of anabolic flux from glucose to cholesterol and fatty acids.

36 rovements were additionally observed for HDL cholesterol and for the ratio of total to HDL cholestero

37 in insulin and glucose, and decreases in HDL cholesterol and ghrelin (Ps < 0.05).

38 levated triglycerides, reduced levels of HDL cholesterol and glucose impairment) on the phenotype of

39 events in proportion to their effects on LDL cholesterol and have good safety profiles, though PCSK9

40 Many sterols, including cholesterol and its precursors and metabolites, are biol

41 nducing the internalization of extracellular cholesterol and its trafficking from the PM to the ER.

42 we demonstrated that MDV gB colocalizes with cholesterol and LAMP-1, suggesting that viral protein tr

43 uation, nondaily statin dosing lowered total cholesterol and LDL-C levels.

44 and third-trimester high-density lipoprotein cholesterol and low-density lipoprotein cholesterol leve

45 ors, including endogenous compounds, such as cholesterol and neurosteroid pregnenolone sulfate (PES).

46 ubiquitin-proteasome pathway in response to cholesterol and other sterol intermediates.

47 y the local concentration of lipids, such as cholesterol and phosphoinositides.

48 n drives bile formation and promotes biliary cholesterol and phospholipid output.

49 es an additional level of control to biliary cholesterol and phospholipid secretion.

50 hobicity, or increased activity of dedicated cholesterol and phospholipid transporters.

51 te the role of ORP2 in endothelial cell (EC) cholesterol and PI(4,5)P(2) distribution, angiogenic sig

52 or SK1-I in WT cells induced accumulation of cholesterol and reduced cholesterol esterification.

53 ases, elevation of (low-density lipoprotein) cholesterol and steatosis in hepatocytes.

54 vertebrate development, connecting glucose, cholesterol and steroid hormone metabolism with early em

55 whether higher low-density lipoprotein (LDL) cholesterol and triglyceride levels and lower high-densi

56 res of adiposity, ~0.1 mmol/l higher non-HDL cholesterol and triglycerides and 0.2 mmol/l higher non-

57 MR analysis demonstrates that LDL cholesterol and triglycerides are associated with advers

58 on and fibrosis after being fed a high-fat, -cholesterol, and -fructose (HFCF) diet.

59 n, total and high-density lipoprotein (dHDL) cholesterol, and adiponectin decreased on the daytime co

60 in propionate with increases in leptin, LDL cholesterol, and blood pressure; and increases in butyra

61 sis independently of low-density lipoprotein cholesterol, and high sensitivity C-reactive protein, wi

62 tional risk factors, low-density lipoprotein cholesterol, and high-sensitivity C-reactive protein.

63 The studied general biomarkers, loliolide, cholesterol, and phytol, all show increasing depletion i

64 rovide critical links among cellular status, cholesterol, and purinergic signaling.

65 educed total cholesterol, triglycerides, LDL-cholesterol, and the atherogenic index of plasma (AIP) s

66 ultivariable MR analysis including apoB, LDL cholesterol, and triglycerides in the same model, apoB r

67 Lipid rafts are tightly packed, cholesterol- and sphingolipid-enriched microdomains with

68 vels, including non-high-density lipoprotein cholesterol, apolipoprotein B, and lipoprotein(a) (all p

69 LDL cholesterol associations were carried out in a sample of

70 protein ORP1L, which transports LDL-derived cholesterol at membrane contacts between the late endoso

71 ed a potential allosteric mechanism by which cholesterol binding regulates the conformation of CD81.

72 dimerization and APP-BACE1 are dependent on cholesterol binding to APP.

73 nhibitors that are known to inhibit cellular cholesterol biosynthesis and are clinically prescribed t

74 arch that demonstrate chemical inhibition of cholesterol biosynthesis compromises neurodevelopment.

75 indings suggest that the upregulation of the cholesterol biosynthesis pathway may negatively impact f

76 that nuclear factor kappa B (NF-kappaB) and cholesterol biosynthesis pathways were activated, and sp

77 predicted an increase in cancer, immune, and cholesterol biosynthesis pathways.

78 in cell proliferation, immune responses, and cholesterol biosynthesis, increased infiltration of neut

79 all three of these enzymes are required for cholesterol biosynthesis, only inhibition of the most up

80 hare the same Delta-14 reductase activity in cholesterol biosynthesis, yet little is known about thei

81 ls that promoted optimal GC polarization and cholesterol biosynthesis.

82 MT5 promoted SREBP1 SDM and the induction of cholesterol biosynthetic pathway enzymes that produce re

83 sis cannot synthesize phosphatidylcholine or cholesterol but encodes enzymes for phosphatidylethanola

84 and interference on the bioaccessibility of cholesterol by in vitro digestion models.

85 es, including phospholipids, neutral lipids, cholesterol, ceramides, and free fatty acids.

86 % CI: 0.09, 11.9) of the variance in 1-y LDL cholesterol changes in the intervention arm but was unas

87 s the rate of lipid mixing is independent of cholesterol composition.

88 High-density lipoprotein (HDL) cholesterol concentration (HDL-C) is an established athe

89 Aster-B GRAM domain binds to membranes in a cholesterol concentration-dependent manner and that the

90 HDL-cholesterol concentrations after the milk diet were lowe

91 The cholesterol content decreased significantly after cannin

92 LDL-C was corrected (LDL-C(corrected)) for cholesterol content in lipoprotein(a).

93 Similarly, reducing the cholesterol content of HBE cells with simvastatin or the

94 These findings signal that the cholesterol content of TRLs and sdLDL influence atheroge

95 , fatty acid profile, nutritional impact and cholesterol content were determined and compared with th

96 Reducing cholesterol content with a cholesterol scavenger (beta-m

97 n its biological activity rather than in its cholesterol content.

98 ions require precise regulation of lysosomal cholesterol content.

99 to inflammatory cytokines, oxidized lipids, cholesterol crystals and other factors.

100 In addition, there was no accumulation of cholesterol crystals or signs of toxicity.

101 somal LDL trafficking, resulting in cellular cholesterol deficiency.

102 two conformations, suggesting the motion for cholesterol delivery to the tunnel.

103 Fluvastatin-mediated cholesterol depletion (-27.8%) lowered VSMC migration di

104 of the trimer) increased virus resistance to cholesterol depletion and to the surface-acting agents.

105 sed rat hippocampal cultures and their acute cholesterol depletion by methyl-beta-cyclodextrin as a t

106 s in virus particle density, suggesting that cholesterol depletion from the HIV-1 envelope membrane r

107 gether, it is concluded that statin-mediated cholesterol depletion may coordinate VSMC migration and

108 Proof is provided that statin-mediated cholesterol depletion remodels total vascular smooth mus

109 tegrin alpha2 expression were unchanged upon cholesterol depletion.

110 s reduced (-24.5%) following statin-mediated cholesterol depletion.

111 e in calcitriol, which is synthesized from a cholesterol derivative.

112 he trained model revealed the involvement of cholesterol-derived metabolites and small-molecules that

113 omposition resulting from the high-fat, high-cholesterol diet in this model.

114 dance of ABC transporter A1 (ABCA1) and thus cholesterol efflux and increasing the abundance and modi

115 Low values of cholesterol efflux capacity (OR(1SD), 0.33; 95% CI, 0.18

116 DL did not exert a synergistic effect on HDL cholesterol efflux capacity in the familial hypercholest

117 Low cholesterol efflux capacity values, pro-oxidant/proinfla

118 artial ACAT inhibition, coupled to increased cholesterol efflux capacity, favorably remodels atherosc

119 tion of HDL particles and facilitating their cholesterol efflux capacity.

120 Many studies of cholesterol efflux in macrophages have focused on the ro

121 Macrophage cholesterol efflux induced in vitro by LDL added to the

122 ipoproteins (HDLs), but other mechanisms for cholesterol efflux likely exist.

123 r demonstrate that cross-linking impairs the cholesterol efflux mediated by apoA-I or HDL3 in vitro a

124 Lysosomal cholesterol egress requires two proteins, NPC1 and NPC2,

125 Although either extraction procedure led to cholesterol enrichment, the UAE-E:W conditions favoured

126 uced accumulation of cholesterol and reduced cholesterol esterification.

127 ty given that NTCP inhibition still promoted cholesterol excretion in Abcg8(-/-) mice.

128 et binding, Pro12A is much more sensitive to cholesterol extraction than Laurdan, which is redistribu

129 emission lifetimes, we could determine that cholesterol facilitated lateral segregation most with th

130 Chemical depletion of cholesterol from HIV-1 particles inactivates their infec

131 The intracellular transport of cholesterol from the PM to the ER is believed to be acti

132 of statin dose (not low-density lipoprotein cholesterol goals), additional tests for risk prediction

133 Lipid abnormalities were identified as total cholesterol >200 mg/dL, 4,558 subjects (11.6%); high-den

134 Adults >=18 years with LDL cholesterol >3 mmol/L (n = 113) were recruited from gene

135 LDL-C) levels >=70 mg/dl or non-high-density cholesterol >=100 mg/dl despite statin therapy.

136 American College of Cardiology Multi-Society cholesterol guideline and 2019 American College of Cardi

137 Plasma levels of high-density lipoprotein cholesterol (HDL-C) decline drastically during sepsis, a

138 hibition of phosphatidylinositol kinases and cholesterol homeostasis reduced replication of all three

139 d with I1061T-NPC1 leading to restoration of cholesterol homeostasis, an effect that is largely drive

140 matory response, early/late E2-response, and cholesterol homeostasis.

141 rter and identify >100 genes involved in LDL-cholesterol import.

142 ) was higher in blubber and fur, followed by cholesterol in brain, liver, kidney, heart, and blood, c

143 a tool to describe the physiological role of cholesterol in glutamatergic synaptic transmission.

144 s and the intracellular accumulation of free cholesterol in lysosomes.

145 another truncated variant, also restored PM cholesterol in ORP1-null cells.

146 Through this approach, we find that cholesterol in the target membrane enhances the efficien

147 nct lipophilic moieties like fatty acids and cholesterol increases ASO accumulation and activity in m

148 ent with the hypothesis that target membrane cholesterol increases lipid mixing efficiency by alterin

149 potential utility of serum sphingolipids as cholesterol-independent markers of risk and even future

150 which augments the activation by PIP(2); and cholesterol inhibits the channel.

151 We propose that this gp41-cholesterol interaction mediates virus-cell fusion by re

152 ide(s) in the ER that can cluster PM-derived cholesterol into transient detergent-resistant membrane

153 Cholesterol is a structural component of cellular membra

154 Cholesterol is an essential component of mammalian cell

155 Cholesterol is an integral component of eukaryotic cell

156 Taken together, these findings suggest that cholesterol is critical for the cannabinoid-GlyR interac

157 cles composed of apolipoproteins, lipids and cholesterol is routinely visualised by transmission elec

158 e 9 (PCSK9) is a key regulator of plasma LDL-cholesterol (LDL-C) and a clinically validated target fo

159 Elevated low-density lipoprotein cholesterol (LDL-C) is associated with increased cardiov

160 vascular disease and low-density lipoprotein cholesterol (LDL-C) levels >=70 mg/dl or non-high-densit

161 e lipoprotein(a) and low-density lipoprotein cholesterol (LDL-C) levels.

162 s lipoprotein(a) and low-density lipoprotein cholesterol (LDL-C).

163 de levels and lower high-density lipoprotein cholesterol level are causal risk factors for changes in

164 The mean baseline LDL cholesterol level in the two groups was 255.1 mg per dec

165 4 weeks before screening and who had an LDL cholesterol level of 130 mg per deciliter (3.4 mmol per

166 At day 510, the percent change in the LDL cholesterol level was a reduction of 39.7% (95% confiden

167 abetes; median low-density lipoprotein [LDL] cholesterol level, 75.0 mg/dL; median triglycerides leve

168 reduced HDL-cholesterol level, increased LDL-cholesterol level, and decreased insulin sensitivity.

169 ipidemia and insulin resistance, reduced HDL-cholesterol level, increased LDL-cholesterol level, and

170 eight and body length, higher hemoglobin and cholesterol levels and a higher frequency of growth plat

171 logistic regression models adjusted for HDL cholesterol levels and cardiovascular risk factors to es

172 ion between baseline low-density lipoprotein cholesterol levels and magnitude of VTE risk reduction.

173 lation between low-density lipoprotein (LDL) cholesterol levels and risk of intracerebral hemorrhage

174 The relationship between cholesterol levels and risk of venous thromboembolism (V

175 y was associated with a reduction in PM free cholesterol levels and the intracellular accumulation of

176 Cellular cholesterol levels are regulated through crosstalk betwe

177 valent (ORION-11 trial) who had elevated LDL cholesterol levels despite receiving statin therapy at t

178 D36KO mice, and circulating triglyceride and cholesterol levels in PPARalphaKO mice.

179 Therefore, high cholesterol levels may decrease the efficacy of daraplad

180 Reductions in LDL cholesterol levels of approximately 50% were obtained wi

181 ster, the effect of high-density lipoprotein cholesterol levels on the risk for small-for-gestational

182 , where the protein machinery that regulates cholesterol levels resides.

183 Analysis of total body lipid and cholesterol levels were also investigated, with no betwe

184 ments for confounders, third-trimester total cholesterol levels were associated with a decreased risk

185 tein cholesterol and low-density lipoprotein cholesterol levels were associated with an increased ris

186 Stroke Prevention by Aggressive Reduction in Cholesterol Levels) trial, atorvastatin was compared wit

187 tors for CVD include low-density lipoprotein cholesterol levels, hypertension, renal disease, age, an

188 eased plasma triglycerides and decreased HDL cholesterol levels, is a major factor contributing to no

189 ssociated with low-density lipoprotein (LDL) cholesterol levels.

190 a gene that, when repressed, can lower blood cholesterol levels.

191 ants in LDLR that have a large effect on LDL cholesterol levels.

192 ients to lower low-density lipoprotein (LDL) cholesterol levels.

193 However, the exact mechanisms of how cholesterol/lipid metabolism in peripheral nervous syste

194 Cholesterol lipoprotein profiles of LHM showed a human-l

195 ichment in SMCs that were adjacent to [(13)C]cholesterol-loaded macrophages-including in cytosolic li

196 Cholesterol lowering may also have beneficial effects in

197 LDL cholesterol lowering significantly reduced the risk of m

198 We aimed to summarise the evidence of LDL cholesterol lowering therapies in older patients.

199 The clinical benefit of LDL cholesterol lowering treatment in older patients remains

200 for systolic or >=85 mmHg for diastolic, HDL cholesterol <40 mg/dL for males and <50 mg/dL for female

201 ly, blocking the ability of IFN to reprogram cholesterol metabolism abrogates cellular protection and

202 at are important hormones that regulate host cholesterol metabolism and energy balance via several nu

203 Collectively, our data define cholesterol metabolism as an integral metabolic pathway

204 Recent work suggests that cholesterol metabolism impacts innate immune responses a

205 ere, we show that DENV infection manipulated cholesterol metabolism in cells residing in low-oxygen m

206 e models to determine the drivers of altered cholesterol metabolism in PDAC and the consequences of i

207 To better understand cholesterol metabolism in situ across the complex functi

208 The key roles of cholesterol metabolism in the activation of inflammasome

209 A diverse array of genetic disorders of cholesterol metabolism support this claim as do multiple

210 monly used pharmaceuticals induce changes in cholesterol metabolism that are similar to changes induc

211 Altering cholesterol metabolism using statins decreased the gener

212 olved in metabolism (e.g., sugar, lipid, and cholesterol metabolism), inflammation, and fibrosis.

213 ges, with up-regulation of genes involved in cholesterol metabolism, scavenger receptors, MERTK, and

214 ssociated protein required for regulation of cholesterol metabolism.

215 Rather than producing cholesterol, microglia/macrophages synthesized desmoster

216 en designed and synthesized as a luminescent cholesterol mimic for the monitoring of cholesterol traf

217 the (19)F-(13)C distance data indicate three cholesterol molecules bound near F673 in each trimer.

218 Assessed individually using MR, LDL cholesterol (odds ratio [OR] 1.66 per 1-standard-deviati

219 While one SD increase in the PRSs for total cholesterol (odds ratio [OR] = 0.92; 95% confidence inte

220 ed on the role of ABC transporters in moving cholesterol onto high-density lipoproteins (HDLs), but o

221 naturally adapts to added molecules such as cholesterol or proteins.

222 ses showed a 1-standard-deviation-higher HDL cholesterol (OR 0.80; 95% CI: 0.75-0.86; P < 0.001) and

223 d a robust effect, with the estimate for LDL cholesterol (OR 0.85; 95% CI: 0.57-1.27; P = 0.44) rever

224 interval [CI] = 0.85-0.99; p = 0.03) and LDL cholesterol (OR = 0.88; 95% CI = 0.81-0.95; p = 0.002) w

225 extracts showed a reduction of bioaccessible cholesterol (p < 0.001) higher than that of phytosterols

226 with decreased low-density-lipoprotein (LDL) cholesterol (P = 1.3 x 10(-8)) without being associated

227 Even with statin treatment to lower LDL cholesterol, patients with diabetes have a high residual

228 distribution of cholesterol to an esterified cholesterol pool.

229 HDL NPs are a cholesterol-poor ligand that binds to the receptor for c

230 hages synthesized desmosterol, the immediate cholesterol precursor.

231 ffect of vitamin D3 supplementation on serum cholesterol profile or surrogate biomarkers of cholester

232 Additionally, PDIM's affinity for cholesterol promoted this phenotype; treatment of zebraf

233 lar docking calculations further reveal that cholesterol regulates cannabinoid enhancement of GlyR fu

234 Such inhibition is fully rescued by cholesterol replenishment in a concentration-dependent m

235 enome-wide CRISPR screen using an endogenous cholesterol reporter and identify >100 genes involved in

236 ever, the capacity of LDL to act as a plasma cholesterol reservoir and its potential impact in suppor

237 he plasma membrane (PM), where most cellular cholesterol resides, and the endoplasmic reticulum (ER),

238 notably upregulation of saturated lipids and cholesterol, resulting in recovery of membrane packing a

239 ted that lower low-density lipoprotein (LDL) cholesterol results in fewer cardiovascular events.

240 addressed by showing that sphingomyelin and cholesterol-rich (SCOR) lipid mixtures with phosphatidyl

241 l-poor ligand that binds to the receptor for cholesterol-rich HDLs, scavenger receptor type B1 (SCARB

242 the formation of ordered domains in a SM and cholesterol-rich leaflet can be suppressed by an opposit

243 the non-raft region, the membrane region of cholesterol-rich lipid raft markedly weakens the membran

244 The ordered environment of cholesterol-rich membrane nanodomains is thought to excl

245 Whether cholesterol-rich microdomains (lipid rafts/caveolae) are

246 atients by 26% per 1 mmol/L reduction in LDL cholesterol (RR 0.74 [95% CI 0.61-0.89]; p=0.0019), with

247 Reducing cholesterol content with a cholesterol scavenger (beta-methylcyclodextrin) or stati

248 content of HBE cells with simvastatin or the cholesterol scavenger beta-methylcyclodextrin also block

249 L-C) and small-dense low-density lipoprotein cholesterol (sdLDL-C) concentrations associate with comp

250 Induction of cholesterol secretion was not a consequence of increased

251 atherogenesis without an increase in plasma cholesterol, seen in traditional models of diabetes mell

252 rstanding of the molecular mechanism of CD81 cholesterol sensing, how this relates to HCV entry, and

253 Therefore, CD81 possesses a potential cholesterol-sensing mechanism; however, its relevance fo

254 rs whose proteolytic activation requires the cholesterol-sensing membrane protein Scap.

255 ements between the peptide and (13)C-labeled cholesterol show that C17 on the D ring and C9 at the in

256 Although 25HC is a potent regulator of cholesterol storage, uptake, efflux and biosynthesis, ho

257 tial distribution and relative abundances of cholesterol sulfate are reported and correlated with the

258 ly, hepatic LGR4 knockdown increased hepatic cholesterol synthesis and decreased the phosphorylation

259 25-hydroxycholesterol (25HC), inhibition of cholesterol synthesis and redistribution of cholesterol

260 ghout the various cell compartments, de novo cholesterol synthesis enriched this lipid in the endopla

261 notype; treatment of zebrafish with statins, cholesterol synthesis inhibitors, decreased spreading an

262 ted with expression of genes involved in the cholesterol synthesis pathway in primary human T-ALL spe

263 coordinated network of regulation along the cholesterol synthesis pathway.

264 G-CoA reductase, the rate-limiting enzyme in cholesterol synthesis, was reduced in the spinal cord GM

265 the ER resulting in normalization of de novo cholesterol synthesis.

266 al cholesterol and alterations in endogenous cholesterol synthesis.

267 ment binding transcription factor 2 (Srebf2)-cholesterol synthesis.

268 t manner, to regulate hepatic acetyl-CoA and cholesterol synthesis.

269 sumption results in significantly higher LDL-cholesterol than nontropical vegetable oils.

270 chickens have normal serum concentrations of cholesterol, their aortic tissues were found to have ele

271 dynamic simulations of CD81 with and without cholesterol; this identified a potential allosteric mech

272 , whereas LDLR uptake would have distributed cholesterol throughout the various cell compartments, de

273 cholesterol synthesis and redistribution of cholesterol to an esterified cholesterol pool.

274 ACAT1) transfers a long-chain fatty acid to cholesterol to form cholesteryl esters that coalesce int

275 mechanisms, but all require the presence of cholesterol to pierce lipid bilayers.

276 589 cells for genes required for LDL-derived cholesterol to reach the ER.

277 As a consequence of reduced delivery of cholesterol to the PM in ORP1-null cells, cholesterol wa

278 Thus, modification of neuronal cholesterol trafficking and of lipid rafts by Nef may co

279 Disruption or dysfunction of cholesterol trafficking leads to numerous human diseases

280 Interruption of cholesterol trafficking within multivesicular bodies (MV

281 cent cholesterol mimic for the monitoring of cholesterol trafficking.

282 TREM2 as a key transcriptional regulator of cholesterol transport and metabolism under conditions of

283 The addition of PS restores cholesterol transport to the ER.

284 s pro-atherosclerotic via effects on reverse cholesterol transportation targeting the ATP binding cas

285 sting; risk restratification strategies; LDL-cholesterol treatment targets; management protocols for

286 (p < 0.01) elevated plasma triglycerides and cholesterol, treatment with MSU-42011 did not increase t

287 cardiometabolic risk markers, including LDL cholesterol, triacylglycerol (TG), fasting glucose (FG),

288 ation of AFSE to diabetic mice reduced total cholesterol, triglycerides, LDL-cholesterol, and the ath

289 ar folate, homocysteine, alpha fetal protein cholesterol, triglycerides, prothrombin time.

290 aluate whether triglyceride-rich lipoprotein cholesterol (TRL-C) and small-dense low-density lipoprot

291 In the ER, excess cholesterol acts to reduce cholesterol uptake, preventing toxic cholesterol accumul

292 mmol/L; CB: 6.11 mmol/L; P = 0.006) and LDL cholesterol (WA: 3.72 mmol/L; CB: 3.86 mmol/L; P = 0.031

293 of cholesterol to the PM in ORP1-null cells, cholesterol was diverted to the ER resulting in normaliz

294 In the urine, an altered level of cholesterol was observed with an increase in calcitriol,

295 ect (p < 0.05), whereas the estimate for LDL cholesterol was reversed, and that for triglycerides lar

296 phosphatidylcholine, Bodipy-PE, and TopFluor-cholesterol were rapidly trafficked to ehrlichiae in inf

297 Decreased levels of apoA-I and HDL cholesterol were robustly associated with increased risk

298 leoylphosphatidylcholine, sphingomyelin, and cholesterol were used to form phase-separated domains.

299 ts design, and the unexpected interaction of cholesterol with CB1, suggestive of its endogenous allos

300 diets) that are inherently relatively low in cholesterol with typical levels similar to the current U