ライフサイエンスコーパス: lipoprotein

1 irs many atheroprotective properties of this lipoprotein.

2 rmediate that then collapses to produce lyso-lipoprotein.

3 a by hydrolyzing triglycerides from packaged lipoproteins.

4 cardial infarction risk from apoB-containing lipoproteins.

5 proteoglycans in a pattern similar to human lipoproteins.

6 equire activation by outer-membrane-anchored lipoproteins.

7 a constituent of human low- and high-density lipoproteins.

8 rapeutic approaches that modulate lipids and lipoproteins.

9 ides (135-499 mg/dL), controlled low-density lipoprotein (41-100 mg/dL), and either established cardi

10 We propose an (89)Zr-labeled high-density lipoprotein ((89)Zr-HDL) nanotracer as a means of monito

11 However, the relationship between Lipoprotein (a) [Lp(a)] and healthy cognitive aging has

12 poprotein cholesterol, apolipoprotein B, and lipoprotein(a) (all p < 0.0001).

13 Increased plasma concentrations of lipoprotein(a) (Lp(a)) are associated with an increased

14 Elevated lipoprotein(a) (Lp[a]) and family history (FHx) of coron

15 D events was related to baseline quartile of lipoprotein(a) (P(trend)=0.0021), and tended to associat

16 mab was associated with baseline quartile of lipoprotein(a) (P(trend)=0.03), but not LDL-C(corrected)

17 ended to associate with baseline quartile of lipoprotein(a) (P(trend)=0.06), but not LDL-C(corrected)

18 This study compared the levels of lipoprotein(a) and associated genetic factors between in

19 Alirocumab-induced reductions of lipoprotein(a) and corrected LDL-C independently predict

20 rmined whether alirocumab-induced changes in lipoprotein(a) and LDL-C independently predicted major a

21 At baseline, median lipoprotein(a) and LDL-C(corrected) were 21 and 75 mg/dL

22 se subtilisin/kexin type 9 inhibitor, lowers lipoprotein(a) and low-density lipoprotein cholesterol (

23 e subtilisin/kexin type 9) inhibitors reduce lipoprotein(a) and low-density lipoprotein cholesterol (

24 Alirocumab reduced lipoprotein(a) by 5.0 mg/dl (IQR: 0 to 13.5 mg/dl), corr

25 Lipoprotein(a) concentration is associated with cardiova

26 essure, and the strong causal association of lipoprotein(a) in coronary artery disease development (b

27 y syndrome, risk of PAD events is related to lipoprotein(a) level and is reduced by alirocumab, parti

28 Baseline lipoprotein(a) levels (median: 21.2 mg/dl; interquartile

29 ependent manner in patients who had elevated lipoprotein(a) levels and established cardiovascular dis

30 Lipoprotein(a) levels are genetically determined and, wh

31 However, within the FH cohort, lipoprotein(a) levels did not differ based on the presen

32 APO(a)-L(Rx) reduced lipoprotein(a) levels in a dose-dependent manner in pati

33 The median baseline lipoprotein(a) levels in the six groups ranged from 204.

34 blished cardiovascular disease and screening lipoprotein(a) levels of at least 60 mg per deciliter (1

35 s in the FH cohort had significantly greater lipoprotein(a) levels than either the general population

36 (Rx) resulted in dose-dependent decreases in lipoprotein(a) levels, with mean percent decreases of 35

37 no approved pharmacologic therapies to lower lipoprotein(a) levels.

38 and if such effects are related to levels of lipoprotein(a) or LDL-C.

39 Lipoprotein(a) was measured at randomization and 4 and 1

40 umab, the change from baseline to Month 4 in lipoprotein(a), but not LDL-C(corrected), was associated

41 Apolipoprotein E, lipoprotein(a), oxidized LDL (low density lipoprotein)'s

42 irocumab, particularly among those with high lipoprotein(a).

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

44 LDL-C [corrected for cholesterol content in lipoprotein(a)] predicted MACE.

45 t heparan sulfate oligosaccharides to remove lipoproteins already deposited in both the extracellular

46 sterile ligands such as oxidized low-density lipoprotein and damage-associated molecular patterns and

47 iated oxidation of Caco-2 cells, low-density lipoprotein and deoxyribonucleic acid than those of the

48 analyzed nuclear magnetic resonance-derived lipoprotein and metabolite profiles in the ANGES cohort

49 s confirmed a shift toward less high-density lipoprotein and more very-low-density lipoprotein and tr

50 m human serum, together with the presence of lipoprotein and protein contaminants.

51 ining lipoproteins, particularly low-density lipoprotein and remnant particles.

52 roprotein (proBFT) that is predicted to be a lipoprotein and that is cleaved into two discrete fragme

53 ensity lipoprotein and more very-low-density lipoprotein and triglyceride particles in depression.

54 PCSK9 loss-of-function resulted in low lipoproteins and decreased hepatic bacterial burden in j

55 justment for baseline concentrations of both lipoproteins and demographic and clinical characteristic

56 ing used to determine the relative impact of lipoproteins and protein aggregates on the isolated EV p

57 ex, subcutaneous adipose tissue, low-density lipoproteins and total cholesterol levels).

58 apoB (quantitating number of apoB-containing lipoproteins) and cholesterol and triglyceride content o

59 tic activity, uptake of oxidized low-density lipoprotein, and cytokine expression.

60 o of low-density lipoprotein to high-density lipoprotein, and dependency on the human donor.

61 PCSK9, low-density lipoprotein, and high-density lipoprotein concentrations

62 ty lipoprotein level, and lower high density lipoprotein, and liver attenuation index on CT scan, and

63 increases in total cholesterol, low-density lipoprotein, and low-density lipoprotein particles, but

64 l concentration in medium-sized high-density lipoprotein, and not large or extra-large high-density l

65 vascular events, blood pressure, low-density lipoproteins, and adiposity-related outcomes, with littl

66 ip of dietary cholesterol with blood lipids, lipoproteins, and cardiovascular disease risk to address

67 ), is required for the biosynthesis of these lipoproteins, and its regulation determines fat mobiliza

68 alterations in body composition, lipids and lipoproteins, and measures of vascular health over the M

69 uding ezetimibe and PCSK9 inhibitors; use of lipoprotein apheresis for severe FH; and addressing barr

70 Extracorporeal lipoprotein apheresis systems employ well-established, p

71 420 mg monthly or 420 mg every 2 weeks if on lipoprotein apheresis.

72 Gram-negative bacterial lipoproteins are triacylated with a thioether-linked dia

73 d compartmentalization; and very low-density lipoprotein assembly and secretion.

74 aa3 was found in HDL, a small amount was not lipoprotein associated.

75 As a consequence, LHM lipoproteins bind to human aortic proteoglycans in a pat

76 ylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1) and solved the s

77 levations in plasma levels of the beneficial lipoprotein biomarkers HDL and ApoA1, as well as total b

78 sex, race, BMI, triglycerides, high-density lipoprotein, blood pressure, and blood glucose.

79 locks cellular uptake of N-acylethanolamides-lipoprotein-borne Hh pathway inhibitors required for Smo

80 ram-positive Firmicutes also have N-acylated lipoproteins, but the enzymes catalyzing N-acylation rem

81 e density of examined soluble, membrane, and lipoproteins by at least 5-fold, affording the opportuni

82 n aortic inflammation or markers of advanced lipoprotein characterization, adiposity, or insulin resi

83 cerides >=135 and <500 mg/dL and low-density lipoprotein cholesterol >40 and <=100 mg/dL and a histor

84 l (LDL-C) level >=70 mg/dl, non-high-density lipoprotein cholesterol >=100 mg/dl, or apolipoprotein B

85 67 [95% CI, 2.38-2.95]), or low high-density lipoprotein cholesterol (2.63 [95% CI, 2.33-2.94]), but

86 ith CVD risk factors, including high-density lipoprotein cholesterol (HDL-C) (beta 0.40, 95% confiden

87 [0.11 mmol/l]; p < 0.001), non-high-density lipoprotein cholesterol (HDL-C) (HR: 1.05; 95% CI: 1.01

88 Plasma levels of high-density lipoprotein cholesterol (HDL-C) decline drastically duri

89 age, age at initiation, and non-high-density lipoprotein cholesterol (HDL-C) level on the expected ra

90 diastolic blood pressure (DBP), high-density-lipoprotein cholesterol (HDL-C), and glycated haemoglobi

91 cholesterol (LDL-cholesterol), high-density lipoprotein cholesterol (HDL-cholesterol), total cholest

92 which causes elevated levels of low-density lipoprotein cholesterol (LDL-C) and increased risk of pr

93 s of total serum cholesterol and low-density lipoprotein cholesterol (LDL-C) at 6 months or more of f

94 howed the benefit of targeting a low-density lipoprotein cholesterol (LDL-C) concentration of <70 mg/

95 Elevated low-density lipoprotein cholesterol (LDL-C) is associated with incre

96 statin therapy, with a baseline low-density lipoprotein cholesterol (LDL-C) level >=70 mg/dl, non-hi

97 rotic cardiovascular disease and low-density lipoprotein cholesterol (LDL-C) levels >=70 mg/dl or non

98 bitors reduce lipoprotein(a) and low-density lipoprotein cholesterol (LDL-C) levels.

99 .26 mmol/l]; p < 0.001), but not low-density lipoprotein cholesterol (LDL-C) or HDL-C, were associate

100 study, higher baseline levels of low-density lipoprotein cholesterol (LDL-C) predicted greater benefi

101 bitor, lowers lipoprotein(a) and low-density lipoprotein cholesterol (LDL-C).

102 change (baseline to week 24) in low-density lipoprotein cholesterol (LDL-C); secondary endpoints inc

103 The main outcomes included low-density lipoprotein cholesterol (LDL-cholesterol), high-density

104 7.31%, -12.57%; p < 0.001), non-high-density lipoprotein cholesterol (MD -18.17%; 95% CI -21.14%, -15

105 CI -21.14%, -15.19%; p < 0.001), low-density lipoprotein cholesterol (MD -22.94%; 95% CI -26.63%, -19

106 I -17.41%, -12.95%; p < 0.001), high-density lipoprotein cholesterol (MD -5.83%; 95% CI -6.14%, -5.52

107 lesterol (TRL-C) and small-dense low-density lipoprotein cholesterol (sdLDL-C) concentrations associa

108 pectively evaluate whether triglyceride-rich lipoprotein cholesterol (TRL-C) and small-dense low-dens

109 P = 0.002), and third-trimester high-density lipoprotein cholesterol and low-density lipoprotein chol

110 de significantly associated with low-density lipoprotein cholesterol based on 3203 subjects and that

111 ge levels with elevated total or low-density lipoprotein cholesterol concentrations.

112 s: targeting of statin dose (not low-density lipoprotein cholesterol goals), additional tests for ris

113 d triglyceride levels and lower high-density lipoprotein cholesterol level are causal risk factors fo

114 The low-density lipoprotein cholesterol level was lower by approximately

115 was no relation between baseline low-density lipoprotein cholesterol levels and magnitude of VTE risk

116 third-trimester, the effect of high-density lipoprotein cholesterol levels on the risk for small-for

117 sity lipoprotein cholesterol and low-density lipoprotein cholesterol levels were associated with an i

118 nal risk factors for CVD include low-density lipoprotein cholesterol levels, hypertension, renal dise

119 to lower blood pressure (BP) and low-density lipoprotein cholesterol levels.

120 mass, high blood pressure, low high-density-lipoprotein cholesterol or high triglycerides, and high

121 95% CI, 1.30-2.76) for total to high-density lipoprotein cholesterol ratio, 2.59 (95% CI, 1.76-3.83)

122 ned by the log of (triglyceride/high-density lipoprotein cholesterol).

123 e atherogenesis independently of low-density lipoprotein cholesterol, and high sensitivity C-reactive

124 ed for traditional risk factors, low-density lipoprotein cholesterol, and high-sensitivity C-reactive

125 nic lipid levels, including non-high-density lipoprotein cholesterol, apolipoprotein B, and lipoprote

126 aminotransferases, elevation of (low-density lipoprotein) cholesterol and steatosis in hepatocytes.

127 duction and improved small dense low-density lipoprotein-cholesterol (sdLDL-C) profiles, QoL and URTI

128 markers, and an increase in apolipoprotein B lipoproteins compared with placebo.

129 9, low-density lipoprotein, and high-density lipoprotein concentrations were lower among patients wit

130 pathophysiological role of triglyceride-rich lipoproteins containing ApoC3.

131 e hypothesize that this interaction promotes lipoprotein deposition onto BrM glycosaminoglycans, init

132 s and two animal models, we demonstrate that lipoprotein-derived fatty acids are an independent regul

133 derived from enhanced uptake of high-density lipoprotein-derived lipids.

134 ing glucose, insulin, total and high-density lipoprotein (dHDL) cholesterol, and adiponectin decrease

135 ial hypercholesterolemia (FH) have increased lipoprotein dicarbonyl adducts and dysfunctional HDL.

136 hear stress with enzyme-modified low-density-lipoprotein (eLDL) with or without TNFalpha promotes mon

137 the RagB substrate-binding surface-anchored lipoprotein forming a closed lid on the RagA TonB-depend

138 ion, and the mice were immunized with the P6 lipoprotein from nontypeable Haemophilus influenzae, usi

139 Restoring lipoprotein function with ApoA-I raising agents or block

140 The murein lipoprotein gene lpp promoted capsule retention through

141 are involved in energy metabolism, including lipoproteins, glucose, creatine, and isoleucine.

142 and severe hypercholesterolemia (low-density lipoprotein >=190 mg/dl), overall prevalence estimates a

143 mg/dL, 4,558 subjects (11.6%); high-density lipoprotein (HDL) <40 mg/dL, 2,078 subjects (5.3%); low-

144 vs. 5.12 mmol/L, p < 0.001) and high-density lipoprotein (HDL) (0.90 to 1.55 mmol/L, p < 0.001) were

145 ux of cholesterol to endogenous high-density lipoprotein (HDL) acceptors.

146 glucose, total cholesterol and high-density lipoprotein (HDL) cholesterol (all p < 0.05).

147 establish a clear link between high-density lipoprotein (HDL) cholesterol and cardiovascular disease

148 High-density lipoprotein (HDL) cholesterol concentration (HDL-C) is a

149 l, high triglyceride level, low high-density lipoprotein (HDL) cholesterol level, impaired fasting gl

150 her trypanosomes by circulating high-density lipoprotein (HDL) complexes called trypanosome lytic fac

151 unique proteome, distinct from high-density lipoprotein (HDL) isolated from donor plasma of the same

152 High-density lipoprotein (HDL) metabolism is facilitated in part by s

153 rmine the potential role of the high-density lipoprotein (HDL) receptor as a target for cholesterol d

154 EL) hydrolyzes phospholipids in high-density lipoprotein (HDL) resulting in reduction in plasma HDL l

155 levels of large and extra-large high-density lipoprotein (HDL) subclasses and decreased levels of ver

156 rculating S1P chaperone ApoM(+) high density lipoprotein (HDL), which signals via endothelial niche S

157 along with better values of the high-density lipoproteins (HDL).

158 sity, hypertriglyceridemia, low high-density lipoprotein [HDL], and elevated blood pressure) (P-trend

159 ters in moving cholesterol onto high-density lipoproteins (HDLs), but other mechanisms for cholestero

160 increases in total cholesterol, low-density lipoproteins, high-density lipoproteins, phospholipids,

161 ceride content of VLDL, intermediate-density lipoproteins (IDLs), and low-density lipoproteins (LDLs)

162 n binding protein A, respectively, which are lipoproteins important for host infection.

163 reveals an unexpected role of staphylococcal lipoproteins in EV biogenesis.

164 n effective therapy for lowering atherogenic lipoproteins in PLHIV with high cardiovascular risk.

165 otease responses in the spleen, high-density lipoproteins in the heart, and glutamatergic signaling i

166 proteins, many of which are predicted to be lipoproteins, in the culture medium of an ETBF strain.

167 s well as frequent and extensive deposits of lipoproteins, including immature lipofuscin, were observ

168 tors such as concentrations of detergents or lipoproteins, incubation time, as well as the order of m

169 ide hydrolase 16 (GH16) family and are often lipoproteins, indicating that they are surface located a

170 Lipoprotein subparticles, lipoprotein-insulin resistance (LP-IR), and GlycA were m

171 The integral membrane protein Lit (lipoprotein intramolecular transacylase) from the opport

172 burgdorferi that controls the expression of lipoproteins involved in host infectivity.

173 utated, meaning that cholesterol uptake from lipoproteins is required for survival.

174 while the plasma increase of APOB-containing lipoproteins is unable to stimulate m-RCT.

175 lyzed apolipoprotein A-1 (ApoA-1)-containing lipoproteins isolated from BrM of elderly human donor ey

176 40 mg/dL, 2,078 subjects (5.3%); low-density lipoprotein (LDL) >130 mg/dL, 2,756 subjects (7.0%); and

177 ich is associated with decreased low-density-lipoprotein (LDL) cholesterol (P = 1.3 x 10(-8)) without

178 tudy investigated whether higher low-density lipoprotein (LDL) cholesterol and triglyceride levels an

179 PC1L1, and PCSK9 associated with low-density lipoprotein (LDL) cholesterol in a genome-wide associati

180 gh total cholesterol level, high low-density lipoprotein (LDL) cholesterol level, high very low-densi

181 o an inverse correlation between low-density lipoprotein (LDL) cholesterol levels and risk of intrace

182 provide sustained reductions in low-density lipoprotein (LDL) cholesterol levels with infrequent dos

183 used in adult patients to lower low-density lipoprotein (LDL) cholesterol levels.

184 I population and associated with low-density lipoprotein (LDL) cholesterol levels.

185 lusively demonstrated that lower low-density lipoprotein (LDL) cholesterol results in fewer cardiovas

186 its in the UK Biobank (UKBB) for low-density lipoprotein (LDL) cholesterol, triglycerides, and apolip

187 d by markedly elevated levels of low-density lipoprotein (LDL) cholesterol.

188 as a high-capacity receptor for low-density lipoprotein (LDL) in endothelial cells that mediates its

189 Low-density lipoprotein (LDL) is heterogeneous, composed of particle

190 in type-9 (PCSK9) is a ligand of low-density lipoprotein (LDL) receptor (LDLR) that promotes LDLR deg

191 peptide and efficiently restored low-density lipoprotein (LDL) receptor levels and cleared extracellu

192 s target enzymes bind tightly to low-density lipoprotein (LDL) receptor-related protein 1 (LRP1), but

193 from receptor-mediated uptake of low-density lipoprotein (LDL), which releases cholesterol in lysosom

194 d three lumenal domains, exports low-density-lipoprotein (LDL)-derived cholesterol from lysosomes.

195 f extracellular cholesterol from low density lipoproteins (LDL) via expression of LDL receptors (LDLR

196 e standard deviation decrease in low-density lipoprotein [LDL] cholesterol 0.76, 95% confidence inter

197 women; 70% with diabetes; median low-density lipoprotein [LDL] cholesterol level, 75.0 mg/dL; median

198 rkers (blood pressure, low- and high-density lipoproteins [LDL and HDL], triglycerides [TGs], and gly

199 Low-density lipoproteins (LDLs) are removed by extracorporeal filtra

200 density lipoproteins (IDLs), and low-density lipoproteins (LDLs).

201 sting blood sugar, triglyceride, low density lipoprotein level, and lower high density lipoprotein, a

202 high-density lipoprotein level, low-density lipoprotein level, history of hypertension, systolic blo

203 obin A1c, duration of diabetes, high-density lipoprotein level, low-density lipoprotein level, histor

204 hibition of CETP would preserve high-density lipoprotein levels and decrease mortality in clinical co

205 Lipoprotein levels were associated with AMD-associated g

206 and percent change in other plasma lipid and lipoprotein levels.

207 in the stationary phase and tethering of the lipoprotein LimB similar throughout the cell cycle.

208 on were unchanged in ppHF dams, but systemic lipoprotein lipase (LPL) activity was increased, suggest

209 Lipoprotein lipase (LPL) is active in capillaries, where

210 The enzyme lipoprotein lipase (LPL) is responsible for breaking dow

211 The binding of lipoprotein lipase (LPL) to GPIHBP1 focuses the intravas

212 uated plasma free fatty acids and attenuated lipoprotein lipase activity consistent with hallmarks of

213 hat sphingomyelin and a proteoglycan mediate lipoprotein lipase sorting in the TGN.

214 ation study (GWAS) of circulating non-fasted lipoprotein lipid traits in the UK Biobank (UKBB) for lo

215 Circulating lipoprotein lipids cause coronary heart disease (CHD).

216 ccounts for the aetiological relationship of lipoprotein lipids with risk of CHD.

217 e activation of PBP1b by FtsN but not by the lipoprotein LpoB.

218 In Escherichia coli, Braun's lipoprotein (Lpp) forms the only covalent tether between

219 s was determined by Western blot analysis of lipoprotein markers APOB and APOE.

220 CSK9 loss-of-function, in the context of low lipoproteins, may result in reduced hepatic bacterial cl

221 a suggest that lymphoma cells dependent upon lipoprotein-mediated cholesterol uptake are also subject

222 Therefore, we aimed to further explore their lipoprotein metabolism and to characterize key hepatic s

223 vasoconstriction, complement activation, and lipoprotein metabolism enrichments.

224 pe 9 (PCSK9), a key regulator of low-density lipoprotein metabolism, is induced by leptin and resisti

225 A limitation is that, owing to the nature of lipoprotein metabolism, measures related to the composit

226 ne phospholipase activity and is involved in lipoprotein metabolism.

227 ting translatable model of human hepatic and lipoprotein metabolism.

228 targeting ability of engineered high-density lipoprotein-mimetic nanoparticles (eHNPs) to cross the B

229 cus faecalis synthesizes a specific lysoform lipoprotein (N-acyl S-monoacylglycerol) chemotype by an

230 rides, fasting glucose, and non-high-density lipoprotein (non-HDL) cholesterol using linear mixed mod

231 ntravascular hydrolysis of triglyceride-rich lipoproteins on the surface of capillary endothelial cel

232 ive protein (HsCRP) and oxidized low-density lipoprotein (Ox-LDL) in adolescents.

233 of the peptidoglycan-binding outer-membrane lipoprotein Pal at division sites by the Tol system.

234 d by measurement of labeled very low-density lipoprotein palmitate via gas chromatography mass specto

235 e fasting and postprandial triglyceride-rich lipoprotein particle (TRLP) concentrations and size in b

236 In analyses of lipoprotein particle components by size, we found these

237 CI -26.63%, -19.25%; p < 0.001), low-density lipoprotein particle number (MD -20.67%; 95% CI -23.84%,

238 CI -6.14%, -5.52%; p < 0.001), high-density lipoprotein particle number (MD -3.21%; 95% CI -6.40%, -

239 -3.75%, 0.74%; p = 0.189), very-low-density lipoprotein particle number (MD 3.79%; 95% CI -9.81%, 17

240 Low-density lipoprotein particle size and high-density lipoprotein,

241 An attractive hypothesis is that remnant lipoprotein particles (RLPs), derived by lipolysis from

242 obic aggregates, such as detergent micelles, lipoprotein particles and even polystyrene latex nanobea

243 lism, measures related to the composition of lipoprotein particles are highly correlated, creating a

244 Finally, lipoprotein particles co-isolated with EVs was determine

245 ions, detergent micelles, latex nanobeads or lipoprotein particles inhibit Lp-PLA(2) possibly by bloc

246 rting to LBs, the conversion of proSP-B into lipoprotein particles, and neonatal viability in mice.

247 elevated cholesterol-effluxing high-density lipoprotein particles, and subjected Apoe (-/-) and APOA

248 ol, low-density lipoprotein, and low-density lipoprotein particles, but no changes in markers of infl

249 to cholesterol in medium-sized high-density lipoprotein particles, is associated with both a lower r

250 LPs constitute a heterogeneous population of lipoprotein particles, varying markedly in size and comp

251 s a model for the lipidated state of ApoE in lipoprotein particles, we incorporated ApoE into phospha

252 n, and not large or extra-large high-density lipoprotein particles.

253 in solutions as complexes with detergents or lipoprotein particles.

254 ly studies established that LDL (low-density lipoprotein) particles could act as efficient intermedia

255 attributable to apolipoprotein B-containing lipoproteins, particularly low-density lipoprotein and r

256 d palmitylated variants of the transmembrane lipoprotein phospholemman (FXYD1).

257 erol, low-density lipoproteins, high-density lipoproteins, phospholipids, and glucose.

258 lesterol levels resulting from reduced liver lipoprotein production.

259 Cholesterol lipoprotein profiles of LHM showed a human-like pattern,

260 When constitutively expressed, one of these lipoproteins promotes resistance to multiple bacteriopha

261 otential therapeutic strategies to alter the lipoprotein/protein profile of these extracellular depos

262 cassette transporter (atp), and low-density lipoprotein receptor chaperone (ldlr), that are under th

263 Here we show that the low-density lipoprotein receptor-related protein 1 (LRP1) controls t

264 ation of a SNX17 cargo receptor, low-density lipoprotein receptor-related protein 1 (LRP1), led to re

265 We demonstrate that the low-density lipoprotein receptor-related protein 4 (LRP4) is reduced

266 We explored the role of low-density lipoprotein receptor-related protein 4 (LRP4), a member

267 y and show that the co-receptor, low-density lipoprotein receptor-related protein 5 (Lrp5), is requir

268 n in Xenopus embryos, stimulated low-density lipoprotein receptor-related protein 6 (LRP6) phosphoryl

269 uction of frizzleds (fz), arrow (low-density lipoprotein receptor-related protein [LRP] 5/6), disheve

270 eported to be endocytosed by the low-density lipoprotein receptor-related protein-1 (LRP-1).

271 -aspartate receptor (NMDA-R) and low-density lipoprotein receptor-related protein-1 (LRP1), which fun

272 nd insulin sensitivity through a low-density lipoprotein receptor-related protein-2 (LRP2)-dependent

273 specific degradation of the LDL (low-density lipoprotein) receptor combined with a 10-week western di

274 Brain lipoprotein receptors have been shown to regulate the me

275 ligase IDOL as a negative regulator of brain lipoprotein receptors.

276 l modulator of HIF, defining a mechanism for lipoprotein regulation that functions in parallel to oxy

277 E, lipoprotein(a), oxidized LDL (low density lipoprotein)'s and large LDL particles, as well as other

278 SAR1B knockdown caused loss of lipoprotein secretion, overexpression of SAR1B but not o

279 nd identify a specific function for SAR1B in lipoprotein secretion, providing insights into the mecha

280 All bacterial lipoproteins share a variably acylated N-terminal cystei

281 lammatory cytokines and oxidized low-density lipoprotein significantly increased in the perfusate thr

282 y lipoprotein particle size and high-density lipoprotein, small and medium particle size (HMSP), Glyc

283 ition and particle concentration measures of lipoprotein subclasses; and 81 lipid and fatty acids rat

284 Lipoprotein subparticles, lipoprotein-insulin resistance

285 TG-component in almost all HDL (high-density lipoprotein) subparticles (HDL-TG), a smaller decrease o

286 of most components of VLDL (very low density lipoprotein) subparticles.

287 Here, we used a deuterium-labeled lipoprotein substrate with reconstituted Lit to investig

288 vate TLR2, which include naturally occurring lipoproteins, synthetic lipopeptides, and small heterocy

289 form complexes with RcsF, a surface-exposed lipoprotein that triggers the Rcs stress response when d

290 y producing a small arsenal of outer-surface lipoproteins that bind host complement components and ma

291 cells, even though there is an abundance of lipoproteins that would allow SHH to travel and signal l

292 LDL (low-density lipoprotein) that has accumulated in the artery wall is

293 characterized by a high ratio of low-density lipoprotein to high-density lipoprotein, and dependency

294 er synthesize cholesterol or take it up from lipoproteins to meet their metabolic requirements.

295 adhesion, phagocytosis, oxidized low-density lipoprotein uptake, and expression of inflammatory marke

296 DL) cholesterol level, high very low-density lipoprotein (VLDL) cholesterol level, high triglyceride

297 ses and decreased levels of very low-density lipoprotein (VLDL), amino acids, and citrate.

298 tic metabolite analysis and very low density lipoprotein (VLDL)-TG secretion assays revealed that hep

299 n, whereby the sequence of the surface-bound lipoprotein VlsE is continually modified through segment

300 f myocardial infarction from apoB-containing lipoproteins, whereas VLDL triglycerides did not explain