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1  ultimately disrupt the interaction with the LDL receptor.
2 SK9 modulates atherosclerosis mainly via the LDL receptor.
3 its role in promoting the degradation of the LDL receptor.
4 cretion is to some extent independent of the LDL receptor.
5 ic expression of SREBP-2 and its target, the LDL receptor.
6 ics into aberrant cells that overexpress the LDL receptor.
7 e resident proteins and an ER-trapped mutant LDL receptor.
8 lator of lipid metabolism by degrading liver LDL receptors.
9 erol levels by regulating the degradation of LDL receptors.
10 large VLDL, which are removed from plasma by LDL receptors.
11 ) receptor family, suggesting involvement of LDL receptors.
12  degradation of the low-density lipoprotein (LDL) receptor.
13 otein that degrades low-density lipoprotein (LDL) receptors.
14                     The lectin-like oxidized LDL receptor 1 (LOX-1) is a key player in the developmen
15 gand scavenger receptor Lectin-like Oxidized LDL Receptor-1 (LOX-1) is associated with vascular dysfu
16 dothelial cells through lectin-like oxidized LDL receptor-1 (LOX-1) signaling, and glycosylation remo
17 elets via its receptor, lectin-like oxidized LDL receptor-1 (LOX-1), and alphabeta amyloid peptide, w
18 aken up by endothelial cells primarily by ox-LDL receptor-1 (LOX-1).
19 ing 15-lipoxygenase and lectin-type oxidized LDL receptor-1 both in vitro and in vivo.
20 ing factor receptor and lectin-like oxidized LDL receptor-1 to attenuate Akt activation and trigger g
21  Arg-164 in frizzled 1 domain and Arg-427 in LDL receptor 5 domain, respectively.
22 s that result in loss of function within the LDL receptor, a major determinant of inherited hyperlipi
23 uptake as a result of increased cell surface LDL receptor abundance.
24 hypercholesterolemia patients with defective LDL receptor activity but no reduction in those who were
25 duced ABCA1-dependent cholesterol efflux and LDL receptor activity in ORP1-null cells.
26 ly absent (null-null) or impaired (non-null) LDL-receptor activity.
27       Consistent with this, Pep2-8 inhibited LDL receptor and EGF(A) domain binding to PCSK9 with IC5
28 an hepatoma cells results in upregulation of LDL receptor and increased LDL uptake in the cells.
29 owed that placental LPL acts in concert with LDL receptor and LRP1.
30 agocytic activity and elevated expression of LDL receptor and pro-inflammatory mediators.
31 ting furin-cleaved PCSK9 is able to regulate LDL receptor and serum cholesterol levels, although some
32 s should be the most effective in preserving LDL receptors and in lowering plasma LDL cholesterol.
33 oclonal antibody, increases the recycling of LDL receptors and reduces LDL cholesterol levels.
34 DL) receptors, increasing the degradation of LDL receptors and reducing the rate at which LDL cholest
35 ulating the hepatic low-density lipoprotein (LDL) receptors and increasing the clearance of LDL-chole
36  binding to hepatic low-density lipoprotein (LDL) receptors and promoting their lysosomal degradation
37 duced genes that promote cholesterol uptake (LDL receptor) and biosynthesis (HMG-CoA reductase).
38 pe 9) is a negative regulator of the hepatic LDL receptor, and clinical studies with PCSK9-inhibiting
39 one, with or without a genetic defect in the LDL receptor, and in subjects intolerant to statins, the
40 EBP-1c, SREBP-2, ChREBP, FATP1, HMGCoAR, and LDL receptor, and increasing Acox1 and ABCA1.
41 es involved in cholesterol biosynthesis, the LDL receptor, and PCSK9; a secreted protein that degrade
42 ced vitamin D deficiency in two backgrounds (LDL receptor- and ApoE-null mice) that resemble humans w
43 gainst the development of atherosclerosis in LDL-receptor/ApoB48-deficient mice.
44 rited disorder caused by mutations either in LDL receptor, apolipoprotein B (APOB), or proprotein con
45 amilial hypercholesterolaemia-causing genes, LDL receptor, apolipoprotein B and PCSK9, the most likel
46 tics and endocytosis of LDL particles by the LDL receptor are common in the general population and in
47  antibodies that inhibit its function on the LDL receptor are evaluated in phase III clinical trials.
48  and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inh
49 e start with a brief introduction to LDL and LDL receptor, as well as the advantages of using rLDL pa
50 In contrast, blocking LDL receptor with RAP (LDL receptor-associated protein) stopped the internaliza
51 ase PCSK9 binds the low-density lipoprotein (LDL) receptor at the surface of hepatocytes, thereby pre
52 ese results are consistent with increases in LDL receptors available to clear IDL and LDL from blood
53 (AT2 +/y) and deficient (AT2 -/y) mice in an LDL receptor -/- background were fed a saturated-fat enr
54                  Incubation with WT enhanced LDL receptor binding activity by 40% (+20% for GT and +0
55 , susceptibility to aggregation, LDL and non-LDL receptor-binding, and aortal deposition.
56 ies showed that MG(min)-LDL was bound by the LDL receptor but not by the scavenger receptor and had i
57 ycle, 4) LDL-induced aneuploidy requires the LDL receptor, but not Ass, showing that LDL works differ
58 esearch on a novel regulatory pathway of the LDL receptor by PCSK9, a new class of such drugs with a
59 protein (LDL) receptor family member, termed LDL receptor class A domain containing 3 (LRAD3), which
60 iculum (ER), where it inhibits production of LDL receptors, completing a feedback loop.
61      PCSK9 stimulates internalization of the LDL-receptor, decreases cholesterol uptake into hepatocy
62 s via DC-ASGPR, but not lectin-like oxidized-LDL receptor, Dectin-1, or DC-specific ICAM-3-grabbing n
63 ean+/-SD LDL cholesterol reductions in the 6 LDL receptor-defective patients were 19.3+/-16% and 26.3
64 ifferent populations including patients with LDL receptor defects (heterozygous familial hypercholest
65 al vectors and tested safety and efficacy in LDL receptor deficient Watanabe Heritable Hyperlipidemic
66                                              LDL receptor-deficient (Ldlr(-/-)) mice transplanted wit
67 by studying the effects of IgM deficiency in LDL receptor-deficient (Ldlr(-/-)) mice.
68                         Moreover, in fat-fed LDL receptor-deficient (Ldlr-/-) mice whose myeloid cell
69                             Western diet-fed LDL receptor-deficient (Ldlr-/-) mice with myeloid-speci
70  ABCG1 in T cells impacts atherosclerosis in LDL receptor-deficient (LDLR-deficient) mice, a model of
71 afb-deficient fetal liver cells in recipient LDL receptor-deficient hyperlipidemic mice revealed acce
72 tivity and activation of coagulation in both LDL receptor-deficient mice and African green monkeys.
73                                     Finally, LDL receptor-deficient mice expressing no (KO/L), normal
74 nistration of Slit2 to atherosclerosis-prone LDL receptor-deficient mice inhibited monocyte recruitme
75                          CAPN6 deficiency in LDL receptor-deficient mice restored CWC22/EJC/Rac1 sign
76                             Reversa mice are LDL receptor-deficient mice that develop atherosclerosis
77       PCPE2-deficient mice were crossed with LDL receptor-deficient mice to obtain LDLr(-/-), PCPE2(-
78                    Diabetic and non-diabetic LDL receptor-deficient mice were fed diets containing 0%
79                        Western type diet fed LDL receptor-deficient mice were transplanted with eithe
80                             Cholesterol-fed, LDL receptor-deficient mice were treated with either an
81 n these transgenic mice were crossed with an LDL receptor-deficient mouse model and were fed a high-f
82 d-type (WT), apolipoprotein E-deficient, and LDL receptor-deficient mouse models.
83 n E (Apoe(-/-)) and low-density lipoprotein (LDL) receptor-deficient (LDLr(-/-)) mice.
84 ike 4 (Dll4) in atheromata and fat tissue in LDL-receptor-deficient mice.
85 exin type 9 (PCSK9) activity on cell-surface LDL receptor degradation.
86 regulation of LDL-cholesterol via control of LDL receptor degradation.
87 ithin:cholesterol acyltransferase (LCAT) and LDL receptor double knock-out mice (Ldlr(-/-)xLcat(-/-)
88  down-regulates the low-density lipoprotein (LDL) receptor, elevating LDL cholesterol and acceleratin
89 ions that work primarily via upregulation of LDL receptor expression (ie, diet, bile acid sequestrant
90 g apolipoprotein B production and secretion, LDL receptor expression and membrane abundance, and LDL
91 lation of LDLR mRNA as a potent regulator of LDL receptor expression in humans.
92 tatin therapies that act via upregulation of LDL receptor expression to reduce LDL-C were associated
93 creased LDL reuptake through upregulation of LDL receptor expression.
94 ipoproteins to leukocytes without changes in LDL-receptor expression.
95 e structures of LDL and its complex with the LDL receptor extracellular domain (LDL.LDLr) at extracel
96 omplement-type ligand binding repeats in the LDL receptor family are thought to mediate the interacti
97                                 Furthermore, LDL receptor family member antagonism with receptor-asso
98 general antagonist for binding of ligands to LDL receptor family members, inhibited APC-induced phosp
99 r affinity found for most protein ligands of LDL receptor family members.
100 e known to be critical for ligand binding to LDL receptor family receptors, relatively small reductio
101 interacting with an endogenous member of the LDL receptor family to have these effects.
102 receptor-related protein 1), a member of the LDL receptor family, acts as an endocytic receptor for B
103 nner that depends upon Lrp4, a member of the LDL receptor family, and muscle-specific kinase (MuSK),
104 hermore, we identified LRP1, a member of the LDL receptor family, as a new LeX carrier protein expres
105                        LDLR, a member of the LDL receptor family, binds to apoE, yet its potential ro
106  for trafficking of megalin, a member of the LDL receptor family, from EE to the ERC by coupling it t
107 e interaction with the largest member of the LDL receptor family, low-density lipoprotein receptor-re
108 licated in driving the ligand binding to the LDL receptor family.
109 d required the engagement of a member of the LDL receptor family.
110 or-related protein 1 (LRP1), a member of the LDL receptor family.
111  identified a novel low-density lipoprotein (LDL) receptor family member, termed LDL receptor class A
112 n antagonist of the low-density lipoprotein (LDL) receptor family, suggesting involvement of LDL rece
113 rs of RAP-dependent low-density lipoprotein (LDL) receptor family.
114 ubstantially raised LDL cholesterol, reduced LDL receptor function, xanthomas, and cardiovascular dis
115 antial reduction in low-density lipoprotein (LDL) receptor function, severely elevated LDL cholestero
116 taining mono- and biallelic mutations of the LDL receptor gene as models of familial hypercholesterol
117 or all members of the evolutionarily ancient LDL receptor gene family, is the major genetic modifier
118 ted prevalence of type 2 diabetes by APOB vs LDL receptor gene was 1.91% vs 1.33% (OR, 0.65 [95% CI,
119    Statins activate low-density lipoprotein (LDL) receptor gene expression, thus lowering plasma LDL
120      Members of the low-density lipoprotein (LDL) receptor gene family have a diverse set of biologic
121 c methods to evaluate the effect of diet and LDL receptor genotype on macrophage foam cell formation
122 e expression of the low-density lipoprotein (LDL) receptor homolog, LpR2.
123 or degradation via inducible degrader of the LDL receptor (IDOL) overexpression, using liver-targeted
124 diates posttranscriptional regulation of the LDL receptor in response to intracellular cholesterol le
125 f plasma Lp(a) levels, including the role of LDL receptors in the clearance of Lp(a), is poorly defin
126  and PCSK9; a secreted protein that degrades LDL receptors in the liver.
127  9 (PCSK9) binds to low-density lipoprotein (LDL) receptors, increasing the degradation of LDL recept
128  recognition process likely governs the ApoE-LDL receptor interaction.
129 e (LCAT) knock-out mice, particularly in the LDL receptor knock-out background, are hypersensitive to
130  native LDL, or ox-LDL and in hyperlipidemic LDL receptor knockout (LDLR(-/-)) mice that was effectiv
131 eloid alpha1AMPK knockout (MAKO) mice on the LDL receptor knockout (LDLRKO) background to investigate
132 8-deficient CD11c+ DCs into Western diet-fed LDL receptor knockout mice and found that the transplant
133                       Human AR expression in LDL receptor knockout mice exacerbates vascular disease,
134 FcgammaRIIB knockout (FcRIIB(-/-)) mice into LDL receptor knockout mice.
135                 The m-RCT rates of the LDLr (LDL receptor)-KO (knockout), LDLr-KO/APOB100, and PCSK9
136 atherosclerotic lesion area was displayed in LDL receptor-KO mice transplanted with ERalpha(-/-) bone
137 mera containing the LDLa module of the human LDL receptor (LB2) demonstrated two key N-terminal regio
138 induced PCSK9 mRNA elevation and upregulated LDL-receptor (LDL-R) via modulation of the transcription
139                            Mice deficient in LDL receptor (Ldlr(-/-)) and mice lacking both TGH and L
140 3) or human apoE4 (E4) mice deficient in the LDL receptor (LDLR(-/-)).
141                            Mice lacking both LDL receptor (LDLR) and Arhgef1 were protected from high
142 lesterolemia because of its ability bind the LDL receptor (LDLR) and enhance its degradation in endos
143  cholesterol (LDL-C) by interacting with the LDL receptor (LDLR) and is an attractive therapeutic tar
144               Hepatic clearance involves the LDL receptor (LDLR) and possibly other receptors.
145                Given that PCSK9 degrades the LDL receptor (LDLR) and prevents the removal of LDL from
146 etary fatty acid composition on, lipoprotein-LDL receptor (LDLR) binding, and hepatocyte uptake, acco
147                             The mechanism of LDL receptor (LDLR) degradation mediated by the proprote
148  importance of elevated circulating LDL, and LDL receptor (LDLR) expression in tumor cells, on the gr
149 at hnRNP K is specifically involved in human LDL receptor (LDLR) gene transcription in HepG2 cells.
150                         Lipid uptake via the LDL receptor (LDLR) has been shown for digalactosylceram
151 protein metabolism caused by a defect in the LDL receptor (LDLR) leading to severe hypercholesterolem
152                                      Hepatic LDL receptor (LDLR) levels regulate the amount of plasma
153                                          The LDL receptor (LDLR) mediates efficient endocytosis of VL
154  hypercholesterolemia is typically caused by LDL receptor (LDLR) mutations that result in elevated le
155 ent of LDL, is known to bind to cell surface LDL receptor (LDLR) or cell surface-bound proteoglycans
156                             LXR inhibits the LDL receptor (LDLR) pathway through transcriptional indu
157 L) is a recently identified regulator of the LDL receptor (LDLR) pathway.
158                        Here we show that the LDL receptor (LDLR) serves as the major entry port of VS
159 sed by mutations in several genes, including LDL receptor (LDLR), apolipoprotein B (APOB), proprotein
160 d by variants in at least 3 different genes: LDL receptor (LDLR), apolipoprotein B-100, and proprotei
161     In humans and animals lacking functional LDL receptor (LDLR), LDL from plasma still readily trave
162 SK9 enhances the cellular degradation of the LDL receptor (LDLR), leading to increased plasma LDL cho
163  This multidomain protein interacts with the LDL receptor (LDLR), promoting receptor degradation.
164  cholesterol uptake receptors, including the LDL receptor (LDLR), the very LDLR, and the scavenger re
165 l levels substantially in both wild-type and LDL receptor (LDLR)-deficient mice.
166 ible degrader of the LDL receptor) regulates LDL receptor (LDLR)-dependent cholesterol uptake, but it
167 wild type LRP6 (LRP6(WT)) and LRP6(R611C) in LDL receptor (LDLR)-mediated LDL uptake.
168 c target for hypercholesterolemia due to its LDL receptor (LDLR)-reducing activity.
169  after its cellular internalization with the LDL receptor (LDLR).
170  IDOL as a sterol-dependent regulator of the LDL receptor (LDLR).
171 olesterol from plasma to liver cells via the LDL receptor (LDLr).
172 mechanisms involving upregulation of hepatic LDL receptor (LDLR).
173 eterozygote mutations R410S and G592E of the LDL receptor (LDLR).
174 rogenesis, we crossed mice deficient for the LDL receptor (Ldlr-/- mice) with mice that express low l
175  miR-33 inhibition in mice deficient for the LDL receptor (Ldlr-/- mice), with established atheroscle
176 density lipoproteins (LDL) via expression of LDL receptors (LDLR) at the cell surface.
177 g the endosomal and lysosomal degradation of LDL receptors (LDLR).
178 icking, such as the low-density lipoprotein (LDL) receptor (LDLR) and the ATP-binding cassette A1 (AB
179 erosis by targeting low density lipoprotein (LDL) receptor (LDLR) degradation, this study investigate
180 9 (PCSK9) modulates low-density lipoprotein (LDL) receptor (LDLR) degradation, thus influencing serum
181 is interaction, the low-density lipoprotein (LDL) receptor (LDLR) has been proposed as a potential en
182 erexpression of the low density lipoprotein (LDL) receptor (LDLR) in HepG2 cells dramatically increas
183                 The low-density lipoprotein (LDL) receptor (LDLR) is a central determinant of circula
184 se bone marrow into low-density lipoprotein (LDL) receptor (LDLr) knockout mice (SMS2(-/-)-->LDLr(-/-
185 equence analysis of low-density lipoprotein (LDL) receptor (LDLR) mRNA did not reveal any amino acid
186 SK9) is a ligand of low-density lipoprotein (LDL) receptor (LDLR) that promotes LDLR degradation in l
187  degradation of the low-density lipoprotein (LDL) receptor (LDLR), and its deficiency in humans resul
188 ve compounds on the low density lipoprotein (LDL) receptor (LDLR).
189 ven to mice lacking low density lipoprotein (LDL) receptors (Ldlr(-/-) mice).
190 ble degrader of the low-density lipoprotein [LDL] receptor [LDLR]) as a posttranscriptional regulator
191 ase subtilisin/kexin type 9 (PCSK9) binds to LDL receptors, leading to their degradation.
192 proteases, binds to low-density lipoprotein (LDL) receptors, leading to their accelerated degradation
193                       Moreover, they reduced LDL receptor levels in HepG2 cells and in mouse liver wi
194 fficiently restored low-density lipoprotein (LDL) receptor levels and cleared extracellular LDL.
195 -mediated cholesterol regulation, as well as LDL-receptor levels.
196 ess of monoclonal antibodies that extend the LDL-receptor lifecycle (and thus result in substantial l
197                     The lectin-like oxidized LDL receptor LOX-1 mediates endothelial cell (EC) uptake
198 ytes in relation to the lectin-like oxidized LDL receptor (LOX-1).
199 alirocumab treatment suggests that increased LDL receptors may also play a role in the reduction of p
200 ed heterozygotes, we propose that increasing LDL receptor-mediated cholesterol clearance by targeting
201 psin in the endoplasmic reticulum, deficient LDL receptor-mediated cholesterol uptake, and elevated l
202 possibility of a causal relationship between LDL receptor-mediated transmembrane cholesterol transpor
203 t and indisputably coexist, and both prevent LDL receptor-mediated uptake and promote macrophage scav
204 /kg/day) and AngII were co-infused into male LDL receptor -/- mice that were either AT2 +/y or -/y.
205                                         Male LDL receptor(-/-) mice were fed a saturated fat-enriched
206 at prevent interaction of PCSK9 with hepatic LDL receptors (monoclonal antibodies, mimetic peptides),
207                                    PCSK9 and LDL receptor mRNA levels in flash-frozen HCC and adjacen
208                                              LDL receptor mRNA was consistantly greater in HCC when c
209 e hepatic expression of apolipoprotein B and LDL receptor mRNAs with respect to the HF levels.
210                                      Type of LDL-receptor mutation, use of ezetimibe, coexistent diab
211  Patients with 2 defective versus 2 negative LDL receptor mutations had mean LDL-C reductions of 23.5
212 gene (APOB) mutations, and receptor-negative LDL receptor mutations were considered more severe than
213                     Low-density lipoprotein (LDL) receptor mutations were considered more severe than
214 se of the high prevalence of modestly severe LDL-receptor mutations in the Netherlands.
215                          Eight patients with LDL receptor-negative or -defective homozygous familial
216 t vascular smooth muscle cells isolated from LDL receptor null (Ldlr(-/-)) mice, which have impaired
217 -atherogenic effects of Enano and L-Enano in LDL receptor null (LDLr-/-) mice.
218              Intravenous administration into LDL receptor null mice of targeted compared to non-targe
219 , on lipid metabolism and atherosclerosis in LDL receptor-null (LDLRKO) mice.
220 xpansion were not significantly different in LDL receptor-null mice fed a saturated fat-enriched diet
221  potentially therapeutic protein can bind to LDL receptors on the BBB and be transcytosed into the CN
222                     These therapies increase LDL receptors on the cell surface and reduce plasma LDL
223 isulfide editing-dependent maturation of the LDL receptor or the reduction-dependent degradation of m
224 import in mammalian cells is mediated by the LDL receptor pathway.
225 st to its previously reported effects on the LDL receptor, PCSK9 did not alter ENaC endocytosis or de
226         To achieve its maximal effect on the LDL receptor, PCSK9 requires autoproteolysis.
227  heparan sulfate proteoglycan (HSPG) and the LDL receptor, plus one docking receptor, SR-BI, signific
228  9 (PCSK9) binds to low-density lipoprotein (LDL) receptors, promoting their degradation and increasi
229 and activating a receptor complex containing LDL receptor protein 4 (Lrp4) and muscle-specific kinase
230       A significant 20% reduction in hepatic LDL receptor protein expression was also observed with e
231 ssion lowered plasma PCSK9 levels, increased LDL receptor protein expression, and restored plasma cho
232  target gene expression, resulting in higher LDL receptor protein levels.
233 llular levels with concomitant reductions of LDL receptor protein.
234           As well as the expected effects on LDL-receptor protein levels in the liver, mice expressin
235 and plasma PCSK9 and resulted in lower LDLR (LDL receptor) protein and increased plasma LDL-C.
236 vered the role of PCSK9 in the regulation of LDL-receptor recycling and identified loss-of-function v
237 uitin ligase IDOL (inducible degrader of the LDL receptor) regulates LDL receptor (LDLR)-dependent ch
238 se subtilisin/kexin type-9 (PCSK9, a hepatic LDL-receptor regulator), inflammation, and adipose tissu
239 a consequence of the disruption of the PCSK9/LDL receptor regulatory axis.
240 of the TGF-beta-dependent signaling pathway: LDL receptor-related protein (LRP-1) and decorin.
241                                              LDL receptor-related protein (LRP1) is an endocytic and
242                                              LDL receptor-related protein (LRP1) is expressed by Schw
243 l surface stimulates association of CRT with LDL receptor-related protein (LRP1) to signal focal adhe
244 sing a haploid genetic screen, we identified LDL receptor-related protein 1 (LRP1) as a host cell rec
245                                              LDL receptor-related protein 1 (LRP1) is a highly modula
246                                          The LDL receptor-related protein 1 (LRP1) is a large endocyt
247                                          The LDL receptor-related protein 1 (LRP1) is a large endocyt
248           Recent studies have shown that the LDL receptor-related protein 1 (LRP1) is a physiological
249 epatic clearance of fVIII is mediated by the LDL receptor-related protein 1 (LRP1), a member of the L
250 ell biology techniques, we report that LRP1 (LDL receptor-related protein 1), a member of the LDL rec
251 hat tPA induces Tyr(4507) phosphorylation of LDL receptor-related protein 1, which in turn leads to t
252 nterstitial fibroblast proliferation through LDL receptor-related protein 1-mediated beta1 integrin a
253 ndent of its protease activity, but required LDL receptor-related protein 1.
254 tion of the cytoplasmic tail of its receptor LDL receptor-related protein 1.
255  identified a contribution of the annexin A6/LDL receptor-related protein 1/thrombospondin 1 (ANXA6/L
256 bular protein extracts that we identified as LDL receptor-related protein 2 (LRP2), also known as meg
257 he closely related WNT signaling coreceptors LDL receptor-related protein 5 (LRP5) and LRP6 had redun
258 through the frizzled class receptor 4 (FZD4)/LDL receptor-related protein 5-6 (LRP5-6)/tetraspanin 12
259 y decreased expression of the Wnt coreceptor LDL receptor-related protein 6 (LRP6) in the mucosal tis
260 Loss-of-function mutations in Wnt coreceptor LDL receptor-related protein 6 (LRP6) underlie early-ons
261       We previously identified a mutation in LDL receptor-related protein 6 (LRP6), LRP6(R611C), that
262 that bind to the Frizzled (FZD) receptor and LDL receptor-related protein 6 (LRP6).
263      These effects required the WNT receptor LDL receptor-related protein 6 (LRP6).
264 ivation was determined by phosphorylation of LDL receptor-related protein 6, a coreceptor of Wnt liga
265 rosophila and zebrafish hearts revealed that LDL receptor-related protein LRP2 is required for cardio
266 ular WNT activation by binding to the Kremen/LDL receptor-related protein receptors, was not seen wit
267 omposed of the receptor tyrosine kinase AXL, LDL receptor-related protein-1 (LRP-1), and RAN-binding
268 tective effect of tPA required its receptor, LDL receptor-related protein-1 (LRP-1).
269         Herein, we show that deletion of the LDL receptor-related protein-1 (LRP1) gene in Schwann ce
270                                              LDL receptor-related protein-1 (LRP1) is an endocytic an
271 death via an autocrine mechanism through the LDL receptor-related protein-1 (LRP1) receptor.
272   The endocytic and cell signaling receptor, LDL receptor-related protein-1 (LRP1), is reported to su
273 iption factor in SCs, unless counteracted by LDL receptor-related protein-1 (LRP1), which serves as a
274 rant peptide Angiopep-2 (An2), which targets LDL receptor-related protein-1 (LRP1).
275      Rapid ERK1/2 activation is dependent on LDL receptor-related protein-1 (LRP1).
276                                        LRP1 (LDL receptor-related protein-1) is a ubiquitous receptor
277 om type I collagen alpha chain, albumin, and LDL receptor-related protein.
278                                              LDL receptor-related proteins 5 and 6 (LRP5/6) are corec
279 ipoprotein E (ApoE) receptors, also known as LDL receptor-related proteins, have distinguished themse
280 of LTP across the Blood Brain Barrier by two LDL receptor-related proteins: LRP1 and Megalin.
281 mes bind tightly to low-density lipoprotein (LDL) receptor-related protein 1 (LRP1), but the molecula
282 nternalized through low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1) to become enzyma
283                     Low-density lipoprotein (LDL) receptor-related protein-1 (LRP1) has been shown to
284 is a ligand for the Low Density Lipoprotein (LDL) Receptor-related Protein-1 (LRP1), a multifunctiona
285                                              LDL-receptor-related protein 6 (LRP6), alongside Frizzle
286 structures of ligands in complex with tandem LDL receptor repeats or tandem CUB domains in other endo
287                  Additional studies with the LDL receptor showed a similar effect.
288 h that contacted by the EGF(A) domain of the LDL receptor, suggesting a competitive inhibition mechan
289                            It fully restored LDL receptor surface levels and LDL particle uptake in P
290 ertase subtilisin/kexin type 9 (PCSK9) binds LDL receptors, targeting them for degradation.
291 s 1.79-fold higher surface expression of the LDL receptor than in noncarriers (P=0.0086).
292                            In the absence of LDL receptors, the large VLDLs accumulate and produce ma
293 ession of PCSK9, a secreted inhibitor of the LDL receptor, thereby limiting their beneficial effects.
294 targets, and that inhibition of ACL leads to LDL receptor upregulation, decreased LDL-C and attenuati
295    To this end, the low-density lipoprotein (LDL) receptor was targeted for degradation via inducible
296 Thus, by inducing hepatic degradation of the LDL receptor, we generated a T2D model of combined kidne
297 ely target cancer cells that overexpress the LDL receptor while showing minor adverse impact on norma
298 oth furin- and hepsin-cleaved PCSK9 bound to LDL receptor with only 2-fold reduced affinity compared
299                        In contrast, blocking LDL receptor with RAP (LDL receptor-associated protein)
300  the role of AT(1a) receptors on leukocytes, LDL receptor(-/-)xAT(1a) receptor(+/+) or AT(1a) recepto

 
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