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1 lation of beta-very low density lipoprotein (beta-VLDL).
2 -/-) mice) internalized beta-migrating VLDL (beta-VLDL).
3 he LDL-receptor and none was able to degrade beta-VLDL.
4 l formation when the atherogenic stimulus is beta-VLDL.
5 ndent uptake of the apoE lipoprotein ligand, beta-VLDL.
6 urce or (b) independent actions of apoE3 and beta-VLDL.
7 ities by 35% and redistributing apoE2 to the beta-VLDL.
8 the same extent as excess unlabeled VLDL or beta-VLDL.
9 of ligand binding to LRP, and apoE-enriched beta-VLDL, a ligand for LRP, reduce PDGF-induced tyrosin
10 holesterol deposition during incubation with beta-VLDL alone, but completely blocked the augmented re
11 n in lipoproteins demonstrated a decrease in beta-VLDL and LDL cholesterol and an increase in HDL cho
15 nd beta-VLDL in coated pits, suggesting that beta-VLDL binding promoted the internalization of the LD
16 ibility, mutagenesis experiments showed that beta-VLDL binding was inhibited by mutations at D203 and
18 an alter neurite outgrowth in the absence of beta-VLDL by constructing Neuro-2a cell lines expressing
19 ontaining beta-very low density lipoprotein (beta-VLDL) can stimulate neurite outgrowth to a signific
21 Under these conditions, which allowed equal beta-VLDL-cholesteryl ester hydrolysis, cholesterol este
24 LR-Y807C using LDLR-immunogold, LDL-gold and beta-VLDL-gold probes revealed enrichment of LDLR-Y807C-
25 ificantly greater extent than apoE4-enriched beta-VLDL in a central nervous system-derived neuronal c
26 obes revealed enrichment of LDLR-Y807C-bound beta-VLDL in coated pits, suggesting that beta-VLDL bind
28 highest capacity in binding to apoE enriched beta-VLDL in vitro and was more effective in removing ap
32 eta-migrating very low density lipoproteins (beta-VLDL) (intestinal and hepatic remnant lipoproteins)
33 ry low-density lipoprotein of beta mobility (beta-VLDL), it was with lower affinity and capacity than
34 studies we conclude that the binding of apoE-beta VLDL, lactoferrin, aprotinin, lipoprotein lipase, a
35 pairs of lipoproteins examined, Ac-LDL plus beta-VLDL, LDL plus beta-VLDL, and LDL plus Ac-LDL, was
36 E (apoE)-beta very low density lipoprotein (beta VLDL), lipoprotein lipase, aprotinin, lactoferrin,
38 Pigeon beta-very-low-density lipoprotein (beta-VLDL), low-density lipoprotein (LDL), and acetylate
39 as rabbit beta-very low density lipoprotein (beta-VLDL), making it difficult to discern the biologica
44 beta-migrating very low-density lipoprotein (beta-VLDL) particles, which contain multiple copies of a
45 ntaining beta-very low density lipoproteins (beta-VLDL) possess similar cell binding and internalizat
46 eta-migrating very low density lipoproteins (beta-VLDL) stimulated cholesteryl [(3)H]oleate depositio
47 teins, or quantitation of 125I-apoE-enriched beta-VLDL, there was a 2-3-fold greater accumulation of
52 oprotein, beta-very low density lipoprotein (beta-VLDL), was internalized by macrophages and hydrolyz
53 cholesterol (75%), triglycerides (117%), and beta-VLDL, while decreasing lipoprotein lipase and hepat
54 ion and degradation of (125)I-labeled LDL or beta-VLDL without altering the amount of lipoprotein bou
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