Fabrication and fluorescence imaging of human low-density lipoprotein coatings for highly efficient capillary electrophoresis separation of basic proteins

2009 ◽  
Vol 30 (8) ◽  
pp. 1362-1371 ◽  
Author(s):  
Junfa Yin ◽  
Yuling Song ◽  
Zhixin Wang ◽  
Hailin Wang
2000 ◽  
Vol 269 (1) ◽  
pp. 25-30 ◽  
Author(s):  
Tomomitsu Ichikawa ◽  
Makoto Yamada ◽  
Daisaku Homma ◽  
Richard J. Cherry ◽  
Ian E.G. Morrison ◽  
...  

2018 ◽  
Vol 97 (6) ◽  
pp. 2230-2238 ◽  
Author(s):  
N. Wang ◽  
Q. Xu ◽  
Y. Liu ◽  
Y. Jin ◽  
P.W. Harlina ◽  
...  

1991 ◽  
Vol 37 (3) ◽  
pp. 317-326 ◽  
Author(s):  
Peter O Kwiterovich ◽  
Mahnaz Motevalli ◽  
Michae Miller ◽  
Paul S Bachorik ◽  
Stephanie D Kafonek ◽  
...  

Abstract Hyperapobetalipoproteinemia (hyperapoB), a familial lipoprotein disorder characterized by an increase in small, dense, low-density lipoprotein (LDL) particles, is strongly associated with coronary artery disease. There are two metabolic defects in hyperapoB: an increased synthesis of a very-low-density lipoprotein in liver, resulting in an overproduction of LDL, and a delayed clearance of post-prandial triglyceride and free fatty acids. To date, defects in the apolipoprotein B gene do not appear to explain the hyperapoB phenotype. Defect(s) in the uptake or intracellular metabolism of free fatty acids have been found in cells from hyperapoB patients. Three basic proteins (BPs)--BP I (Mr 14,000, pI 9.10), BP II (Mr 27,500, pI 8.48), and BP III (Mr 55,000, pI 8.73)--were isolated from normal human serum. Compared with normal fibroblasts, cultured hyperapoB fibroblasts incubated with BP I, which appears to be the same protein as acylation-stimulating protein (ASP), showed 50% less stimulation of triglyceride acylation and cholesterol esterification, whereas BP II markedly stimulated cholesteryl ester formation, and BP III caused no difference in response vs normal fibroblasts. However, in cultured normal human monocyte macrophages, BP III, but not BP I or BP II, stimulated cholesteryl esterification two- to threefold. BP I, BP II, and BP III may provide new insights into normal metabolism of lipids, lipoproteins, and free fatty acids and the pathophysiology of hyperapoB.


2002 ◽  
Vol 23 (20) ◽  
pp. 3615-3622 ◽  
Author(s):  
Laura Ceriotti ◽  
Takayuki Shibata ◽  
Britta Folmer ◽  
Bruce H. Weiller ◽  
Matthew A. Roberts ◽  
...  

Author(s):  
Dean A. Handley ◽  
Cynthia M. Arbeeny ◽  
Larry D. Witte

Low density lipoproteins (LDL) are the major cholesterol carrying particles in the blood. Using cultured cells, it has been shown that LDL particles interact with specific surface receptors and are internalized via a coated pit-coated vesicle pathway for lysosomal catabolism. This (Pathway has been visualized using LDL labeled to ferritin or colloidal gold. It is now recognized that certain lysomotropic agents, such as chloroquine, inhibit lysosomal enzymes that degrade protein and cholesterol esters. By interrupting cholesterol ester hydrolysis, chloroquine treatment results in lysosomal accumulation of cholesterol esters from internalized LDL. Using LDL conjugated to colloidal gold, we have examined the ultrastructural effects of chloroquine on lipoprotein uptake by normal cultured fibroblasts.


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