ApoA-II versus apoA-I: Two for one is not always a good deal

Arteriosclerosis, Thrombosis, and Vascular Biology

Volumn 21, Issue 12, 2001, Pages 1870-1872

  Castellani, Lawrence W ^a   Lusis, Aldons J ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

APOLIPOPROTEIN A1; APOLIPOPROTEIN A2; HIGH DENSITY LIPOPROTEIN;

ATHEROGENESIS; ATHEROSCLEROSIS; DISEASE PREDISPOSITION; EDITORIAL; FATTY ACID METABOLISM; HUMAN; LIPID METABOLISM; LIPID TRANSPORT; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL;

EID: 0035571569     PISSN: 10795642     EISSN: None     Source Type: Journal    
DOI: 10.1161/atvb.21.12.1870     Document Type: Editorial

References (25)

1. Identification of a sequence of apolipoprotein A-I associated with the activation of lecithin: Cholesterol acyltransferase
2. Human serum paraoxonase/arylesterase's retained hydrophobic N-terminal leader sequence associates with HDLs by binding phospholipids: Apolipoprotein A-I stabilizes activity
3. Apolipoprotein A-I deficiency: Biochemical and metabolic characteristics
4. Inhibition of early atherogenesis in transgenic mice by human apolipoprotein AI
5. Structure and function of apolipoprotein A-I and high-density lipoprotein
6. Cholesterol efflux from cultured adipose cells is mediated by LpAI particles but not by LpAI AII particles
7. Cholesterol efflux, lecithin-cholesterol acyltransferase activity, and pre-beta particle formation by serum from human apolipoprotein A-I and apolipoprotein A-I/apolipoprotein A-II transgenic mice consistent with the latter being less effective for reverse cholesterol transport
8. Overexpression of apolipoprotein AII in transgenic mice converts high density lipoproteins to proinflammatory particles
9. A splice-junction mutation responsible for familial apolipoprotein A-II deficiency: A splice-junction mutation responsible for familial apolipoprotein A-II deficiency
10. Atherosclerosis in transgenic mice overexpressing apolipoprotein A-II
11. Influence of the apoA-II gene locus on HDL levels and fatty streak development in mice
12. Human apolipoprotein A-II is a pro-atherogenic molecule when it is expressed in transgenic mice at a level similar to that in humans: Evidence of a potentially relevant species-specific interaction with diet
13. Expression of human apolipoprotein A-II and its effect on high density lipoproteins in transgenic mice
14. Evidence for linkage of the apolipoprotein A-II locus to plasma apolipoprotein A-II and free fatty acid levels in mice and humans
15. Studies with apolipoprotein A-II transgenic mice indicate a role for HDLs in adiposity and insulin resistance
16. Human evidence that the apolipoprotein a-II gene is implicated in visceral fat accumulation and metabolism of triglyceride-rich lipoproteins
17. Dramatically decreased high density lipoprotein cholesterol, increased remnant clearance, and insulin hypersensitivity in apolipoprotein A-II knockout mice suggest a complex role for apolipoprotein A-II in atherosclerosis susceptibility
18. Arg123-Tyr166 domain of human apoA-I is critical for HDL-mediated inhibition of macrophage honing and early atherosclerosis in mice
19. Structure-function relationships
20. A new synthetic class A amphipathic peptide analogue protects mice from diet-induced atherosclerosis
21. Three arginine residues in apolipoprotein A-I are critical for activation of lecithin: Cholesterol acyltransferase
22. Effect of overexpression of human apoA-I in C57BL/6 and C57BL/6 apoE-deficient mice on 2 lipoprotein-associated enzymes, platelet activating factor acetylhydrolase and paraoxonase. Comparison of adenovirus-mediated human apoA-I gene transfer and human apoA-I transgenesis
23. Cysteine substitutions in apolipoprotein A-I primary structure modulate paraoxonase activity
24. Oxidized low density lipoprotein-induced activation of NF-kB and subsequent expression of a variety of proinflammatory and proatherogenic genes are defective in monocyte-derived macrophages from CD36-deficient mice
25. Hepatobiliary cholesterol transport is not impaired in Abca1-null mice lacking HDL