Trimerization of Apolipoprotein A-I Retards Plasma Clearance and Preserves Antiatherosclerotic Properties
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E. Falk | S. Moestrup | J. Graversen | M. Etzerodt | H. Thøgersen | J. Christensen | J. Nieland | J. M. Laurberg | M. H. Andersen
[1] P. Shah,et al. Apolipoprotein A-I/HDL infusion therapy for plaque stabilization-regression: a novel therapeutic approach. , 2007, Current pharmaceutical design.
[2] P. Barter,et al. The rationale for using apoA‐I as a clinical marker of cardiovascular risk , 2006, Journal of internal medicine.
[3] E. Rubin,et al. HDLs in apoA-I transgenic Abca1 knockout mice are remodeled normally in plasma but are hypercatabolized by the kidney Published, JLR Papers in Press, July 16, 2005. DOI 10.1194/jlr.M500179-JLR200 , 2005, Journal of Lipid Research.
[4] S. Kaul,et al. Differential Effects of Apolipoprotein A-I–Mimetic Peptide on Evolving and Established Atherosclerosis in Apolipoprotein E-Null Mice , 2004, Circulation.
[5] J. Tavernier,et al. Phosphorylation by Protein Kinase CK2 Modulates the Activity of the ATP Binding Cassette A1 Transporter* , 2004, Journal of Biological Chemistry.
[6] Paul Schoenhagen,et al. Effect of recombinant ApoA-I Milano on coronary atherosclerosis in patients with acute coronary syndromes: a randomized controlled trial. , 2003, JAMA.
[7] A. Beaudet,et al. Long-Term Stable Expression of Human Apolipoprotein A-I Mediated by Helper-Dependent Adenovirus Gene Transfer Inhibits Atherosclerosis Progression and Remodels Atherosclerotic Plaques in a Mouse Model of Familial Hypercholesterolemia , 2003, Circulation.
[8] J. Ordóñez‐Llanos,et al. Mechanisms of HDL deficiency in mice overexpressing human apoA-II DOI 10.1194/jlr.M200081-JLR200 , 2002, Journal of Lipid Research.
[9] S. Reddy,et al. High-density lipoprotein and the dynamics of atherosclerotic lesions. , 2001, Circulation.
[10] W. Davidson,et al. A proteolytic method for distinguishing between lipid-free and lipid-bound apolipoprotein A-I. , 2001, Journal of lipid research.
[11] N. Srivastava,et al. High density lipoprotein, apolipoprotein A-1, and coronary artery disease , 2000, Molecular and Cellular Biochemistry.
[12] R. A. Srivastava,et al. High density lipoprotein, apolipoprotein A-I, and coronary artery disease. , 2000, Molecular and cellular biochemistry.
[13] D. Sparks,et al. Role of the kidney in regulating the metabolism of HDL in rabbits: evidence that iodination alters the catabolism of apolipoprotein A-I by the kidney. , 2000, Biochemistry.
[14] J. Graversen,et al. The heparin-binding site in tetranectin is located in the N-terminal region and binding does not involve the carbohydrate recognition domain. , 2000, The Biochemical journal.
[15] D. Rader,et al. Regression of atherosclerosis induced by liver-directed gene transfer of apolipoprotein A-I in mice. , 1999, Circulation.
[16] A. Chapelle,et al. The intrinsic factor–vitamin B12 receptor, cubilin, is a high-affinity apolipoprotein A-I receptor facilitating endocytosis of high-density lipoprotein , 1999, Nature Medicine.
[17] G. Franceschini,et al. Recombinant apolipoproteins for the treatment of vascular diseases. , 1999, Atherosclerosis.
[18] H. Hobbs,et al. Kinetic characteristics and regulation of HDL cholesteryl ester and apolipoprotein transport in the apoA-I 2 / 2 mouse , 1998 .
[19] L. Woollett,et al. Kinetic parameters for high density lipoprotein apoprotein AI and cholesteryl ester transport in the hamster. , 1997, The Journal of clinical investigation.
[20] L. Ellgaard,et al. Dissection of the domain architecture of the alpha2macroglobulin-receptor-associated protein. , 1997, European journal of biochemistry.
[21] A. Jonas,et al. Properties of an N-terminal proteolytic fragment of apolipoprotein AI in solution and in reconstituted high density lipoproteins , 1995, The Journal of Biological Chemistry.
[22] G. Kaysen,et al. Apolipoprotein AI levels are increased in part as a consequence of reduced catabolism in nephrotic rats. , 1995, The American journal of physiology.
[23] S. Eisenberg,et al. Human HDL cholesterol levels are determined by apoA-I fractional catabolic rate, which correlates inversely with estimates of HDL particle size. Effects of gender, hepatic and lipoprotein lipases, triglyceride and insulin levels, and body fat distribution. , 1994, Arteriosclerosis and thrombosis : a journal of vascular biology.
[24] G. Franceschini,et al. In vivo metabolism of a mutant form of apolipoprotein A-I, apo A-IMilano, associated with familial hypoalphalipoproteinemia. , 1993, The Journal of clinical investigation.
[25] B. Paigen,et al. Synthetic low and high fat diets for the study of atherosclerosis in the mouse. , 1990, Journal of lipid research.
[26] D. Steinberg,et al. Tissue sites of degradation of apoprotein A-I in the rat. , 1983, The Journal of biological chemistry.
[27] M. Pal,et al. HDL elevators and mimetics--emerging therapies for atherosclerosis. , 2007, Cardiovascular & hematological agents in medicinal chemistry.
[28] A. von Eckardstein,et al. High density lipoproteins and arteriosclerosis. Role of cholesterol efflux and reverse cholesterol transport. , 2001, Arteriosclerosis, thrombosis, and vascular biology.
[29] A. Jonas. Reconstitution of high-density lipoproteins. , 1986, Methods in enzymology.