A. Lusis

发表

Complex genetic contribution of the Apo AI-CIII-AIV gene cluster to familial combined hyperlipidemia. Identification of different susceptibility haplotypes.

J. Rotter, A. Lusis, T. D. de Bruin, 1997, The Journal of clinical investigation.

Multilocus genetic determinants of LDL particle size in coronary artery disease families.

R. Krauss, J. Rotter, A. Lusis, 1996, American journal of human genetics.

Minimally Modified Lipoproteins in Diabetes

F. Parhami, M. Territo, M. Navab, 1992, Diabetes.

A genome scan for familial combined hyperlipidemia reveals evidence of linkage with a locus on chromosome 11.

J. Rotter, A. Lusis, H. Allayee, 1999, American journal of human genetics.

Dietary regulation of fibrinolytic factors.

A. Lusis, M. Mehrabian, R. Barnard, 1990, Atherosclerosis.

Genetic variation in lipoprotein (a) levels in families enriched for coronary artery disease is determined almost entirely by the apolipoprotein (a) gene locus.

J. Rotter, A. Lusis, R. Gray, 1995, American journal of human genetics.

Production of erythroid-potentiating activity by a human T-lymphoblast cell line.

N. Bersch, S. Quan, D. Golde, 1980, Proceedings of the National Academy of Sciences of the United States of America.

Purification and characterization of a human T-lymphocyte-derived granulocyte-macrophage colony-stimulating factor.

D. Golde, A. J. Lusis, D. Quon, 1981, Blood.

An undifferentiated variant derived from the human acute myelogenous leukemia cell line (KG-1).

H. Koeffler, D. Golde, R. Sparkes, 1980, Blood.

Genome scan for adiposity in Dutch dyslipidemic families reveals novel quantitative trait loci for leptin, body mass index and soluble tumor necrosis factor receptor superfamily 1A

R. Cantor, A. Lusis, H. Allayee, 2000, International Journal of Obesity.

Novel genes for familial combined hyperlipidemia.

A. J. Lusis, L. Peltonen, J. Rotter, 1999, Current opinion in lipidology.

Apolipoprotein A-I/C-III/A-IV gene cluster in familial combined hyperlipidemia: effects on LDL-cholesterol and apolipoproteins B and C-III.

J. Rotter, A. Lusis, T. D. de Bruin, 1996, Journal of lipid research.

Systems genetics uncovers microbe-lipid-host connections in the murine gut

H. Blackwell, F. Rey, G. Keele, 2021, bioRxiv.

Families with familial combined hyperlipidemia and families enriched for coronary artery disease share genetic determinants for the atherogenic lipoprotein phenotype.

R. Krauss, J. Rotter, A. Lusis, 1998, American journal of human genetics.

Stimulatory activity for human pluripotent hemopoietic progenitors produced by a human T-lymphocyte cell line.

D. Golde, A. Fauser, H. Messner, 1981, Stem cells.

Neutrophil migration inhibition factor from T lymphocytes (NIF-T): partial purification by antibody affinity chromatography and further characterization.

D. Golde, L. Spolter, R. Weisbart, 1982, Clinical immunology and immunopathology.

Linkage of a candidate gene locus to familial combined hyperlipidemia: lecithin:cholesterol acyltransferase on 16q.

J. Rotter, A. Lusis, H. Allayee, 1999, Arteriosclerosis, thrombosis, and vascular biology.

Human leukemia cell line K562 responds to erythroid-potentiating activity

D. Golde, A. Lusis, C. Gauwerky, 1982 .

Contribution of the hepatic lipase gene to the atherogenic lipoprotein phenotype in familial combined hyperlipidemia.

R. Cantor, R. Krauss, J. Rotter, 2000, Journal of lipid research.

Atherosclerosis: basic mechanisms. Oxidation, inflammation, and genetics.

P. Edwards, A. Lusis, L. Demer, 1995, Circulation.

HDL and the inflammatory response induced by LDL-derived oxidized phospholipids.

D. Shih, A. Lusis, S. Reddy, 2001, Arteriosclerosis, thrombosis, and vascular biology.

Induction of heme oxygenase-1 inhibits the monocyte transmigration induced by mildly oxidized LDL.

A. Lusis, N. Leitinger, M. Navab, 1997, The Journal of clinical investigation.

Interaction of monocytes with cocultures of human aortic wall cells involves interleukins 1 and 6 with marked increases in connexin43 message.

A. Lusis, M. Navab, T. Rajavashisth, 1991, The Journal of clinical investigation.

The Yin and Yang of oxidation in the development of the fatty streak. A review based on the 1994 George Lyman Duff Memorial Lecture.

P. Edwards, D. Shih, A. Lusis, 1996, Arteriosclerosis, thrombosis, and vascular biology.

Minimally modified low density lipoprotein is biologically active in vivo in mice.

A. Lusis, M. Mehrabian, L. Demer, 1991, The Journal of clinical investigation.

Mildly oxidized LDL induces an increased apolipoprotein J/paraoxonase ratio.

G. Fonarow, A. Lusis, M. Brennan, 1997, The Journal of clinical investigation.

Paraoxonase and coronary heart disease.

G. Fonarow, D. Shih, A. Lusis, 2002, Current opinion in lipidology.

The role of high-density lipoproteins in oxidation and inflammation.

D. Shih, A. Lusis, M. Navab, 2001, Trends in cardiovascular medicine.

Overexpression of apolipoprotein AII in transgenic mice converts high density lipoproteins to proinflammatory particles.

A. Lusis, L. Castellani, C. Hedrick, 1997, The Journal of clinical investigation.

Modified Lipoproteins and Atherogenesis

A. Lusis, M. Territo, J. Berliner, 1992 .

Role of the GRO family of chemokines in monocyte adhesion to MM-LDL-stimulated endothelium.

A. Lusis, T. Kirchgessner, J. Berliner, 1994, The Journal of clinical investigation.

Biochemistry. An absorbing study of cholesterol.

H. Allayee, B. Laffitte, A. Lusis, 2000, Science.

Hb Switching in neonatal cultures. Increase of Hb A synthesis in presence of an erythroid potentiating activity (EPA)

W. Vainchenker, U. Testa, D. Golde, 1982, Journal of cellular physiology.