Renee LeBoeuf, PhD
Research Professor, Department of Medicine, Division of Metabolism, Endocrinology and Nutrition
Email Address: email@example.com
Division of Metabolism, Endocrinology and Nutrition Website: http://depts.washington.edu/metab/
Dr. LeBoeuf received her MS in Biophysics from the University of Oregon and her PhD in Biochemistry/Biophysics from the State University of New York in Buffalo, NY. Her post-doctoral work studying biotransformation enzymes was performed with Dr. Beverly Paigen in the Department of Molecular Biology, Roswell Park Memorial Institute in Buffalo, NY. This was followed by work as a Postdoctoral Fellow and Assistant Professor while in the Molecular Biology Institute and the Department of Lipid Biology, University of California, Los Angeles, CA.
Dr. LeBoeuf is currently a Research Professor of Medicine and the Director of the Seattle Mouse Metabolic Phenotype Center (www.mmpc.org). She is a member of the Diabetes and Obesity Center of Excellence and the Center for Cardiovascular Biology. Dr. LeBoeuf has been continuously funded by federal and private grants to study the genetics of atherosclerosis and diabetes. Dr. LeBoeuf currently is the principle investigator of two NIH RO1 grants and a member of several program project grants. Dr. LeBoeuf has trained dozens of graduate students and postdoctoral fellows during her faculty career at UCLA and the UW.
The LeBoeuf lab has several ongoing projects in the areas of vascular disease, diabetes-accelerated atherosclerosis and renal diseases, and obesity. They are interested in the identification and functional characterization of genes involved in these disorders. They utilize the mouse as a genetic model for these diseases because the mouse genome is well defined and metabolic diseases in this organism are similar to those seen in humans.
Genetic and dietary factors contributing to atherosclerosis
Atherosclerosis remains the most prevalent cause of morbidity and mortality in the United States. The reduction of blood cholesterol levels through the use of statins has reduced risk for many individuals but it is clear that plasma lipid levels are not the only factor precipitating this disease. We have a history of mapping and characterizing genes involved in lipid metabolism and atherosclerosis and participating in the development of the mouse system in which to study atherosclerosis (see Past Accomplishments below). Although we continue to identify genes involved in specific features of atherosclerotic disease, we are focusing current work on understanding how specific cytokines influence disease initiation and progression.
Tumor necrosis factor-alpha (TNF) is a key inflammatory mediator implicated in all stages of the atherosclerotic process. Although TNF contributions are generally considered as pro-atherogenic, we have shown that TNF makes a biphasic contribution to atherosclerosis. During the initiation phase of atherogenesis, TNF retards lesion formation by reducing the rate of cholesterol accumulation in macrophages through reduction of scavenger receptors and possible enhancement of cholesterol efflux. However, as foam cells form and accumulate in number, increased levels of TNF secreted from these cells result in negative outcomes (e.g. apoptosis, proliferation of smooth muscle cells and insult to endothelial cells). Thus, TNF participates in adaptive and maladaptive processes at the artery wall.
We have also found that loss of the major TNF receptor (R1) is associated with accelerated initiation of atherosclerosis, suggesting that R1 is protective with respect to lesion initiation. In contrast, loss of R1 in advanced lesions reduced lesion progression, suggesting that R1 aggravates lesion progression. The identification of molecular mechanisms involved in these dual activities of TNF receptor(s) is a goal for this project.
Genetic factors contributing to carotid artery intimal thickening
Restenosis of the carotid artery in individuals treated with bare wire and drug treated stents remains a major problem. Nearly 25% of all individuals receiving stents must undergo retreatment to eliminate new blockages to avoid suffering major stroke events. Why a sub-set of individuals is most susceptible to restenotic events is not clear. Dozen of genes have been proposed to be involved in restenosis and we can either check the role of each gene one by one, or take a broader genetic and genomic approach to uncovering key pathways predisposing individuals to restenosis.
In order to identify key molecular pathways and in an effort to identify important therapeutic targets, we are using a genomics approach to identify key genetic regulators of intimal hyperplasia using a carotid artery injury model. Current work shows that between FVB and C57B/6 mouse strains, there are 2 major genes responsible for differences in injury responses between these strains. Chromosomal interval reduction through additional genetic analyses coupled to gene expression microarray analyses are being used to uncover specific gene pathways which then can be tested for treatment relevance among human subjects in classic association studies.
Diabetes-accelerated atherosclerosis and renal diseases
Cardiovascular diseases are accelerated in individuals with diabetes and are the leading cause of morbidity and mortality in this population. In addition, microvascular diseases involving the retinal and kidney are also strongly manifested due to diabetes. Acute and chronic elevations in circulating levels of glucose, free fatty acids and lipoproteins as well as fluctuating insulin levels are among the contributing factors suggested to accelerate atherosclerosis. However, the precise mechanisms by which these factors lead to accelerated disease are not clear.
For diabetes-accelerated atherosclerosis and renal diseases, several basic questions remain to be answered. At what stage of atherosclerosis and renal lesion development is diabetes most damaging? Do lesions differ in their composition from individuals with, as compared to without diabetes? Are molecular mechanisms leading to atherosclerosis/renal disease accentuated during diabetes or are new molecular pathways invoked by the diabetic state? If the latter is the case, can diabetes-specific molecular pathways be identified? It is of crucial importance to answer these questions in order to design therapeutic interventions for the millions of individuals suffering with diabetes mellitus.
To address these questions, we have developed several mouse models of diabetic vascular and renal diseases. Several models are better suited for studies of lesion initiation, and several are better for studies of advanced lesion progression. Using genetic engineering and classic genetic studies, we are testing the role of specific genes contributing to diabetes-accelerated vascular diseases. One model has demonstrated that diabetic mice, but not non-diabetic mice, show increased levels of collagen in medial and adventitial regions of the aorta. Such changes may lead to arterial stiffness, a key aberrant consequence of diabetes in human vascular disease. Can accumulation of collagen and other matrix proteins be slowed through better diabetes control, diet manipulations or specific drug interventions?
Both hyperglycemia and hyperlipidemia are evident in individuals with type 2 diabetes. To better understand how these factors influence artery wall biology, we are using gene expression microarrays to identify factors at the aortic wall which are responsive to elevated glucose versus elevated lipids. This information will be used to modulate the expression of genes predisposing the aorta to further metabolic insults.
Obesity, inflammation and cholesterol metabolism
Obesity is now considered an inflammatory disease because of the influx of macrophages into adipose tissue and the release of inflammatory cytokines which may participate in promoting insulin resistance. TNF receptors are important players in both the inflammation and insulin resistance scenarios. However, we have found that loss of both TNF receptors results in a worsening of the obesity component in mice challenged with high fat diets. Thus, one project in the lab is to understand the role of TNF receptor signaling pathways in obesity.
Obesity, dieting and cholesterol metabolism
It is clear from many literature sources, that loss of body weight through dieting and multiple body weight cycling are risk factors for gall bladder and liver diseases. Adipose tissue serves as the largest ‘sink’ in the body for free cholesterol and the only tissue able to dispose of excess cholesterol is the liver through conversion of cholesterol into bile acids. It is therefore of the utmost importance to understand how adipose tissue mobilizes the massive levels of free cholesterol upon loss of body fat and whether this can be regulated or controlled to improve outcomes with respect to gall bladder and liver diseases.
Little is known about the mechanisms by which adipose tissue releases cholesterol, whether triglyceride lipolysis and cholesterol efflux are coordinately regulated, to what lipoprotein particles or other intermediate storage points this cholesterol is shuttled, and how the liver stores and mediates disposal of the vast quantities of cholesterol during dieting. These are the directions to which we are focusing part of our studies.
Kanter JE, Averill MM, Leboeuf RC, Bornfeldt KE. Diabetes-accelerated atherosclerosis and inflammation. Circ Res. 2008, 103(8):e116-7.
Li YI, Elmer G, Leboeuf RC. Tanshinone IIA reduces macrophage death induced by hydrogen peroxide by upregulating glutathione peroxidase. Life Sci. 2008 83:557-62. Epub 2008 Aug 16.
Zhang WJ, Bird KE, McMillen TS, LeBoeuf RC, Hagen TM, Frei B.
Dietary alpha-lipoic acid supplementation inhibits atherosclerotic lesion development in apolipoprotein E-deficient and apolipoprotein E/low-density lipoprotein receptor-deficient mice. Circulation. 2008 117:421-8.
Hall TR, Bogdani M, Leboeuf RC, Kirk EA, Maziarz M, Banga JP, Oak S, Pennington CA, Hampe CS. Modulation of diabetes in NOD mice by GAD65-specific monoclonal antibodies is epitope specific and accompanied by anti-idiotypic antibodies. Immunology. 2008 123(4):547-54.
Katz R, Hamilton JA, Pownall HJ, Deckelbaum RJ, Hillard CJ, Leboeuf RC, Watkins PA.
Brain uptake and utilization of fatty acids, lipids & lipoproteins: recommendations for future research. J Mol Neurosci. 2007 33(1):146-50.
Ajioka RS, LeBoeuf RC, Gillespie RR, Amon LM, Kushner JP. Mapping genes responsible for strain-specific iron phenotypes in murine chromosome substitution strains. Blood Cells Mol Dis. 2007 39(2):199-205.
Kanter JE, Johansson F, LeBoeuf RC, Bornfeldt KE. Do glucose and lipids exert independent effects on atherosclerotic lesion initiation or progression to advanced plaques? Circ Res. 2007 100(6):769-81. Review.
McMillen TS, Heinecke JW, LeBoeuf RC. Expression of human myeloperoxidase by macrophages promotes atherosclerosis in mice. Circulation. 2005 111(21):2798-804.
Ladiges WC, Knoblaugh SE, Morton JF, Korth MJ, Sopher BL, Baskin CR, MacAuley A, Goodman AG, LeBoeuf RC, Katze MG. Pancreatic beta-cell failure and diabetes in mice with a deletion mutation of the endoplasmic reticulum molecular chaperone gene P58IPK. Diabetes. 2005 54(4):1074-81.
O’Brien KD, McDonald TO, Kunjathoor V, Eng K, Knopp EA, Lewis K, Lopez R, Kirk EA, Chait A, Wight TN, deBeer FC, LeBoeuf RC. Serum amyloid A and lipoprotein retention in murine models of atherosclerosis. Arterioscler Thromb Vasc Biol. 2005 25(4):785-90.
Shultz JM, Zhu XD, Knopp RH, Leboeuf RC, Rosenfeld ME. Norgestimate and medroxyprogesterone acetate do not attenuate the atheroprotective effects of 17beta-estradiol in ovariectomized, apolipoprotein E-deficient mice. Fertil Steril. 2004 82 Suppl 3:1133-9.
Mühlfeld AS, Spencer MW, Hudkins KL, Kirk E, LeBoeuf RC, Alpers CE. Hyperlipidemia aggravates renal disease in B6.ROP Os/+ mice. Kidney Int. 2004 66(4):1393-402.
Spencer MW, Mühlfeld AS, Segerer S, Hudkins KL, Kirk E, LeBoeuf RC, Alpers CE. Hyperglycemia and hyperlipidemia act synergistically to induce renal disease in LDL receptor-deficient BALB mice. Am J Nephrol. 2004 24(1):20-31.
Schreyer SA, Lystig TC, Vick CM, LeBoeuf RC. Mice deficient in apolipoprotein E but not LDL receptors are resistant to accelerated atherosclerosis associated with obesity. Atherosclerosis. 2003 171(1):49-55.
Vidal J, Verchere CB, Andrikopoulos S, Wang F, Hull RL, Cnop M, Olin KL, LeBoeuf RC, O’Brien KD, Chait A, Kahn SE. The effect of apolipoprotein E deficiency on islet amyloid deposition in human islet amyloid polypeptide transgenic mice. Diabetologia. 2003 46(1):71-9. Epub
Shie FS, LeBoeuf RC, Jin LW. Early intraneuronal Abeta deposition in the hippocampus of APP transgenic mice. Neuroreport. 2003 Jan 20;14(1):123-9. Erratum in: Neuroreport. 2004 15(12):1993. LeBoeur, Renée C [corrected to LeBoeuf, Renée C].
Wen M, Segerer S, Dantas M, Brown PA, Hudkins KL, Goodpaster T, Kirk E, LeBoeuf RC, Alpers CE. Renal injury in apolipoprotein E-deficient mice. Lab Invest. 2002 82(8):999-1006.
Brown ML, Yui K, Smith JD, LeBoeuf RC, Weng W, Umeda PK, Li R, Song R, Gianturco SH, Bradley WA. The murine macrophage apoB-48 receptor gene (Apob-48r): homology to the human receptor. J Lipid Res. 2002 43(8):1181-91.
Shie FS, Jin LW, Cook DG, Leverenz JB, LeBoeuf RC. Diet-induced hypercholesterolemia enhances brain A beta accumulation in transgenic mice. Neuroreport. 2002 13(4):455-9.
Kunjathoor VV, Chiu DS, O’Brien KD, LeBoeuf RC. Accumulation of biglycan and perlecan, but not versican, in lesions of murine models of atherosclerosis. Arterioscler Thromb Vasc Biol. 2002 22(3):462-8.
Schreyer SA, Vick CM, LeBoeuf RC. Loss of lymphotoxin-alpha but not tumor necrosis factor-alpha reduces atherosclerosis in mice. J Biol Chem. 2002 277(14):12364-8.
Schreyer SA, Vick C, Lystig TC, Mystkowski P, LeBoeuf RC. LDL receptor but not apolipoprotein E deficiency increases diet-induced obesity and diabetes in mice. Am J Physiol Endocrinol Metab. 2002 282(1):E207-14.
Schreyer SA, Cummings DE, McKnight GS, LeBoeuf RC. Mutation of the RIIbeta subunit of protein kinase A prevents diet-induced insulin resistance and dyslipidemia in mice.
Diabetes. 2001 50(11):2555-62.
Kirk EA, Heinecke JW, LeBoeuf RC. Iron overload diminishes atherosclerosis in apoE-deficient mice. J Clin Invest. 2001 107(12):1545-53.
Deeg MA, Bowen RF, Williams MD, Olson LK, Kirk EA, LeBoeuf RC. Increased expression of GPI-specific phospholipase D in mouse models of type 1 diabetes. Am J Physiol Endocrinol Metab. 2001 281(1):E147-54.
Mystkowski P, Shankland E, Schreyer SA, LeBoeuf RC, Schwartz RS, Cummings DE, Kushmerick M, Schwartz MW. Validation of whole-body magnetic resonance spectroscopy as a tool to assess murine body composition. Int J Obes Relat Metab Disord. 2000 24(6):719-24.
Kirk EA, Dinauer MC, Rosen H, Chait A, Heinecke JW, LeBoeuf RC. Impaired superoxide production due to a deficiency in phagocyte NADPH oxidase fails to inhibit atherosclerosis in mice. Arterioscler Thromb Vasc Biol. 2000 20(6):1529-35.
Clee SM, Bissada N, Miao F, Miao L, Marais AD, Henderson HE, Steures P, McManus J, McManus B, LeBoeuf RC, Kastelein JJ, Hayden MR. Plasma and vessel wall lipoprotein lipase have different roles in atherosclerosis. J Lipid Res. 2000 41(4):521-31.
Harte RA, Kirk EA, Rosenfeld ME, LeBoeuf RC. Initiation of hyperinsulinemia and hyperleptinemia is diet dependent in C57BL/6 mice. Horm Metab Res. 1999 31(10):570-5.
Eldar-Finkelman H, Schreyer SA, Shinohara MM, LeBoeuf RC, Krebs EG. Increased glycogen synthase kinase-3 activity in diabetes- and obesity-prone C57BL/6J mice. Diabetes. 1999 48(8):1662-6.
Knopp EA, Arndt TL, Eng KL, Caldwell M, LeBoeuf RC, Deeb SS, O’Brien KD. Murine phospholipid hydroperoxide glutathione peroxidase: cDNA sequence, tissue expression, and mapping. Mamm Genome. 1999 10(6):601-5.
Crawford RS, Kirk EA, Rosenfeld ME, LeBoeuf RC, Chait A. Dietary antioxidants inhibit development of fatty streak lesions in the LDL receptor-deficient mouse. Arterioscler Thromb Vasc Biol. 1998 18(9):1506-13.
LeBoeuf RC, Caldwell M, Guo Y, Metz C, Davitz MA, Olson LK, Deeg MA. Mouse glycosylphosphatidylinositol-specific phospholipase D (Gpld1) characterization. Mamm Genome. 1998 9(9):710-4.
Schreyer SA, Chua SC Jr, LeBoeuf RC. Obesity and diabetes in TNF-alpha receptor- deficient mice. J Clin Invest. 1998 102(2):402-11.
Kirk EA, Sutherland P, Wang SA, Chait A, LeBoeuf RC. Dietary isoflavones reduce plasma cholesterol and atherosclerosis in C57BL/6 mice but not LDL receptor-deficient mice. J Nutr. 1998 128(6):954-9.
Schreyer SA, Wilson DL, LeBoeuf RC. C57BL/6 mice fed high fat diets as models for diabetes-accelerated atherosclerosis. Atherosclerosis. 1998 136(1):17-24.
Chiu DS, Oram JF, LeBoeuf RC, Alpers CE, O’Brien KD. High-density lipoprotein-binding protein (HBP)/vigilin is expressed in human atherosclerotic lesions and colocalizes with apolipoprotein E. Arterioscler Thromb Vasc Biol. 1997 17(11):2350-8.
Clee SM, Zhang H, Bissada N, Miao L, Ehrenborg E, Benlian P, Shen GX, Angel A, LeBoeuf RC, Hayden MR. Relationship between lipoprotein lipase and high density lipoprotein cholesterol in mice: modulation by cholesteryl ester transfer protein and dietary status. J Lipid Res. 1997 38(10):2079-89.
Schreyer SA, Peschon JJ, LeBoeuf RC. Accelerated atherosclerosis in mice lacking tumor necrosis factor receptor p55. J Biol Chem. 1996 271(42):26174-8.
Fukuchi K, Ho L, Younkin SG, Kunkel DD, Ogburn CE, LeBoeuf RC, Furlong CE, Deeb SS, Nochlin D, Wegiel J, Wisniewski HM, Martin GM. High levels of circulating beta-amyloid peptide do not cause cerebral beta-amyloidosis in transgenic mice. Am J Pathol. 1996 149(1):219-27.
LeBoeuf RC, Caldwell M, Tu A, Albers JJ. Phospholipid transfer protein maps to distal mouse chromosome 2. Genomics. 1996 34(2):259-60.
Ohman T, Dang N, LeBoeuf RC, Furlong CE, Fukuchi K. Expression of apolipoprotein E inhibits aggregation of the C-terminal fragments of beta-amyloid precursor protein. Neurosci Lett. 1996 210(1):65-8.
Kunjathoor VV, Wilson DL, LeBoeuf RC. Increased atherosclerosis in streptozotocin-induced diabetic mice. J Clin Invest. 1996 97(7):1767-73.
Leboeuf RC, Tolson D, Heinecke JW. Dissociation between tissue iron concentrations and transferrin saturation among inbred mouse strains. J Lab Clin Med. 1995 126(2):128-36.
Kirk EA, Moe GL, Caldwell MT, Lernmark JA, Wilson DL, LeBoeuf RC. Hyper- and hypo-responsiveness to dietary fat and cholesterol among inbred mice: searching for level and variability genes. J Lipid Res. 1995 36(7):1522-32.
LeBoeuf RC, Xia YR, Oram JF, Lusis AJ. Mapping of the gene for high-density lipoprotein binding protein (Hdlbp) to proximal mouse chromosome 1. Genomics. 1994 23(1):296-8.
Liu MS, Jirik FR, LeBoeuf RC, Henderson H, Castellani LW, Lusis AJ, Ma Y, Forsythe IJ, Zhang H, Kirk E, et al. Alteration of lipid profiles in plasma of transgenic mice expressing human lipoprotein lipase. J Biol Chem. 1994 269(15):11417-24.
LeBoeuf RC, Caldwell M, Kirk E. Regulation by nutritional status of lipids and apolipoproteins A-I, A-II, and A-IV in inbred mice. J Lipid Res. 1994 35(1):121-33.
LeBoeuf RC, Veldee MS. Genetically determined body weight loss in mice fed diets containing salmon oil. J Nutr. 1993 123(3):547-58.
Kasim SE, LeBoeuf RC, Khilnani S, Tallapaka L, Dayananda D, Jen KL. Mechanisms of triglyceride-lowering effect of an HMG-CoA reductase inhibitor in a hypertriglyceridemic animal model, the Zucker obese rat. J Lipid Res. 1992 33(1):1-7.
Querfeld U, LeBoeuf RC, Salusky IB, Nelson P, Laidlaw S, Fine RN. Lipoproteins in children treated with continuous peritoneal dialysis. Pediatr Res. 1991 29(2):155-9.
Doolittle MH, LeBoeuf RC, Warden CH, Bee LM, Lusis AJ. A polymorphism affecting apolipoprotein A-II translational efficiency determines high density lipoprotein size and composition. J Biol Chem. 1990 265(27):16380-8.
LeBoeuf RC, Doolittle MH, Montcalm A, Martin DC, Reue K, Lusis AJ. Phenotypic characterization of the Ath-1 gene controlling high density lipoprotein levels and susceptibility to atherosclerosis. J Lipid Res. 1990 31(1):91-101.
Paigen B, Nesbitt MN, Mitchell D, Albee D, LeBoeuf RC. Ath-2, a second gene determining atherosclerosis susceptibility and high density lipoprotein levels in mice. Genetics. 1989 122(1):163-8.
Kirchgessner TG, LeBoeuf RC, Langner CA, Zollman S, Chang CH, Taylor BA, Schotz MC, Gordon JI, Lusis AJ. Genetic and developmental regulation of the lipoprotein lipase gene: loci both distal and proximal to the lipoprotein lipase structural gene control enzyme expression. J Biol Chem. 1989 264(3):1473-82.
Seldin MF, Morse HC 3rd, Reeves JP, Scribner CL, LeBoeuf RC, Steinberg AD. Genetic analysis of autoimmune gld mice. I. Identification of a restriction fragment length polymorphism closely linked to the gld mutation within a conserved linkage group.
J Exp Med. 1988 167(2):688-93.
Seldin MF, Morse HC, LeBoeuf RC, Steinberg AD. Establishment of a molecular genetic map of distal mouse chromosome 1: further definition of a conserved linkage group syntenic with human chromosome 1q. Genomics. 1988 2(1):48-56.
Lusis AJ, Taylor BA, Quon D, Zollman S, LeBoeuf RC. Genetic factors controlling structure and expression of apolipoproteins B and E in mice. J Biol Chem. 1987 262(16):7594-604.
Paigen B, Mitchell D, Reue K, Morrow A, Lusis AJ, LeBoeuf RC. Ath-1, a gene determining atherosclerosis susceptibility and high density lipoprotein levels in mice. Proc Natl Acad Sci USA. 1987 84(11):3763-7.
Miller CG, Lee TD, LeBoeuf RC, Shively JE. Primary structure of apolipoprotein A-II from inbred mouse strain BALB/c. J Lipid Res. 1987 28(3):311-9.
Williams SC, Bruckheimer SM, Lusis AJ, LeBoeuf RC, Kinniburgh AJ. Mouse apolipoprotein A-IV gene: nucleotide sequence and induction by a high-lipid diet. Mol Cell Biol. 1986 6(11):3807-14.
Kasim SE, LeBoeuf RC, Rockett MJ, Page J, Keyser AJ. The effects of oral agent or insulin treatments on the plasma lipoproteins and the plasma lipoprotein lipase activator in diabetic patients. Horm Metab Res. 1986 18(3):190-3.
Lusis AJ, LeBoeuf RC. Genetic control of plasma lipid transport: mouse model.
Methods Enzymol. 1986;128:877-94.
Lusis AJ, West R, Mehrabian M, Reuben MA, LeBoeuf RC, Kaptein JS, Johnson DF, Schumaker VN, Yuhasz MP, Schotz MC, et al. Cloning and expression of apolipoprotein B, the major protein of low and very low density lipoproteins. Proc Natl Acad Sci U S A.1985 82(14):4597-601.
LeBoeuf RC, Miller C, Shively JE, Schumaker VN, Balla MA, Lusis AJ. Human apolipoprotein B: partial amino acid sequence. FEBS Lett. 1984 170(1):105-8.
Ben-Zeev O, Lusis AJ, LeBoeuf RC, Nikazy J, Schotz MC. Evidence for independent genetic regulation of heart and adipose lipoprotein lipase activity. J Biol Chem. 1983 258(22):13632-6.
LeBoeuf RC, Puppione DL, Schumaker VN, Lusis AJ. Genetic control of lipid transport in mice. I. Structural properties and polymorphisms of plasma lipoproteins. J Biol Chem. 1983 258(8):5063-70.
Lusis AJ, Taylor BA, Wangenstein RW, LeBoeuf RC. Genetic control of lipid transport in mice. II. Genes controlling structure of high density lipoproteins. J Biol Chem. 1983 258(8):5071-8.
Leboeuf R, Havens M, Tabron D, Paigen B. Arylhydrocarbon hydroxylase
Biochim Biophys Acta. 1981 658(2):348-55.
Vaught JB, Gurtoo HL, Parker NB, LeBoeuf R, Doctor G. Effect of smoking on benzo(a)pyrene metabolism by human placental microsomes. Cancer Res. 1979 39(8):3177-83.
Within the Diabetes and Obesity Center of Excellence and its Affiliated Members
John (Jack) Oram, PhD
Jay Heinecke, MD
Michael Schwartz, MD
Karin Bornfeldt, PhD
Alan Chait, MD
Phuong-Oanh Mai, MS