메뉴 건너뛰기




Volumn 8, Issue 4, 1997, Pages 219-224

High density lipoprotein and coronary heart disease: Insights from mutations leading to low high density lipoprotein

Author keywords

[No Author keywords available]

Indexed keywords

APOLIPOPROTEIN A1; HIGH DENSITY LIPOPROTEIN; HIGH DENSITY LIPOPROTEIN CHOLESTEROL; LIPOPROTEIN LIPASE; PHOSPHATIDYLCHOLINE STEROL ACYLTRANSFERASE;

EID: 0030878533     PISSN: 09579672     EISSN: None     Source Type: Journal    
DOI: 10.1097/00041433-199708000-00005     Document Type: Review
Times cited : (55)

References (46)
  • 1
    • 0031029838 scopus 로고    scopus 로고
    • Isolated low HDL cholesterol as a risk factor for coronary heart disease mortality. A 21-year follow-up of 8000 men
    • Goldbourt U, Yaari S, Medalie JH: Isolated low HDL cholesterol as a risk factor for coronary heart disease mortality. A 21-year follow-up of 8000 men. Arterioscler Thromb Vasc Biol 1997, 17:107 113.
    • (1997) Arterioscler Thromb Vasc Biol , vol.17 , pp. 107-113
    • Goldbourt, U.1    Yaari, S.2    Medalie, J.H.3
  • 2
    • 0029893460 scopus 로고    scopus 로고
    • Angiographically silent atherosclerosis detected by intravascular ultrasound in patients with familial hypercholesterolemia and familial combined hyperlipidemia: Correlation with high density lipoproteins
    • Hausmann D, Johnson JA, Sudhir K, Mullen WL, Friedrich G, Fitzgerald PJ, Chou TM, Ports TA, Kane JP, Malloy MJ, Yock PG: Angiographically silent atherosclerosis detected by intravascular ultrasound in patients with familial hypercholesterolemia and familial combined hyperlipidemia: correlation with high density lipoproteins. J Am Coll Cardiol 1996, 27:1562 1570. The extent of atherosclerosis in coronary and iliac arteries was investigated in 48 asymptomatic hyperlipidemic patients, using intravascular ultrasound imaging. The authors concluded that intravascular ultrasound detects plaque more frequently than angiography; by stepwise multiple regression analysis, the strongest predictors for plaque extent and severity were plasma HDL-cholesterol and total/HDL-cholesterol ratio.
    • (1996) J Am Coll Cardiol , vol.27 , pp. 1562-1570
    • Hausmann, D.1    Johnson, J.A.2    Sudhir, K.3    Mullen, W.L.4    Friedrich, G.5    Fitzgerald, P.J.6    Chou, T.M.7    Ports, T.A.8    Kane, J.P.9    Malloy, M.J.10    Yock, P.G.11
  • 3
    • 0030045883 scopus 로고    scopus 로고
    • High density lipoproteins and coronary heart disease
    • Barter PJ, Rye KA: High density lipoproteins and coronary heart disease. Atherosclerosis 1996, 121:1 12.
    • (1996) Atherosclerosis , vol.121 , pp. 1-12
    • Barter, P.J.1    Rye, K.A.2
  • 4
    • 0028280609 scopus 로고
    • The properties of HDL in genetically engineered mice
    • Schultz JR, Rudin EM: The properties of HDL in genetically engineered mice. Curr Opin Lipidol 1994, 5:126 137.
    • (1994) Curr Opin Lipidol , vol.5 , pp. 126-137
    • Schultz, J.R.1    Rudin, E.M.2
  • 6
    • 9544221670 scopus 로고    scopus 로고
    • Inhibition of atherosclerosis development in cholesterol-fed human apolipoprotein A-I-transgenic rabbits
    • Duverger N, Kruth H, Emmanuel F, Caillaud JM, Viglietta C, Castro GR, Tailleux A, Fievet C, Fruchart JC, Houdebine LM et al.: Inhibition of atherosclerosis development in cholesterol-fed human apolipoprotein A-I-transgenic rabbits. Circulation 1996, 94:713 717. In this study the authors demonstrate that the overexpression of human apoA-I in rabbits enhances plasma HDL levels and protects the aorta from diet-induced atherosclerosis.
    • (1996) Circulation , vol.94 , pp. 713-717
    • Duverger, N.1    Kruth, H.2    Emmanuel, F.3    Caillaud, J.M.4    Viglietta, C.5    Castro, G.R.6    Tailleux, A.7    Fievet, C.8    Fruchart, J.C.9    Houdebine, L.M.10
  • 7
    • 0029832009 scopus 로고    scopus 로고
    • Apolipoprotein A-I and B levels and the risk of ischemic heart disease during a five-year follow-up of men in the Quebec cardiovascular study
    • Lamarche B, Moorjani S, Lupien PJ, Cantin B, Bernard PM, Dagenais GR, Despres JP: Apolipoprotein A-I and B levels and the risk of ischemic heart disease during a five-year follow-up of men in the Quebec cardiovascular study. Circulation 1996, 94:273-278.
    • (1996) Circulation , vol.94 , pp. 273-278
    • Lamarche, B.1    Moorjani, S.2    Lupien, P.J.3    Cantin, B.4    Bernard, P.M.5    Dagenais, G.R.6    Despres, J.P.7
  • 8
    • 0029948968 scopus 로고    scopus 로고
    • Increased coronary heart disease in Japanese-American men with mutation in the cholesteryl ester transfer protein gene despite increased HDL levels
    • Zhong S, Sharp DS, Grove JS, Bruce C, Yano K, Curb JD, Tall AR: Increased coronary heart disease in Japanese-American men with mutation in the cholesteryl ester transfer protein gene despite increased HDL levels. J Clin Invest 1996, 97:2917 2923. A large cross-sectional examination of the relationship between mutations in the cholesteryl ester transfer protein gene and CDH.
    • (1996) J Clin Invest , vol.97 , pp. 2917-2923
    • Zhong, S.1    Sharp, D.S.2    Grove, J.S.3    Bruce, C.4    Yano, K.5    Curb, J.D.6    Tall, A.R.7
  • 9
    • 0029937359 scopus 로고    scopus 로고
    • Cholesteryl ester transfer protein: Friend or foe?
    • Fielding CJ, Havel RJ: Cholesteryl ester transfer protein: friend or foe? J Clin Invest 1996, 97:2687 2688.
    • (1996) J Clin Invest , vol.97 , pp. 2687-2688
    • Fielding, C.J.1    Havel, R.J.2
  • 10
    • 0029657764 scopus 로고    scopus 로고
    • A novel A→G mutation in intron 1 of the hepatic lipase gene leads to alternative splicing resulting in enzyme deficiency
    • Brand K, Dugi KA, Brunzell JD, Nevin DN, Santamarina-Fojo S: A novel A→G mutation in intron 1 of the hepatic lipase gene leads to alternative splicing resulting in enzyme deficiency. J Lipid Res 1996, 37:1213 1223.
    • (1996) J Lipid Res , vol.37 , pp. 1213-1223
    • Brand, K.1    Dugi, K.A.2    Brunzell, J.D.3    Nevin, D.N.4    Santamarina-Fojo, S.5
  • 11
    • 0029820675 scopus 로고    scopus 로고
    • Apolipoprotein function in health and disease. Insights from natural mutations
    • Franceschini G: Apolipoprotein function in health and disease. Insights from natural mutations. Eur J Clin Invest 1996, 26:733 746. A recent review examining the effect of natural apolipoprotein mutants on lipoprotein metabolism and cardiovascular risk.
    • (1996) Eur J Clin Invest , vol.26 , pp. 733-746
    • Franceschini, G.1
  • 12
    • 0030482546 scopus 로고    scopus 로고
    • A cysteine-containing truncated apoA-I variant associated with HDL deficiency
    • Moriyama K, Sasaki J, Takada Y, Matsunaga A, Fukui J, Albers JJ, Arakawa K: A cysteine-containing truncated apoA-I variant associated with HDL deficiency. Arterioscler Thromb Vasc Biol 1996, 16:1416 1423. The authors describe a novel mutation in the apoA-I gene identified in a Japanese woman with HDL deficiency, xanthomas, corneal opacities and partial LCAT and cholesteryl ester transfer protein deficiency, but no evidence of CHD.
    • (1996) Arterioscler Thromb Vasc Biol , vol.16 , pp. 1416-1423
    • Moriyama, K.1    Sasaki, J.2    Takada, Y.3    Matsunaga, A.4    Fukui, J.5    Albers, J.J.6    Arakawa, K.7
  • 13
    • 0029783094 scopus 로고    scopus 로고
    • Effects of deletion of the carboxyl-terminal domain of ApoA-I or of its substitution with helices of ApoA-II on in vitro and in vivo lipoprotein association
    • Holvoet P, Zhao Z, Deridder E, Dhoest A, Collen D: Effects of deletion of the carboxyl-terminal domain of ApoA-I or of its substitution with helices of ApoA-II on in vitro and in vivo lipoprotein association. J Biol Chem 1996, 271:19395 19401.
    • (1996) J Biol Chem , vol.271 , pp. 19395-19401
    • Holvoet, P.1    Zhao, Z.2    Deridder, E.3    Dhoest, A.4    Collen, D.5
  • 14
    • 10144236519 scopus 로고    scopus 로고
    • Compound heterozygosity for a structural apolipoprotein A-I variant, apoA-I(L141R)Pisa, and an apolipoprotein A-I null allele in patients with absence of HDL cholesterol, corneal opacifications, and coronary heart disease
    • Miccoli R, Bertolotto A, Navalesi R, Odoguardi L, Boni A, Wessling J, Funke H, Wiebusch H, Eckardstein A, Assmann G: Compound heterozygosity for a structural apolipoprotein A-I variant, apoA-I(L141R)Pisa, and an apolipoprotein A-I null allele in patients with absence of HDL cholesterol, corneal opacifications, and coronary heart disease. Circulation 1996, 94:1622 1628. The paper describes an Italian family with HDL deficiency caused by compound heterozygosity for a nucleotide deletion and a missense mutation in the apoA-I gene, and premature atherosclerosis.
    • (1996) Circulation , vol.94 , pp. 1622-1628
    • Miccoli, R.1    Bertolotto, A.2    Navalesi, R.3    Odoguardi, L.4    Boni, A.5    Wessling, J.6    Funke, H.7    Wiebusch, H.8    Eckardstein, A.9    Assmann, G.10
  • 18
    • 0029967616 scopus 로고    scopus 로고
    • Identification of two apolipoprotein variants, A-I Karatsu (Tyr 100→His) and A-I Kurume (His 162→GIn)
    • Moriyama K, Sasaki J, Matsunaga A, Takada Y, Kagimoto M, Arakawa K: Identification of two apolipoprotein variants, A-I Karatsu (Tyr 100→His) and A-I Kurume (His 162→GIn). Clin Genet 1996, 49:79-84.
    • (1996) Clin Genet , vol.49 , pp. 79-84
    • Moriyama, K.1    Sasaki, J.2    Matsunaga, A.3    Takada, Y.4    Kagimoto, M.5    Arakawa, K.6
  • 20
    • 0029948966 scopus 로고    scopus 로고
    • Hereditary hepatic and systemic amyloidosis caused by a new deletion/insertion mutation in the apolipoprotein AI gene
    • Booth DR, Tan SY, Booth SE, Tennent GA, Hutchinson WL, Hsuan JJ, Totty NF, Truong O, Soutar AK, Hawkins PN et al.: Hereditary hepatic and systemic amyloidosis caused by a new deletion/insertion mutation in the apolipoprotein AI gene. J Clin Invest 1996, 97:2714 2721. A novel amyloidogenic variant of apoA-I was identified in a Spanish family with autosomal-dominant nonneurophatic hereditary amyloidosis.
    • (1996) J Clin Invest , vol.97 , pp. 2714-2721
    • Booth, D.R.1    Tan, S.Y.2    Booth, S.E.3    Tennent, G.A.4    Hutchinson, W.L.5    Hsuan, J.J.6    Totty, N.F.7    Truong, O.8    Soutar, A.K.9    Hawkins, P.N.10
  • 21
    • 0029937074 scopus 로고    scopus 로고
    • Complete deficiency of plasma lecithin-cholesterol acyltransferase (LCAT) activity due to a novel homozygous mutation (Gly-30-Ser) in the LCAT gene
    • Owen JS, Wiebusch H, Cullen P, Watts GF, Lima VL, Funke H, Assmann G: Complete deficiency of plasma lecithin-cholesterol acyltransferase (LCAT) activity due to a novel homozygous mutation (Gly-30-Ser) in the LCAT gene. Hum Mutat 1996, 8:79-82.
    • (1996) Hum Mutat , vol.8 , pp. 79-82
    • Owen, J.S.1    Wiebusch, H.2    Cullen, P.3    Watts, G.F.4    Lima, V.L.5    Funke, H.6    Assmann, G.7
  • 22
    • 0030034348 scopus 로고    scopus 로고
    • A new molecular defect in the lecithin: Cholesterol acyltransferase (LCAT) gene associated with fish eye disease
    • Contacos C, Sullivan DR, Rye KA, Funke H, Assmann G: A new molecular defect in the lecithin: cholesterol acyltransferase (LCAT) gene associated with fish eye disease. J Lipid Res 1996, 37:35-44.
    • (1996) J Lipid Res , vol.37 , pp. 35-44
    • Contacos, C.1    Sullivan, D.R.2    Rye, K.A.3    Funke, H.4    Assmann, G.5
  • 23
    • 0030017367 scopus 로고    scopus 로고
    • An intronic mutation in a lariat branchpoint sequence is a direct cause of an inherited human disorder (fish-eye disease)
    • Kuivenhoven JA, Weibusch H, Pritchard PH, Funke H, Benne R, Assmann G, Kastelein JJ: An intronic mutation in a lariat branchpoint sequence is a direct cause of an inherited human disorder (fish-eye disease). J Clin Invest 1996, 98:358 364.
    • (1996) J Clin Invest , vol.98 , pp. 358-364
    • Kuivenhoven, J.A.1    Weibusch, H.2    Pritchard, P.H.3    Funke, H.4    Benne, R.5    Assmann, G.6    Kastelein, J.J.7
  • 24
    • 0030019949 scopus 로고    scopus 로고
    • Two novel molecular defects in the LCAT gene are associated with fish eye disease
    • Kuivenhoven JA, Stalenhoef AF, Hill JS, Demacker PN, Errami A, Kastelein JJ, Pritchard PH: Two novel molecular defects in the LCAT gene are associated with fish eye disease. Arterioscler Thromb Vasc Biol 1996, 16:294 303. An interesting study describing a new case of FED caused by compound heterozygosity for two different mutations in the LCAT gene, associated with premature coronary artery disease. A review of clinical data on previously published cases of partial LCAT deficiency raises questions on the risk of atherosclerosis in this syndrome.
    • (1996) Arterioscler Thromb Vasc Biol , vol.16 , pp. 294-303
    • Kuivenhoven, J.A.1    Stalenhoef, A.F.2    Hill, J.S.3    Demacker, P.N.4    Errami, A.5    Kastelein, J.J.6    Pritchard, P.H.7
  • 27
    • 0029845121 scopus 로고    scopus 로고
    • Potential gene therapy for lecithin-cholesterol acyltransferase (LCAT)-deficient and hypoalphalipoproteinemic patients with adenovirus-mediated transfer of human LCAT gene
    • Seguret-Mace S, Latta-Mahieu M, Castro G, Luc G, Fruchart JC, Rubin E, Denefle P, Duverger N: Potential gene therapy for lecithin-cholesterol acyltransferase (LCAT)-deficient and hypoalphalipoproteinemic patients with adenovirus-mediated transfer of human LCAT gene. Circulation 1996, 94:2177 2184. A gene therapy approach to prevent atherosclerosis in hypoalphalipoproteinemia.
    • (1996) Circulation , vol.94 , pp. 2177-2184
    • Seguret-Mace, S.1    Latta-Mahieu, M.2    Castro, G.3    Luc, G.4    Fruchart, J.C.5    Rubin, E.6    Denefle, P.7    Duverger, N.8
  • 28
    • 0030056398 scopus 로고    scopus 로고
    • Molecular pathobiology of the human lipoproteln lipase gene
    • Murthy V, Julien P, Gagne C: Molecular pathobiology of the human lipoproteln lipase gene. Pharmacol Ther 1996, 70:101 135.
    • (1996) Pharmacol Ther , vol.70 , pp. 101-135
    • Murthy, V.1    Julien, P.2    Gagne, C.3
  • 29
    • 0030006214 scopus 로고    scopus 로고
    • Homozygosity for two point mutations in the lipoprotein lipase (LPL) gene in a patient with familial LPL deficiency: LPL(Asp9→Asn, Tyr262→His)
    • Rouis M, Lohse P, Dugi KA, Beg OU, Ronan R, Talley GD, Brunzell JD, Santamarina-Fojo S: Homozygosity for two point mutations in the lipoprotein lipase (LPL) gene in a patient with familial LPL deficiency: LPL(Asp9→Asn, Tyr262→His). J Lipid Res 1996, 37:651 661.
    • (1996) J Lipid Res , vol.37 , pp. 651-661
    • Rouis, M.1    Lohse, P.2    Dugi, K.A.3    Beg, O.U.4    Ronan, R.5    Talley, G.D.6    Brunzell, J.D.7    Santamarina-Fojo, S.8
  • 30
    • 0029808302 scopus 로고    scopus 로고
    • Premature atherosclerosis in patients with familial chylomicronemia caused by mutations in the lipoprotein lipase gene
    • Benlian P, de Gennes JL, Foubert L, Zhang H, Gagne SE, Hayden MR: Premature atherosclerosis in patients with familial chylomicronemia caused by mutations in the lipoprotein lipase gene. N Engl J Med 1996, 335:848-854. The association of premature atherosclerosis with LPL deficiency is still controversial. This study describes four patients with chylomicronemia caused by mutations in the LPL gene who developed atherosclerosis before the age of 55 years.
    • (1996) N Engl J Med , vol.335 , pp. 848-854
    • Benlian, P.1    De Gennes, J.L.2    Foubert, L.3    Zhang, H.4    Gagne, S.E.5    Hayden, M.R.6
  • 31
    • 15844426908 scopus 로고    scopus 로고
    • Alterations in plasma lipoproteins and apolipoprotelns before the age of 40 in heterozygotes for lipoprotein lipase deficiency
    • Bijvoet S, Gagne SE, Moorjani S, Gagne C, Henderson HE, Fruchart JC, Dallongeville J, Alaupovic P, Prins M, Kastelein JJ, Hayden MR: Alterations in plasma lipoproteins and apolipoprotelns before the age of 40 in heterozygotes for lipoprotein lipase deficiency. J Lipid Res 1996, 37:640 650. The lipid/lipoprotein profile in a single large French-Canadian family with the P207L mutation in the LPL gene. The study shows significant disturbances in lipoprotein metabolism in heterozygote carriers, clearly supporting the key role of LPL in determining the lipid composition of lipoproteins. Alterations are sometimes evident before the age of 20 years and would predict an increased susceptibility to atherosclerosis.
    • (1996) J Lipid Res , vol.37 , pp. 640-650
    • Bijvoet, S.1    Gagne, S.E.2    Moorjani, S.3    Gagne, C.4    Henderson, H.E.5    Fruchart, J.C.6    Dallongeville, J.7    Alaupovic, P.8    Prins, M.9    Kastelein, J.J.10    Hayden, M.R.11
  • 33
    • 0030602890 scopus 로고    scopus 로고
    • Common sequence variants of lipoproteln lipase: Standardized studies of in vitro expression and catalytic function
    • Zhang H, Henderson H, Gagne SE, Clee SM, Miao L, Liu G, Hayden MR: Common sequence variants of lipoproteln lipase: standardized studies of in vitro expression and catalytic function. Biochim Biophys Acta 1996, 1302:159 166.
    • (1996) Biochim Biophys Acta , vol.1302 , pp. 159-166
    • Zhang, H.1    Henderson, H.2    Gagne, S.E.3    Clee, S.M.4    Miao, L.5    Liu, G.6    Hayden, M.R.7
  • 34
    • 0029815358 scopus 로고    scopus 로고
    • A frequently occurring mutation in the lipoprotein lipase gene (Asn291Ser) results in altered postprandial chylomicron triglyceride and retinyl palmitate response in normolipidemic carriers
    • Pimstone SN, Clee SM, Gagne SE, Miao L, Zhang H, Stein EA, Hayden MR: A frequently occurring mutation in the lipoprotein lipase gene (Asn291Ser) results in altered postprandial chylomicron triglyceride and retinyl palmitate response in normolipidemic carriers. J Lipid Res 1996, 37:1675 1684.
    • (1996) J Lipid Res , vol.37 , pp. 1675-1684
    • Pimstone, S.N.1    Clee, S.M.2    Gagne, S.E.3    Miao, L.4    Zhang, H.5    Stein, E.A.6    Hayden, M.R.7
  • 35
  • 37
    • 0030452127 scopus 로고    scopus 로고
    • Regulatory mutations in the human lipoprotein lipase gene in patients with familial combined hyperlipidemia and coronary artery disease
    • Yang WS, Nevin DN, Iwasaki L, Peng R, Brown BG, Brunzell JD, Deeb SS: Regulatory mutations in the human lipoprotein lipase gene in patients with familial combined hyperlipidemia and coronary artery disease. J Lipid Res 1996, 37:2627 2637
    • (1996) J Lipid Res , vol.37 , pp. 2627-2637
    • Yang, W.S.1    Nevin, D.N.2    Iwasaki, L.3    Peng, R.4    Brown, B.G.5    Brunzell, J.D.6    Deeb, S.S.7
  • 39
    • 0030587872 scopus 로고    scopus 로고
    • The Asp9 Asn mutation in the lipoprotein lipase gene is associated with increased progression of coronary atherosclerosis
    • Jukema JW, van Boven AJ, Groenemeijer B, Zwinderman AH, Reiber JH, Bruschke AV, Henneman JA, Molhoek GP, Bruin T, Jansen H, Gagne E et al.: The Asp9 Asn mutation in the lipoprotein lipase gene is associated with increased progression of coronary atherosclerosis. Circulation 1996, 94:1913 1918. Heterozygosity for a LPL mutation in patients enrolled in the REGRESS trial causes minor changes in plasma lipids but is associated with more progression of coronary atherosclerosis.
    • (1996) Circulation , vol.94 , pp. 1913-1918
    • Jukema, J.W.1    Van Boven, A.J.2    Groenemeijer, B.3    Zwinderman, A.H.4    Reiber, J.H.5    Bruschke, A.V.6    Henneman, J.A.7    Molhoek, G.P.8    Bruin, T.9    Jansen, H.10    Gagne, E.11
  • 43
    • 0029082507 scopus 로고
    • Defective removal of cellular cholesterol and phospholiplds by apolipoprotein A-I in Tangier Disease
    • Francis GA, Knopp RH, Oram JF: Defective removal of cellular cholesterol and phospholiplds by apolipoprotein A-I in Tangier Disease. J Clin Invest 1995, 96:78-87.
    • (1995) J Clin Invest , vol.96 , pp. 78-87
    • Francis, G.A.1    Knopp, R.H.2    Oram, J.F.3
  • 44
    • 0029007219 scopus 로고
    • HDL-mediated efflux of intracellular cholesterol is impaired in fibroblasts from Tangier disease patients
    • Rogler G, Trumbach B, Klima B, Lackner KJ, Schmitz G: HDL-mediated efflux of intracellular cholesterol is impaired in fibroblasts from Tangier disease patients. Arterioscler Thromb Vasc Biol 1995, 15:683 690.
    • (1995) Arterioscler Thromb Vasc Biol , vol.15 , pp. 683-690
    • Rogler, G.1    Trumbach, B.2    Klima, B.3    Lackner, K.J.4    Schmitz, G.5
  • 45
    • 0029088622 scopus 로고
    • Activation of phosphatidylinositol-specific phospholipase C in response to HDL3 and LDL is markedly reduced in cultured fibroblasts from Tangier patients
    • Drobnik W, Mollers C, Resink T, Schmitz G: Activation of phosphatidylinositol-specific phospholipase C in response to HDL3 and LDL is markedly reduced in cultured fibroblasts from Tangier patients. Arterioscler Thromb Vasc Biol 1995, 15:1369 1377.
    • (1995) Arterioscler Thromb Vasc Biol , vol.15 , pp. 1369-1377
    • Drobnik, W.1    Mollers, C.2    Resink, T.3    Schmitz, G.4
  • 46
    • 0029852937 scopus 로고    scopus 로고
    • Defective regulation of phosphatidylcholine-specific phospholipases C and D in a kindred with Tangier disease. Evidence for the involvement of phosphatidylcholine breakdown in HDL-mediated cholesterol efflux mechanisms
    • Walter M, Reinecke H, Gerdes U, Noter JR, Hobbel G, Seedorf U, Assmann G: Defective regulation of phosphatidylcholine-specific phospholipases C and D in a kindred with Tangier disease. Evidence for the involvement of phosphatidylcholine breakdown in HDL-mediated cholesterol efflux mechanisms. J Clin Invest 1996, 98: 2315 2323. An in-vitro study in fibroblasts investigating signaling pathways involved in HDL-mediated mobilization of intracellular cholesterol and phospholipids, which are defective in TD.
    • (1996) J Clin Invest , vol.98 , pp. 2315-2323
    • Walter, M.1    Reinecke, H.2    Gerdes, U.3    Noter, J.R.4    Hobbel, G.5    Seedorf, U.6    Assmann, G.7


* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.