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Apolipoprotein characterization

In this in vitro system, the presence of serum in cell culture medium is not necessary, but the type of transwell is important (the total amount of H-triglycerides secreted was two-fold higher when using 3 pm versus 1 pm pore size transwells), and oleic acid supplementation is required for the formation and secretion of CMs as well as the transport of 3-carotene through Caco-2 cells. Finally, the presence of Tween 40 does not affect CM synthesis and secretion in this in vitro cell culture system. Thus, CMs secreted by Caco-2 cells were characterized as particles rich in newly synthesized H-triglycerides (90% of total secreted) containing apolipoprotein B (30% of total secreted) and H-phospholipids (20% of total secreted) and with an average diameter of 60 nm. These characteristics are close to those of CMs secreted in vivo by enterocytes. ... [Pg.153]

Finally, clinical chemistry of Lp(a) and apolipoprotein (a) is characterized by a variety of problems, caused by the structural complexity and heterogeneity of Lp(a), the homology of apo(a) with plasminogen, and the lack of standardization of analytical methods. [Pg.74]

Rainwater DK, Kammerer CM, VandeBerg JL, Hixson JE. Characterization of the genetic elements controlling lipoprotein(a) concentrations in Mexican Americans. Evidence for at least three controlling elements linked to LPA, the locus encoding apolipoprotein(a). Atherosclerosis 1997 128 22333. [Pg.272]

B9. Brown, W. V., Levy, R. I., and Fredrickson, D. S., Further characterization of apolipoproteins from the human plasma very low-density lipoproteins. J. Biol. Chem. 245, 6588-6594 (1970). [Pg.145]

Familial dysbetalipoproteinemia (type III) is characterized by the accumulation of chylomicron and VLDL remnants, which are enriched in cholesterol compared to their precursors. The primary molecular cause of familial dysbetalipoproteinemia (type III) is the homozygous presence of the apolipoprotein E2 (apoE2) isoform, which is associated with recessive inheritance of the disorder [62]. However, only 1 in 50 homozygotes for apoE2 will develop type III hyperlipoproteinemia, which is clinically characterized by palmar and tuberous xanthomas, arcus lipoides, and premature atherosclerosis of coronary, peripheral, and cerebral arteries. Precipitating factors include diabetes mellitus, renal disease, hemochromatosis, but also familial hypercholesterolemia. In addition, some rare mutations in the apoE gene have been found to cause dominant and more penetrant forms of type III hyperlipoproteinemia. [Pg.506]

Tsurupa, G., Ho-Tin-Noe, B., Angles-Cano, E., and Medved, L. (2003). Identification and characterization of novel lysine-independent apolipoprotein(a)-binding sites in fibrin (ogen) alphaC-domains./. Biol. Chem. 278, 37154-37159. [Pg.297]

Zannis VI, Breslow JL, SanGiacomo TR, Aden DP, Knowles BB. Characterization of the major apolipoproteins secreted by two human hepatoma cell lines. Biochemistry. 1981, 20 7089-7096. [Pg.165]

Karathanasis SK, Zannis VI, Breslow JL. Isolation and characterization of the human apolipoprotein A-I gene. Proc Natl Acad Sci USA. 1983, 80 6147-6151. [Pg.166]

Perhaps the clearest demonstration of HDL heterogeneity was that by Suenram et al. (S61). When specific antisera to apolipoproteins A-I, A-II, B, C-III, D, E, and F were set up in double diffusion analyses against HDL, reactions of nonidentity were observed between each possible combination of these antisera. The only exception was a reaction of partial identity between antisera to apoA-I and apoA-II, indicating two types of apoA-contain-ing lipoproteins, a major class containing both proteins and a minor one containing only apoA-I. The other apolipoproteins in HDL therefore appear each to be largely peculiar to their own lipoprotein particles, and the nomenclature LpC, LpD, etc., has been used by Alaupovic and co-workers to describe lipoproteins characterized by a single apolipoprotein class (A5-A7). [Pg.264]

J4. Jackson, R. L., and Gotto, A. M., Jr., A study of the cystine-containing apolipoprotein of human plasma high density lipoproteins Characterization of cyanogen bromide and tryptic fragments. Biochim. Biophys. Acta 285, 36-47 (1972). [Pg.281]

K18. Kostner, G., Studies of the composition and structure of human serum lipoproteins Isolation and partial characterization of apolipoprotein A-UI. Biochim. Biophys. Acta 336, 383-395 (1974). [Pg.282]

L23. Lux, S. E., and John, K. M., Further characterization of the polymorphic forms of a human high density apolipoprotein, apoLp-Gln-I (apoA-I). Biochim. Biophys. Acta 278, 266-270 (1972). [Pg.284]

M6. Mahadevan, V., and Soloff, L. A., A method for isolating human plasma lecithimcho-lesterol acyltransferase without using anti-apolipoprotein D, and its characterization. Biochim. Biophys. Acta 752, 89-97 (1983). [Pg.285]

Olofsson, S.-O., McConathy, W. J., and Alaupovic, P., Isolation and partial characterization of a new acidic apolipoprotein (apolipoprotein F) from high density lipoprotein of human plasma. Biochemistry 17, 1032-1036 (1978). [Pg.288]

Shore, V. G., Shore, B., and Lewis, S. B., Isolation and characterization of two threonine-poor apolipoproteins of human plasma high density lipoproteins. Biochemistry 17, 2174-2179 (1978). [Pg.293]

Ul. Utermann, G., Isolation and partial characterization of an arginine-rich apolipoprotein from human plasma very-low-density lipoproteins Apolipoprotein E. Hoppe Seylers Z. Physiol. Chem. 356, 1113-1121 (1975). [Pg.295]

VI. Vaith, P., Assmann, G., and Uhlenbruck, G., Characterization of the oligosaccharide side chain of apolipoprotein C-III from human plasma very low density lipoprotein. Biochim. Biophys. Acta 541, 234-240 (1978). [Pg.296]

The clinical picture is characterized by xanthomas, particularly on the tendons (especially the Achilles tendon). Xanthomas consist of cholesterol and cholestanol. The enzyme defect also results in disturbed vitamin D metabolism. Osteoporosis is thus observed quite often, with a tendency towards spontaneous fractures. (208) Striking clinical features are cerebral functional disorders (from deviant behaviour to severe dementia, motor disturbances and convulsions) as well as peripheral neurological symptoms caused by cholestanol deposits. (211) High concentrations of apolipoprotein B and cholestanol are found in the CSF. (213) Treatment is based on the administration of chenodeoxycholic acid (750 mg/day). Effectiveness is improved if HMG-CoA reductase inhibitors (e. g. pravastatin) are used concomitantly. (207, 212)... [Pg.599]

Despite similar mean body weights (olanzapine 84 kg versus risperidone 81 kg), 32% of those who took olanzapine were characterized by the atherogenic metabolic triad (hyperinsulinemia and raised apolipoprotein B and small-density LDL concentrations) compared with only 5% of those who took risperidone. [Pg.2464]


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See also in sourсe #XX -- [ Pg.255 , Pg.256 ]




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