Relevant bibliographies by topics / Apolipoprotein B-100

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  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Apolipoprotein B-100'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Apolipoprotein B-100"

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Welty, Francine K., Alice H. Lichtenstein, P. Hugh R. Barrett, Gregory G. Dolnikowski, Jose M. Ordovas, and Ernst J. Schaefer. "Decreased Production and Increased Catabolism of Apolipoprotein B-100 in Apolipoprotein B-67/B-100 Heterozygotes." Arteriosclerosis, Thrombosis, and Vascular Biology 17, no. 5 (May 1997): 881–88. http://dx.doi.org/10.1161/01.atv.17.5.881.

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Herbert, P. N., J. S. Hyams, D. N. Bernier, M. M. Berman, A. L. Saritelli, K. M. Lynch, A. V. Nichols, and T. M. Forte. "Apolipoprotein B-100 deficiency. Intestinal steatosis despite apolipoprotein B-48 synthesis." Journal of Clinical Investigation 76, no. 2 (August 1, 1985): 403–12. http://dx.doi.org/10.1172/jci111986.

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Edge, Stephen B., Jeffrey M. Hoeg, Philip D. Schneider, and H. Bryan Brewer. "Apolipoprotein B synthesis in humans: Liver synthesizes only apolipoprotein B-100." Metabolism 34, no. 8 (August 1985): 726–30. http://dx.doi.org/10.1016/0026-0495(85)90022-8.

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Huet, G., M. C. Dieu, A. Martin, G. Grard, J. M. Bard, P. Fossati, and P. Degand. "Heterozygous hypobetalipoproteinemia with fasting chylomicronemia." Clinical Chemistry 37, no. 2 (February 1, 1991): 296–300. http://dx.doi.org/10.1093/clinchem/37.2.0296.

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Abstract We describe a disorder in which low-density lipoprotein (LDL)-cholesterol and apolipoprotein B are in low concentration (0.47 mmol/L and 0.28 g/L, respectively) and chylomicrons are still present in plasma after an 18-h fast. The d less than 1.006 fraction was isolated by flotation ultracentrifugation and the apolipoproteins were analyzed by electrophoresis, immunoblotting with anti-apolipoprotein B-100 antiserum, and isoelectric focusing. In the d less than 1.006 fraction of the fasting serum, we found an apolipoprotein B form with the same apparent molecular mass as apolipoprotein B-48 and similar in amount to apolipoprotein B-100 (respective percentages, 46% and 54%). The monosialylated form of the apolipoprotein C-III was severely decreased. After an oral fat load, the repartition of the two species of apolipoprotein B did not change greatly (respective percentages, 60% and 40%), and the concentration of serum triglyceride increased only from 1.20 to 1.65 mmol/L.
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Chulkova, T. M., and V. V. Tertov. "Degradation of human apolipoprotein B-100 by apolipoprotein(a)." FEBS Letters 336, no. 2 (December 27, 1993): 327–29. http://dx.doi.org/10.1016/0014-5793(93)80830-n.

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Schaefer, Juergen R., Hubert Scharnagl, Manfred W. Baumstark, Horst Schweer, Loren A. Zech, Hansjörg Seyberth, Karl Winkler, Armin Steinmetz, and Winfried März. "Homozygous Familial Defective Apolipoprotein B-100." Arteriosclerosis, Thrombosis, and Vascular Biology 17, no. 2 (February 1997): 348–53. http://dx.doi.org/10.1161/01.atv.17.2.348.

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Decroli, Eva. "KADAR APOLIPOPROTEIN B 100 SERUM PADA PENDERITA NEFROPATI DIABETIKUM." Majalah Kedokteran Andalas 38, no. 2 (December 8, 2015): 99. http://dx.doi.org/10.22338/mka.v38.i2.p99-107.2015.

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AbstrakPenelitian ini bertujuan untuk mengetahui kadar Apolipoprotein B 100 serum pada penderita nefropati diabetikum. Metode penelitian ini dengan desain cross sectional yang bersifat deskriptif analitik. Populasi adalah semua pasien yang menderita diabetes mellitus tipe 2 yang dirawat di bagian penyakit dalam atau kontrol ke poliklinik khusus metabolik endokrin RSU Dr. M. Djamil Padang. Sampel penelitian adalah pasien diabetes mellitus tipe 2 dengan proteinuria positif yang memenuhi kriteria inklusi dan ekslusi yang diambil secara konsekutif. Sampel penelitian diambil dari darah vena dalam keadaaan puasa selama 12 jam. Pemeriksaan apolipoprotein B 100 serum dilakukan di laboratorium klinik swasta, dengan menggunakan metode imunoturbidimetri. Albumin creatinin ratio merupakan perbandingan kadar albumin urin terhadap kreatinin urin dengan metode pemeriksaan imunoturbidimetri. Pada penelitian ini didapatkan rerata kadar Apolipoprotein B 100 serum yaitu 86,10 mg/dl (nilai normal 66-101 mg/dl) dengan standar deviasi 27,997. Simpulan: Tidak terdapat peningkatan kadar apolipoprotein B 100 serum pada penderita nefropati diabetikum.AbstractThis study aims to examine Apolipoprotein B 100 serum level in diabetic nephropathy patient. Study design was cross sectional with analytic descriptive. Population is all type 2 diabetes mellitus inpatient and outpatient in internal medicine M Djamil hospital. Sample is all type 2 diabetes mellitus consecutive patient with positive proteinuria and fullfilled inclusion and exclusion criteria. Vein blood was taken after 12 hours-fasting. Apolipoprotein B 100 serum check at non-governmental laboratory by immunoturbidimetry methode. Albumin creatinin ratio check by immunoturbidimetry methode. Result: Apolipoprotein B 100 serum level is 86.10 mg/dl (normal value 66-101 mg/dl) with standar deviation 27.997. Conclusion: There is no significant enhancement of apolipoprotein B 100 serum level in diabetic nephropathy patient.
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Innerarity, TL, RW Mahley, KH Weisgraber, TP Bersot, RM Krauss, GL Vega, SM Grundy, W. Friedl, J. Davignon, and BJ McCarthy. "Familial defective apolipoprotein B-100: a mutation of apolipoprotein B that causes hypercholesterolemia." Journal of Lipid Research 31, no. 8 (August 1990): 1337–49. http://dx.doi.org/10.1016/s0022-2275(20)42605-7.

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Soria, L. F., E. H. Ludwig, H. R. Clarke, G. L. Vega, S. M. Grundy, and B. J. McCarthy. "Association between a specific apolipoprotein B mutation and familial defective apolipoprotein B-100." Proceedings of the National Academy of Sciences 86, no. 2 (January 1, 1989): 587–91. http://dx.doi.org/10.1073/pnas.86.2.587.

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Chen, G. C., S. Zhu, D. A. Hardman, J. W. Schilling, K. Lau, and J. P. Kane. "Structural Domains of Human Apolipoprotein B-100." Journal of Biological Chemistry 264, no. 24 (August 1989): 14369–75. http://dx.doi.org/10.1016/s0021-9258(18)71687-6.

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Dissertations / Theses on the topic "Apolipoprotein B-100"

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Mahala, Bonginkosi. "Familial Defective binding apolipoprotein B-100 the Cape Town Experience." Master's thesis, University of Cape Town, 2009. http://hdl.handle.net/11427/3421.

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Wang, Xingyu. "An immunochemical analysis of human apolipoprotein B-100 structure-function relationships." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ32458.pdf.

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Rubinsztein, David Chaim. "Monogenic hypercholesterolemia in South Africans : familial hypercholesterolemia in Indians and familial defective apolipoprotein B-100." Doctoral thesis, University of Cape Town, 1993. http://hdl.handle.net/11427/27142.

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LDL-receptor mutations and familial defective apolipoprotein B-100 (codon 3500) (FOB), the known causes of monogenic hypercholesterolemia (MH), have similar clinical features. The nature of the mutations responsible for MH in South Africans of Indian origin was previously unknown. Similarly, the mutations in the LDL-receptor gene of a South African Black FH homozygote had also not been characterised. The aim of this thesis was to identify and analyse the LDL-receptor mutations in the Indian homozygotes NS, D, AV and AA and in the Black homozygote JL. In addition, the possible importance of FOB as a cause of MH in South Africans was also assessed. The patient NS was characterized as having two "Null" LDL-receptor alleles. His skin fibroblasts expressed no detectable LDL-receptor protein and very low levels of LDL-receptor mRNA of approximately normal size. Since NS' s LDLreceptor promoter sequence was normal, his alleles are likely to harbour exonic point mutations or minor rearrangements that cause premature stop codons. The patient D was found to be a heteroallelic homozygote. Two new point mutations in the LDL receptor, Asp₆₉ -Tyr and Glu₁₁₉-Lys, were identified. D's fibroblasts expressed about 30% of the normal surf ace complement of receptors that bound LDL poorly. This low number could at least be partially explained by their decreased stability. These mutations were not identified in any other Indian FH or hypercholesterolemic patients. Patients AV and AA were both shown to be homoallelic homozygotes for the Pro₆₆₄ -Leu mutation. This mutation was identified in 4 unrelated Muslim families of Gujerati origin suggesting that the mutation arose from this area in India. Contrary to previous reports (Knight et al. 1990, Soutar et al. 1989), neither LOL nor β-VLDL binding were shown to be affected by this mutation. These mutant receptors were rapidly degraded. Thus the disease FH in these subjects is presumably due to the low steady-state level of mature receptors that are functionally normal but exhibit accelerated turnover. The Pedi FH homozygote, JL, expressed very few LOL receptors due to decreased receptor synthesis associated with low mRNA levels and not due to enhanced degradation. One of JL's LOL receptor alleles has a 3 b.p. deletion in repeat 1 of the promoter (G. Zuilani, H. Hobbs and L.F. de Waal, personal communication). The nature of the defect in his other allele is unknown. The importance of FOB as a cause of monogenic hypercholesterolemia in the South African Indian, "Coloured" and Afrikaner populations was determined by screening hypercholesterolemic subjects with or without xanthomata. The absence of FOB in such patients, in whom the relevant common or founder South African mutations were excluded, suggested that this disorder was rarer in these groups than in North America and Europe. FOB was identified in two different families of mixed British and Afrikaner ancestry. One family contained individuals who were heterozygous for the FOB mutation, as well as the FH Afrikaner-1 and the FH Afrikaner-2 LOL-receptor mutations. In addition, 4 compound heterozygotes, who had both FOB and the FH Afrikaner-1 mutation and one individual whu inherited all 3 defects, were identified. This family allowed us to characterise the compound heterozygotes with one mutant LOLreceptor allele and FOB as having a condition that was probably intermediate in severity between the FH heterozygote and homozygote states.
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Alberty, Deborah J. "A study of time and temperature variables affecting apolipoprotein B-100 on iodipamide ethyl ester particles /." Online version of thesis, 1993. http://hdl.handle.net/1850/11252.

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Bamji-Mirza, Michelle. "Defining an Intracellular Role of Hepatic Lipase in the Formation of Very Low Density Lipoproteins and High Density Lipoproteins." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20134.

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Hepatic lipase (HL) plays a pivotal role in the catabolism of apolipoprotein (apo)B-containing lipoproteins and high density lipoprotein (HDL) particles through its reported catalytic and non-catalytic extracellular functions. The current study tested the hypothesis that HL expression might impair formation and secretion of hepatic derived very low density lipoproteins (VLDL) and apoA-I (nascent HDL). Stable or transient expression of human HL (hHL) in McA-RH7777 cells resulted in decreased incorporation of [3H]glycerol into cell-associated and secreted (VLDL-associated) 3H-triacylglcyerol (TAG) relative to control cells. Stable expression of catalytically-inactive hHL (hHLSG) also resulted in decreased secretion of VLDL-associated 3H-TAG whereas cell-associated 3H-TAG levels were unchanged. Expression of hHL or hHLSG increased cell-associated 35S-apoB100 with relatively no change in secreted 35S-apoB100. Importantly, hHL or hHLSG expression resulted in reduced 3H-TAG associated with the microsomal lumen lipid droplets (LLD), and increased relative expression of ApoB and genes involved in lipogenesis and fatty acyl oxidation. Transient expression of hHL in HL-null primary hepatocytes, mediated by adenoviral gene transfer, resulted in decreased steady-state levels of cell-associated and secreted apoA-I and reduced rates of synthesis and secretion of 35S-apoA-I. HL-null hepatocytes exhibited increased levels of secreted 35S-apoA-I relative to wildtype hepatocytes while cell-associated 35S-apoA-I levels were normal. Transient expression of a hHL chimera (hHLmt), in which the C-terminus of hHL was replaced with mouse HL sequences, exerted an inhibitory effect on apoA-I production similar to that of hHL even though hHLmt was secreted less effectively than hHL with impaired exit from the endoplasmic reticulum (ER) as compared with hHL. In contrast, stable expression of hHL in McA-RH7777 cells resulted in a dose-dependent increase in cell-associated and secreted 35S-apoA-I levels. These studies demonstrate that hHL has an intracellular (but non-catalytic) role in reducing the content of the LLD and ultimately the buoyancy of secreted VLDL particles, and that the N-terminal sequences of ER-residing hHL directly or indirectly modulates the production and secretion of apoA-I (nascent HDL) from hepatocytes.
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Vauhkonen, Matti. "Surface structure of human low density lipoproteins carbohydrate structure of apolipoprotein B-100 and properties of the surface lipid layer /." Helsinki : Finnish Society of Sciences and Letters, 1990. http://catalog.hathitrust.org/api/volumes/oclc/22137261.html.

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Brinkmann, Jan Ole [Verfasser]. "Vessel function of the atherosclerotic low-density-lipoprotein-receptor-deficient apolipoprotein-B-100-only mouse / Jan Ole Brinkmann." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2008. http://d-nb.info/102325784X/34.

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Delporte, Cédric. "Etude des modifications de l'apolipoprotéine B-100 induites par la myéloperoxydase à l'aide de la chromatographie liquide couplée à la spectrométrie de masse." Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209655.

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Les maladies cardiovasculaires constituent la première cause de décès dans le monde et l’athérosclérose est le premier facteur causal de ces maladies. Parmi les multiples facteurs de risque athéromateux, un facteur est souvent décrit :la modification des lipoprotéines de basse densité (LDLs). Bien que le phénomène d’athérogénèse ne soit pas encore complètement résolu, il est actuellement admis que les LDLs natives passent la paroi vasculaire et s’accumulent au niveau sous-endothélial où elles sont oxydées et endocytées par les macrophages. Une théorie plus récente indique que les LDLs peuvent être également modifiées dans la circulation.

Néanmoins, le processus par lequel ces lipoprotéines sont modifiées reste hautement controversé. Depuis quelques années, le modèle de modification des LDLs par la myéloperoxydase est apparu comme un modèle physiopathologique contrairement au modèle longuement utilisé de l’oxydation des LDLs par le cuivre. La myéloperoxydase est une enzyme présente dans les granules primaires des neutrophiles mais qui lors d’inflammations chroniques, comme dans l’athérosclérose, peut se retrouver dans le milieu extracellulaire et former un oxydant puissant qui attaque les protéines, les lipides ou les acides nucléiques. Les LDLs modifiées par la myéloperoxydase ne sont plus reconnues par le récepteur membranaire spécifique pour les LDLs. De plus, très peu d’études ont décrit à ce jour les modifications apportées par la myéloperoxydase aux LDLs.

Dans ce contexte, nous avons étudié la spécificité de la myéloperoxydase à modifier les LDLs. Dans ce modèle, la partie protéique de la lipoprotéine est majoritairement touchée. C’est pourquoi nous avons développé et optimisé des méthodes d’analyse par spectrométrie de masse de l’apolipoprotéine B-100, la seule protéine de la LDL. De plus, l’activité de la myéloperoxydase à la surface des LDLs a également été investiguée.

Les résultats de ce travail montrent que la myéloperoxydase s’attaque de manière spécifique aux LDLs et que le modèle chimique utilisant de l’acide hypochloreux pour mimer l’action de la myéloperoxydase n’est pas parfait. Enfin, nous avons également observé des changements dans l’activité enzymatique lorsque la myéloperoxydase est adsorbée à la surface des LDLs.


Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished

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Cummings, Michael Hunter. "Application of a stable isotope mass-spectrometry method to examine the regulation of very-low-density lipoprotein apolipoprotein B-100 in physiological and pathological states." Thesis, St George's, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307608.

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Mero-Matikainen, Niina. "Postprandial metabolism of HLD and apolipoproteins B-48 and B-100." Helsinki : University of Helsinki, 1999. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/mero-matikainen/.

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Book chapters on the topic "Apolipoprotein B-100"

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Leung, Alexander K. C., William Lane M. Robson, Carsten Büning, Johann Ockenga, Janine Büttner, Hartmut Schmidt, Antonio V. Delgado-Escueta, et al. "Ligand-defective Apolipoprotein B-100, Familial." In Encyclopedia of Molecular Mechanisms of Disease, 1175–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_616.

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Desnick, Robert J., Orlando Guntinas-Lichius, George W. Padberg, Gustav Schonfeld, Xiaobo Lin, Maurizio Averna, Pin Yue, et al. "Familial Ligand-defective Apolipoprotein B-100." In Encyclopedia of Molecular Mechanisms of Disease, 635. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_9174.

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Chan, Lawrence. "Structure-Function Relationships of Apolipoprotein B-100." In Drugs Affecting Lipid Metabolism, 45–47. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1703-6_6.

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Gregg, Richard E., and H. Bryan Brewer. "The Role of Apolipoprotein E in Modulating the Metabolism of Apolipoprotein B-48 and Apolipoprotein B-100 Containing Lipoproteins in Humans." In Lipoprotein Deficiency Syndromes, 289–98. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-1262-8_25.

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Beg, Zafarul H., John A. Stonik, Jeffrey M. Hoeg, and H. Bryan Brewer. "Post-Translational Modification by Covalent Phosphorylation of Human Apolipoprotein B-100." In Methods in Protein Structure Analysis, 355–67. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-1031-8_31.

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Truong, Phuong Kim, Cong Van Bui, Thuan Duc Lao, and Thuy Huyen Ai Le. "Detection of Defective Apolipoprotein B-100 R3500Q Mutation Caused Familial Hypercholesterolemia in Vietnamese Patients." In 6th International Conference on the Development of Biomedical Engineering in Vietnam (BME6), 275–79. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4361-1_46.

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Cardin, Alan D., Richard L. Jackson, Virginia H. Donaldson, Julie Chao, and Harry S. Margolius. "Processing of Apolipoprotein B-100 of Human Plasma Low Density Lipoproteins by Tissue and Plasma Kallikreins." In Kinins IV, 195–202. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5143-6_27.

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Pownall, Henry J., Diane H. Bick, Kay T. Kimball, Danièle Zoch, and Christie M. Ballantyne. "Acute Effects of Alcohol on the Turnover of Very Low Density Lipoprotein (VLDL) Apolipoprotein B-100 in Normolipidemic Subjects." In Moderate Alcohol Consumption and Cardiovascular Disease, 47–52. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4307-3_5.

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Lackner, K. J., W. März, G. Wolter, H. Sartor, and W. Gross. "Anabolic Steroids do not Change mRNA Levels and Protein Secretion of Apolipoprotein A-I and B-100 in HepG2 Cells." In Recent Developments in Lipid and Lipoprotein Research, 151–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84855-1_18.

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Yang, Chao-Yuh, Zi-Wei Gu, Lawrence Chan, Henry J. Pownall, and Antonio M. Gotto. "Structure and Functional Domains of Human Apolipoprotein B-100: A Strategy to Elucidate the Structure Information of a Large Protein." In Methods in Protein Sequence Analysis, 466–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73834-0_62.

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Conference papers on the topic "Apolipoprotein B-100"

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DUC, LAO, LE HUYEN, NGUYEN HOANG, and TRUONG KIM. "Detection and haplotype analysis of defective Apolipoprotein B 100 R3500Q mutation in Familial hypercholesterolemia in Vietnamese patients by AS PCR Allele specific PCR." In Fourth International Conference On Advances in Applied Science and Environmental Technology- ASET 2016. Institute of Research Engineers and Doctors, 2016. http://dx.doi.org/10.15224/978-1-63248-097-2-46.

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