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  • Humans  (125)
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  • 1998  (125)
  • 1
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    A physical map of 30,000 human genes (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-23
    Description: A map of 30,181 human gene-based markers was assembled and integrated with the current genetic map by radiation hybrid mapping. The new gene map contains nearly twice as many genes as the previous release, includes most genes that encode proteins of known function, and is twofold to threefold more accurate than the previous version. A redesigned, more informative and functional World Wide Web site (www.ncbi.nlm.nih.gov/genemap) provides the mapping information and associated data and annotations. This resource constitutes an important infrastructure and tool for the study of complex genetic traits, the positional cloning of disease genes, the cross-referencing of mammalian genomes, and validated human transcribed sequences for large-scale studies of gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deloukas, P -- Schuler, G D -- Gyapay, G -- Beasley, E M -- Soderlund, C -- Rodriguez-Tome, P -- Hui, L -- Matise, T C -- McKusick, K B -- Beckmann, J S -- Bentolila, S -- Bihoreau, M -- Birren, B B -- Browne, J -- Butler, A -- Castle, A B -- Chiannilkulchai, N -- Clee, C -- Day, P J -- Dehejia, A -- Dibling, T -- Drouot, N -- Duprat, S -- Fizames, C -- Fox, S -- Gelling, S -- Green, L -- Harrison, P -- Hocking, R -- Holloway, E -- Hunt, S -- Keil, S -- Lijnzaad, P -- Louis-Dit-Sully, C -- Ma, J -- Mendis, A -- Miller, J -- Morissette, J -- Muselet, D -- Nusbaum, H C -- Peck, A -- Rozen, S -- Simon, D -- Slonim, D K -- Staples, R -- Stein, L D -- Stewart, E A -- Suchard, M A -- Thangarajah, T -- Vega-Czarny, N -- Webber, C -- Wu, X -- Hudson, J -- Auffray, C -- Nomura, N -- Sikela, J M -- Polymeropoulos, M H -- James, M R -- Lander, E S -- Hudson, T J -- Myers, R M -- Cox, D R -- Weissenbach, J -- Boguski, M S -- Bentley, D R -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):744-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sanger Centre, Hinxton Hall, Hinxton, Cambridge CB10 1SA UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9784132" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Human/*genetics ; Expressed Sequence Tags ; Gene Expression ; Genetic Markers ; *Genome, Human ; Human Genome Project ; Humans ; Internet ; *Physical Chromosome Mapping ; Rats ; Sequence Tagged Sites
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Requirement for IL-13 independently of IL-4 in experimental asthma (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-18
    Description: The pathogenesis of asthma reflects, in part, the activity of T cell cytokines. Murine models support participation of interleukin-4 (IL-4) and the IL-4 receptor in asthma. Selective neutralization of IL-13, a cytokine related to IL-4 that also binds to the alpha chain of the IL-4 receptor, ameliorated the asthma phenotype, including airway hyperresponsiveness, eosinophil recruitment, and mucus overproduction. Administration of either IL-13 or IL-4 conferred an asthma-like phenotype to nonimmunized T cell-deficient mice by an IL-4 receptor alpha chain-dependent pathway. This pathway may underlie the genetic associations of asthma with both the human 5q31 locus and the IL-4 receptor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3897229/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3897229/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grunig, G -- Warnock, M -- Wakil, A E -- Venkayya, R -- Brombacher, F -- Rennick, D M -- Sheppard, D -- Mohrs, M -- Donaldson, D D -- Locksley, R M -- Corry, D B -- 03344/PHS HHS/ -- 47412/PHS HHS/ -- K08 HL003344/HL/NHLBI NIH HHS/ -- T32 HL07185/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2261-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, San Francisco General Hospital, University of California San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856950" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Allergens/immunology ; Animals ; Asthma/genetics/*immunology/pathology/physiopathology ; Bronchial Hyperreactivity ; Bronchoalveolar Lavage Fluid/cytology ; Chromosomes, Human, Pair 5 ; Goblet Cells/pathology ; Humans ; Immunoglobulin Fc Fragments ; Interleukin-13/antagonists & inhibitors/genetics/pharmacology/*physiology ; Interleukin-13 Receptor alpha1 Subunit ; Interleukin-4/genetics/pharmacology/*physiology ; Mice ; Mice, Inbred BALB C ; Ovalbumin/immunology ; Phenotype ; Receptors, Interleukin/genetics/immunology/physiology ; Receptors, Interleukin-13 ; Receptors, Interleukin-4/genetics/physiology ; Recombinant Fusion Proteins/pharmacology ; Th2 Cells/immunology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    AIDS vaccine development (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Agosto, M -- Allan, J -- Benson, C -- Berger, E A -- Blumenthal, R -- Burton, D -- Clements, J -- Coffin, J -- Connor, R -- Cullen, B -- Desrosiers, R -- Dimitrov, D -- Doms, R -- Emerman, M -- Feinberg, M -- Fultz, P -- Gerard, C -- Gonsalves, G -- Haase, A -- Haigwood, N -- Hirsch, V -- Ho, D -- Hoxie, J A -- Hu, S L -- Zingale, D -- New York, N.Y. -- Science. 1998 May 8;280(5365):803, 804-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9599148" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines/immunology ; Acquired Immunodeficiency Syndrome/prevention & control ; *Clinical Trials as Topic ; HIV Envelope Protein gp120/immunology ; HIV-1/immunology ; Humans ; National Institutes of Health (U.S.) ; United States
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    The Lost Colony and Jamestown droughts (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-09
    Description: Tree-ring data from Virginia indicate that the Lost Colony of Roanoke Island disappeared during the most extreme drought in 800 years (1587-1589) and that the alarming mortality and the near abandonment of Jamestown Colony occurred during the driest 7-year episode in 770 years (1606-1612). These extraordinary droughts can now be implicated in the fate of the Lost Colony and in the appalling death rate during the early occupations at Jamestown, the first permanent English settlement in America.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stahle, D W -- Cleaveland, M K -- Blanton, D B -- Therrell, M D -- Gay, D A -- New York, N.Y. -- Science. 1998 Apr 24;280(5363):564-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tree-Ring Laboratory, Department of Geography, University of Arkansas, Fayetteville, AR 72701, USA. dstahle@comp.uark.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9554842" target="_blank"〉PubMed〈/a〉
    Keywords: Climate ; Disasters/*history ; Fresh Water ; History, 16th Century ; History, 17th Century ; Humans ; *Mortality ; Nutrition Disorders/history ; Starvation/history ; Virginia
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Mutation of a gene encoding a protein with extracellular matrix motifs in Usher syndrome type IIa (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: Usher syndrome type IIa (OMIM 276901), an autosomal recessive disorder characterized by moderate to severe sensorineural hearing loss and progressive retinitis pigmentosa, maps to the long arm of human chromosome 1q41 between markers AFM268ZD1 and AFM144XF2. Three biologically important mutations in Usher syndrome type IIa patients were identified in a gene (USH2A) isolated from this critical region. The USH2A gene encodes a protein with a predicted size of 171.5 kilodaltons that has laminin epidermal growth factor and fibronectin type III motifs; these motifs are most commonly observed in proteins comprising components of the basal lamina and extracellular matrixes and in cell adhesion molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eudy, J D -- Weston, M D -- Yao, S -- Hoover, D M -- Rehm, H L -- Ma-Edmonds, M -- Yan, D -- Ahmad, I -- Cheng, J J -- Ayuso, C -- Cremers, C -- Davenport, S -- Moller, C -- Talmadge, C B -- Beisel, K W -- Tamayo, M -- Morton, C C -- Swaroop, A -- Kimberling, W J -- Sumegi, J -- 5PO1 DC01813-05/DC/NIDCD NIH HHS/ -- DC03402/DC/NIDCD NIH HHS/ -- EY07003/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1998 Jun 12;280(5370):1753-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9624053" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Adhesion Molecules/chemistry ; Chromosome Mapping ; Chromosomes, Human, Pair 1 ; Cochlea/chemistry ; Epidermal Growth Factor/chemistry ; Extracellular Matrix Proteins/chemistry/*genetics/physiology ; Female ; Fibronectins/chemistry ; Frameshift Mutation ; Gene Expression ; Genes, Recessive ; Glycosylation ; Hearing Loss, Sensorineural/*genetics ; Humans ; Laminin/chemistry ; Male ; Molecular Sequence Data ; Pedigree ; Retina/chemistry ; Retinitis Pigmentosa/*genetics ; Syndrome ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Mutation-specific functional impairments in distinct tau isoforms of hereditary FTDP-17 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-04
    Description: Tau proteins aggregate as cytoplasmic inclusions in a number of neurodegenerative diseases, including Alzheimer's disease and hereditary frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). Over 10 exonic and intronic mutations in the tau gene have been identified in about 20 FTDP-17 families. Analyses of soluble and insoluble tau proteins from brains of FTDP-17 patients indicated that different pathogenic mutations differentially altered distinct biochemical properties and stoichiometry of brain tau isoforms. Functional assays of recombinant tau proteins with different FTDP-17 missense mutations implicated all but one of these mutations in disease pathogenesis by reducing the ability of tau to bind microtubules and promote microtubule assembly.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hong, M -- Zhukareva, V -- Vogelsberg-Ragaglia, V -- Wszolek, Z -- Reed, L -- Miller, B I -- Geschwind, D H -- Bird, T D -- McKeel, D -- Goate, A -- Morris, J C -- Wilhelmsen, K C -- Schellenberg, G D -- Trojanowski, J Q -- Lee, V M -- New York, N.Y. -- Science. 1998 Dec 4;282(5395):1914-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9836646" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Brain/*metabolism ; Cerebellum/metabolism ; Chromosomes, Human, Pair 17 ; Dementia/*genetics/metabolism ; Frontal Lobe/metabolism ; Humans ; Microtubules/*metabolism ; Mutation ; Mutation, Missense ; Parkinson Disease, Secondary/*genetics/metabolism ; Phosphorylation ; Protein Isoforms/chemistry/genetics/metabolism ; Recombinant Proteins/metabolism ; Solubility ; Syndrome ; tau Proteins/chemistry/*genetics/*metabolism
    Print ISSN: 0036-8075
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  • 7
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    Quantitation of HIV-1-specific cytotoxic T lymphocytes and plasma load of viral RNA (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-16
    Description: Although cytotoxic T lymphocytes (CTLs) are thought to be involved in the control of human immunodeficiency virus-type 1 (HIV-1) infection, it has not been possible to demonstrate a direct relation between CTL activity and plasma RNA viral load. Human leukocyte antigen-peptide tetrameric complexes offer a specific means to directly quantitate circulating CTLs ex vivo. With the use of the tetrameric complexes, a significant inverse correlation was observed between HIV-specific CTL frequency and plasma RNA viral load. In contrast, no significant association was detected between the clearance rate of productively infected cells and frequency of HIV-specific CTLs. These data are consistent with a significant role for HIV-specific CTLs in the control of HIV infection and suggest a considerable cytopathic effect of the virus in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogg, G S -- Jin, X -- Bonhoeffer, S -- Dunbar, P R -- Nowak, M A -- Monard, S -- Segal, J P -- Cao, Y -- Rowland-Jones, S L -- Cerundolo, V -- Hurley, A -- Markowitz, M -- Ho, D D -- Nixon, D F -- McMichael, A J -- MO1-RR00102/RR/NCRR NIH HHS/ -- U01AI41534/AI/NIAID NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1998 Mar 27;279(5359):2103-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Medicine, Nuffield Department of Medicine, Oxford OX3 9DS, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9516110" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-HIV Agents/therapeutic use ; CD4 Lymphocyte Count ; Coloring Agents ; Cytopathogenic Effect, Viral ; Cytotoxicity, Immunologic ; Flow Cytometry ; Gene Products, gag ; Gene Products, pol ; HIV Infections/drug therapy/*immunology/*virology ; HIV-1/genetics/*physiology ; HLA-A Antigens ; Humans ; Lymphocyte Count/*methods ; Oligopeptides ; RNA, Viral/*blood ; Sensitivity and Specificity ; T-Lymphocytes, Cytotoxic/*immunology ; Viral Load ; Viremia
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Anterior cingulate cortex, error detection, and the online monitoring of performance (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-23
    Description: An unresolved question in neuroscience and psychology is how the brain monitors performance to regulate behavior. It has been proposed that the anterior cingulate cortex (ACC), on the medial surface of the frontal lobe, contributes to performance monitoring by detecting errors. In this study, event-related functional magnetic resonance imaging was used to examine ACC function. Results confirm that this region shows activity during erroneous responses. However, activity was also observed in the same region during correct responses under conditions of increased response competition. This suggests that the ACC detects conditions under which errors are likely to occur rather than errors themselves.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carter, C S -- Braver, T S -- Barch, D M -- Botvinick, M M -- Noll, D -- Cohen, J D -- K08MH01306/MH/NIMH NIH HHS/ -- R01MH52864/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1998 May 1;280(5364):747-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Western Psychiatric Institute and Clinic, School of Medicine, University of Pittsburgh, 3811 O'Hara Street, Pittsburgh, PA 15213, USA. cscarter+@pitt.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9563953" target="_blank"〉PubMed〈/a〉
    Keywords: Brain Mapping ; Cognition/*physiology ; Frontal Lobe/*physiology ; Gyrus Cinguli/*physiology ; Humans ; Magnetic Resonance Imaging
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Inhibition of a Mycobacterium tuberculosis beta-ketoacyl ACP synthase by isoniazid (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-11
    Description: Although isoniazid (isonicotinic acid hydrazide, INH) is widely used for the treatment of tuberculosis, its molecular target has remained elusive. In response to INH treatment, saturated hexacosanoic acid (C26:0) accumulated on a 12-kilodalton acyl carrier protein (AcpM) that normally carried mycolic acid precursors as long as C50. A protein species purified from INH-treated Mycobacterium tuberculosis was shown to consist of a covalent complex of INH, AcpM, and a beta-ketoacyl acyl carrier protein synthase, KasA. Amino acid-altering mutations in the KasA protein were identified in INH-resistant patient isolates that lacked other mutations associated with resistance to this drug.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mdluli, K -- Slayden, R A -- Zhu, Y -- Ramaswamy, S -- Pan, X -- Mead, D -- Crane, D D -- Musser, J M -- Barry, C E 3rd -- AI37004/AI/NIAID NIH HHS/ -- Z01 AI000783-11/Intramural NIH HHS/ -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1607-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tuberculosis Research Unit, Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute for Allergy and Infectious Diseases (NIAID), National Institutes of Health, Hamilton, MT 59840, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616124" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Oxoacyl-(Acyl-Carrier-Protein) Synthase/*antagonists & ; inhibitors/chemistry/genetics ; Acyl Carrier Protein/chemistry/genetics/metabolism ; Amino Acid Sequence ; Antitubercular Agents/*pharmacology ; Drug Resistance, Microbial ; Enzyme Inhibitors/pharmacology ; Fatty Acids/metabolism ; Genes, Bacterial ; Humans ; Isoniazid/*pharmacology ; Molecular Sequence Data ; Molecular Weight ; Mutation ; Mycobacterium tuberculosis/drug effects/*enzymology/genetics ; Mycolic Acids/metabolism ; Tuberculosis/microbiology ; Up-Regulation
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  • 10
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    An MTP inhibitor that normalizes atherogenic lipoprotein levels in WHHL rabbits (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-23
    Description: Patients with abetalipoproteinemia, a disease caused by defects in the microsomal triglyceride transfer protein (MTP), do not produce apolipoprotein B-containing lipoproteins. It was hypothesized that small molecule inhibitors of MTP would prevent the assembly and secretion of these atherogenic lipoproteins. To test this hypothesis, two compounds identified in a high-throughput screen for MTP inhibitors were used to direct the synthesis of a highly potent MTP inhibitor. This molecule (compound 9) inhibited the production of lipoprotein particles in rodent models and normalized plasma lipoprotein levels in Watanabe-heritable hyperlipidemic (WHHL) rabbits, which are a model for human homozygous familial hypercholesterolemia. These results suggest that compound 9, or derivatives thereof, has potential applications for the therapeutic lowering of atherogenic lipoprotein levels in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wetterau, J R -- Gregg, R E -- Harrity, T W -- Arbeeny, C -- Cap, M -- Connolly, F -- Chu, C H -- George, R J -- Gordon, D A -- Jamil, H -- Jolibois, K G -- Kunselman, L K -- Lan, S J -- Maccagnan, T J -- Ricci, B -- Yan, M -- Young, D -- Chen, Y -- Fryszman, O M -- Logan, J V -- Musial, C L -- Poss, M A -- Robl, J A -- Simpkins, L M -- Slusarchyk, W A -- Sulsky, R -- Taunk, P -- Magnin, D R -- Tino, J A -- Lawrence, R M -- Dickson, J K Jr -- Biller, S A -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):751-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Metabolic Diseases, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, NJ 08543-4000, USA. Wetterau_John_R@msmail.bms.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9784135" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine Transaminase/blood ; Animals ; Apolipoproteins B/*blood ; Aspartate Aminotransferases/blood ; Carrier Proteins/*antagonists & inhibitors ; Cholesterol/*blood ; Cricetinae ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Drug Design ; Drug Evaluation, Preclinical ; Fluorenes/chemistry/pharmacokinetics/*pharmacology ; Humans ; Hyperlipidemias/blood/drug therapy ; Hyperlipoproteinemia Type II/*blood/drug therapy ; Lipids/blood ; Lipoproteins/blood ; Liver/metabolism ; Mice ; Piperidines/chemistry/pharmacokinetics/*pharmacology ; Rabbits ; Rats ; Triglycerides/*blood/metabolism ; Tumor Cells, Cultured
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