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  • Mice  (29)
  • Mice, Inbred C57BL
  • 1995-1999  (9)
  • 1990-1994  (20)
  • 1945-1949
  • 1940-1944
Collection
Keywords
Publisher
Years
  • 1995-1999  (9)
  • 1990-1994  (20)
  • 1945-1949
  • 1940-1944
  • 1985-1989  (15)
Year
  • 1
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    Type 1 neurofibromatosis gene: identification of a large transcript disrupted in three NF1 patients (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-13
    Description: Von Recklinghausen neurofibromatosis (NF1) is a common autosomal dominant disorder characterized by abnormalities in multiple tissues derived from the neural crest. No reliable cellular phenotypic marker has been identified, which has hampered direct efforts to identify the gene. The chromosome location of the NF1 gene has been previously mapped genetically to 17q11.2, and data from two NF1 patients with balanced translocations in this region have further narrowed the candidate interval. The use of chromosome jumping and yeast artificial chromosome technology has now led to the identification of a large (approximately 13 kilobases) ubiquitously expressed transcript (denoted NF1LT) from this region that is definitely interrupted by one and most likely by both translocations. Previously identified candidate genes, which failed to show abnormalities in NF1 patients, are apparently located within introns of NF1LT, on the antisense strand. A new mutation patient with NF1 has been identified with a de novo 0.5-kilobase insertion in the NF1LT gene. These observations, together with the high spontaneous mutation rate of NF1 (which is consistent with a large locus), suggest that NF1LT represents the elusive NF1 gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wallace, M R -- Marchuk, D A -- Andersen, L B -- Letcher, R -- Odeh, H M -- Saulino, A M -- Fountain, J W -- Brereton, A -- Nicholson, J -- Mitchell, A L -- NS23410/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):181-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Ann Arbor, MI.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2134734" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Northern ; Blotting, Southern ; Cell Line ; Cloning, Molecular ; DNA, Neoplasm/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Hybrid Cells ; Male ; Mice ; Molecular Sequence Data ; Mutation ; Neurofibromatosis 1/*genetics ; Protein Biosynthesis ; RNA, Neoplasm/*genetics ; Transcription, Genetic ; *Translocation, Genetic ; Tumor Cells, Cultured
    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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    Induction of inflammatory arthropathy resembling rheumatoid arthritis in mice transgenic for HTLV-I (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-30
    Description: Human T cell leukemia virus type-I (HTLV-I) is the etiologic agent of adult T cell leukemia and has also been suggested to be involved in other diseases such as chronic arthritis or myelopathy. To elucidate pathological roles of the virus in disease, transgenic mice were produced that carry the HTLV-I genome. At 2 to 3 months of age, many of the mice developed chronic arthritis resembling rheumatoid arthritis. Synovial and periarticular inflammation with articular erosion caused by invasion of granulation tissues were marked. These observations suggest a possibility that HTLV-I is one of the etiologic agents of chronic arthritis in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iwakura, Y -- Tosu, M -- Yoshida, E -- Takiguchi, M -- Sato, K -- Kitajima, I -- Nishioka, K -- Yamamoto, K -- Takeda, T -- Hatanaka, M -- New York, N.Y. -- Science. 1991 Aug 30;253(5023):1026-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Medical Science, University of Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1887217" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis, Rheumatoid/*genetics/pathology/physiopathology ; Genes, Viral ; Human T-lymphotropic virus 1/*genetics ; Inflammation ; Joints/pathology ; Mice ; Mice, Inbred Strains ; Mice, Transgenic ; RNA, Messenger/genetics ; Repetitive Sequences, Nucleic Acid ; Viral Envelope Proteins/genetics
    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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  • 3
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    Deposits of amyloid beta protein in the central nervous system of transgenic mice (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-19
    Description: Alzheimer's disease is characterized by widespread deposition of amyloid in the central nervous system. The 4-kilodalton amyloid beta protein is derived from a larger amyloid precursor protein and forms amyloid deposits in the brain by an unknown pathological mechanism. Except for aged nonhuman primates, there is no animal model for Alzheimer's disease. Transgenic mice expressing amyloid beta protein in the brain could provide such a model. To investigate this possibility, the 4-kilodalton human amyloid beta protein was expressed under the control of the promoter of the human amyloid precursor protein in two lines of transgenic mice. Amyloid beta protein accumulated in the dendrites of some but not all hippocampal neurons in 1-year-old transgenic mice. Aggregates of the amyloid beta protein formed amyloid-like fibrils that are similar in appearance to those in the brains of patients with Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wirak, D O -- Bayney, R -- Ramabhadran, T V -- Fracasso, R P -- Hart, J T -- Hauer, P E -- Hsiau, P -- Pekar, S K -- Scangos, G A -- Trapp, B D -- New York, N.Y. -- Science. 1991 Jul 19;253(5017):323-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Therapeutics Inc., Miles Research Center, West Haven, CT 06516.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1857970" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics/pathology ; Amyloid beta-Peptides/analysis/*genetics ; Animals ; Base Sequence ; Brain/*metabolism/pathology ; DNA/genetics ; Hippocampus/ultrastructure ; Humans ; Mice ; Mice, Transgenic ; Microscopy, Electron ; Molecular Sequence Data ; Neurofibrils/ultrastructure ; Oligonucleotide Probes ; Restriction Mapping
    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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  • 4
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    Disappearance of the lymphoid system in Bcl-2 homozygous mutant chimeric mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-17
    Description: The bcl-2 proto-oncogene can prevent the death of many cell types. Mice were generated that were chimeric for the homozygous inactivation of bcl-2. Lymphocytes without Bcl-2 differentiated into phenotypically mature cells. However, in vitro, the mature T cells that lacked Bcl-2 had shorter life-spans and increased sensitivity to glucocorticoids and gamma-irradiation. In contrast, stimulation of CD3 inhibited the death of these cells. T and B cells with no Bcl-2 disappeared from the bone marrow, thymus, and periphery by 4 weeks of age. Thus, Bcl-2 was dispensable for lymphocyte maturation, but was required for a stable immune system after birth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakayama, K -- Negishi, I -- Kuida, K -- Shinkai, Y -- Louie, M C -- Fields, L E -- Lucas, P J -- Stewart, V -- Alt, F W -- AI 15322/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 17;261(5128):1584-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8372353" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3/immunology ; Apoptosis ; B-Lymphocytes/cytology/*immunology ; Base Sequence ; Bone Marrow/immunology ; Bone Marrow Cells ; Cell Line ; Chimera ; Homozygote ; Humans ; Lymphoid Tissue/cytology/immunology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Proto-Oncogene Proteins/genetics/*physiology ; Proto-Oncogene Proteins c-bcl-2 ; Proto-Oncogenes ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/cytology/*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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  • 5
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    Uncovering of functional alternative CTLA-4 counter-receptor in B7-deficient mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-05
    Description: B7 delivers a costimulatory signal through CD28, resulting in interleukin-2 secretion and T cell proliferation. Blockade of this pathway results in T cell anergy. The in vivo role of B7 was evaluated with B7-deficient mice. These mice had a 70 percent decrease in costimulation of the response to alloantigen. Despite lacking B7 expression, activated B cells from these mice bound CTLA-4 and GL1 monoclonal antibody, demonstrating that alternative CTLA-4 ligand or ligands exist. These receptors are functionally important because the residual allogenic mixed lymphocyte responses were blocked by CTLA4Ig. Characterization of these CTLA-4 ligands should lead to strategies for manipulating the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freeman, G J -- Borriello, F -- Hodes, R J -- Reiser, H -- Hathcock, K S -- Laszlo, G -- McKnight, A J -- Kim, J -- Du, L -- Lombard, D B -- CA 40216/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Nov 5;262(5135):907-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematologic Malignancies, Dana-Farber Cancer Institute, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7694362" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antigens, CD ; Antigens, CD80/genetics/*immunology/metabolism ; Antigens, Differentiation/immunology/*metabolism ; B-Lymphocytes/*immunology ; Base Sequence ; CTLA-4 Antigen ; Cell Line ; *Immunoconjugates ; Interleukin-2/secretion ; Isoantigens/immunology ; Lymphocyte Activation ; Lymphocyte Culture Test, Mixed ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; T-Lymphocytes/*immunology ; Transfection
    Print ISSN: 0036-8075
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  • 6
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    Interleukin-2 receptor gamma chain: a functional component of the interleukin-4 receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-17
    Description: The interleukin-2 (IL-2) receptor gamma chain (IL-2R gamma) is an essential component of high- and intermediate-affinity IL-2 receptors. IL-2R gamma was demonstrated to be a component of the IL-4 receptor on the basis of chemical cross-linking data, the ability of IL-2R gamma to augment IL-4 binding affinity, and the requirement for IL-2R gamma in IL-4-mediated phosphorylation of insulin receptor substrate-1. The observation that IL-2R gamma is a functional component of the IL-4 receptor, together with the finding that IL-2R gamma associates with the IL-7 receptor, begins to elucidate why deficiency of this common gamma chain (gamma c) has a profound effect on lymphoid function and development, as seen in X-linked severe combined immunodeficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Russell, S M -- Keegan, A D -- Harada, N -- Nakamura, Y -- Noguchi, M -- Leland, P -- Friedmann, M C -- Miyajima, A -- Puri, R K -- Paul, W E -- New York, N.Y. -- Science. 1993 Dec 17;262(5141):1880-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Pulmonary and Molecular Immunology, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266078" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Cell Line, Transformed ; Genetic Linkage ; Humans ; Insulin Receptor Substrate Proteins ; Interleukin-4/metabolism ; L Cells (Cell Line) ; Mice ; Molecular Sequence Data ; Phosphoproteins/metabolism ; Phosphorylation ; Receptors, Interleukin-2/chemistry/genetics/*metabolism ; Receptors, Interleukin-4 ; Receptors, Mitogen/chemistry/genetics/*metabolism ; Severe Combined Immunodeficiency/genetics/immunology ; Signal Transduction ; Transfection ; X Chromosome
    Print ISSN: 0036-8075
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  • 7
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    Increased activity of L-type Ca2+ channels exposed to serum from patients with type I diabetes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-02
    Description: Type I diabetes [insulin-dependent diabetes mellitus (IDDM)] is an autoimmune disease associated with the destruction of pancreatic beta cells. Serum from patients with IDDM increased L-type calcium channel activity of insulin-producing cells and of GH3 cells derived from a pituitary tumor. The subsequent increase in the concentration of free cytoplasmic Ca2+ ([Ca2+]i) was associated with DNA fragmentation typical of programmed cell death or apoptosis. These effects of the serum were prevented by adding a blocker of voltage-activated L-type Ca2+ channels. When the serum was depleted of immunoglobulin M (IgM), it no longer affected [Ca2+]i. An IgM-mediated increase in Ca2+ influx may thus be part of the autoimmune reaction associated with IDDM and contribute to the destruction of beta cells in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Juntti-Berggren, L -- Larsson, O -- Rorsman, P -- Ammala, C -- Bokvist, K -- Wahlander, K -- Nicotera, P -- Dypbukt, J -- Orrenius, S -- Hallberg, A -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):86-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rolf Luft Center for Diabetes Research, Department of Endocrinology, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7686306" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Pyridinecarboxylic acid, ; 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ; ester/pharmacology ; Animals ; Apoptosis ; Calcium/*metabolism ; Calcium Channels/drug effects/*metabolism ; DNA Damage ; Diabetes Mellitus, Type 1/*immunology ; Humans ; Immunoglobulin M/*physiology ; Islets of Langerhans/drug effects/*metabolism ; Membrane Potentials ; Mice ; Pituitary Neoplasms/metabolism ; Tumor Cells, Cultured ; Verapamil/pharmacology
    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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    Aggressive behavior and altered amounts of brain serotonin and norepinephrine in mice lacking MAOA (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-23
    Description: Deficiency in monoamine oxidase A (MAOA), an enzyme that degrades serotonin and norepinephrine, has recently been shown to be associated with aggressive behavior in men of a Dutch family. A line of transgenic mice was isolated in which transgene integration caused a deletion in the gene encoding MAOA, providing an animal model of MAOA deficiency. In pup brains, serotonin concentrations were increased up to ninefold, and serotonin-like immunoreactivity was present in catecholaminergic neurons. In pup and adult brains, norepinephrine concentrations were increased up to twofold, and cytoarchitectural changes were observed in the somatosensory cortex. Pup behavioral alterations, including trembling, difficulty in righting, and fearfulness were reversed by the serotonin synthesis inhibitor parachlorophenylalanine. Adults manifested a distinct behavioral syndrome, including enhanced aggression in males.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2844866/" 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/PMC2844866/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cases, O -- Seif, I -- Grimsby, J -- Gaspar, P -- Chen, K -- Pournin, S -- Muller, U -- Aguet, M -- Babinet, C -- Shih, J C -- K05 MH 00796/MH/NIMH NIH HHS/ -- R01 MH 37020/MH/NIMH NIH HHS/ -- R37 MH 39085/MH/NIMH NIH HHS/ -- R37 MH039085/MH/NIMH NIH HHS/ -- R37 MH039085-23/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1995 Jun 23;268(5218):1763-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre National de la Recherche Scientifique (CNRS), Unite de Recherche Associee (URA), Institut Curie, Orsay, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7792602" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression/*physiology ; Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Southern ; Brain/*metabolism ; Disease Models, Animal ; Dopamine/metabolism ; Female ; Interferon-beta/genetics ; Male ; Mice ; Mice, Inbred C3H ; Mice, Transgenic ; Molecular Sequence Data ; Monoamine Oxidase/*deficiency ; Norepinephrine/*metabolism ; Sequence Deletion ; Serotonin/*metabolism
    Print ISSN: 0036-8075
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  • 9
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    Inactivation of the mouse Huntington's disease gene homolog Hdh (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-07-21
    Description: Huntington's disease (HD) is a dominant neurodegenerative disorder caused by expansion of a CAG repeat in the gene encoding huntingtin, a protein of unknown function. To distinguish between "loss of function" and "gain of function" models of HD, the murine HD homolog Hdh was inactivated by gene targeting. Mice heterozygous for Hdh inactivation were phenotypically normal, whereas homozygosity resulted in embryonic death. Homozygotes displayed abnormal gastrulation at embryonic day 7.5 and were resorbing by day 8.5. Thus, huntingtin is critical early in embryonic development, before the emergence of the nervous system. That Hdh inactivation does not mimic adult HD neuropathology suggests that the human disease involves a gain of function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duyao, M P -- Auerbach, A B -- Ryan, A -- Persichetti, F -- Barnes, G T -- McNeil, S M -- Ge, P -- Vonsattel, J P -- Gusella, J F -- Joyner, A L -- NS16367/NS/NINDS NIH HHS/ -- NS32765/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 Jul 21;269(5222):407-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurogenetics Unit, Massachusetts General Hospital, Charlestown 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7618107" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Ectoderm/cytology ; Embryonic and Fetal Development ; Female ; Gene Targeting ; Genotype ; Heterozygote ; Homozygote ; Humans ; Huntington Disease/*genetics ; Male ; Mesoderm/cytology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Nerve Tissue Proteins/*genetics/physiology ; Nuclear Proteins/*genetics/physiology ; Phenotype ; Stem Cells/metabolism
    Print ISSN: 0036-8075
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  • 10
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    E5531, a pure endotoxin antagonist of high potency (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-04-07
    Description: Shock due to Gram-negative bacterial sepsis is a consequence of acute inflammatory response to lipopolysaccharide (LPS) or endotoxin released from bacteria. LPS is a major constituent of the outer membrane of Gram-negative bacteria, and its terminal disaccharide phospholipid (lipid A) portion contains the key structural features responsible for toxic activity. Based on the proposed structure of nontoxic Rhodobacter capsulatus lipid A, a fully stabilized endotoxin antagonist E5531 has been synthesized. In vitro, E5531 demonstrated potent antagonism of LPS-mediated cellular activation in a variety of systems. In vivo, E5531 protected mice from LPS-induced lethality and, in cooperation with an antibiotic, protected mice from a lethal infection of viable Escherichia coli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Christ, W J -- Asano, O -- Robidoux, A L -- Perez, M -- Wang, Y -- Dubuc, G R -- Gavin, W E -- Hawkins, L D -- McGuinness, P D -- Mullarkey, M A -- New York, N.Y. -- Science. 1995 Apr 7;268(5207):80-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Elsai Research Institute, Andover, MA 01810-2441, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7701344" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BCG Vaccine/immunology ; Cytokines/secretion ; Drug Design ; Endotoxins/*antagonists & inhibitors ; Escherichia coli Infections/immunology ; Gram-Negative Bacteria/immunology ; Humans ; In Vitro Techniques ; Lipid A/*analogs & derivatives/chemical synthesis/chemistry/pharmacology ; Lipopolysaccharides/antagonists & inhibitors ; Macrophages/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Monocytes/immunology ; Moxalactam/pharmacology ; Nitric Oxide/metabolism ; Rhodobacter capsulatus/immunology ; Tumor Necrosis Factor-alpha/secretion
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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