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  • 1
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    Age-associated inclusions in normal and transgenic mouse brain (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jucker, M -- Walker, L C -- Martin, L J -- Kitt, C A -- Kleinman, H K -- Ingram, D K -- Price, D L -- New York, N.Y. -- Science. 1992 Mar 13;255(5050):1443-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1542796" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*metabolism ; Amyloid beta-Peptides/*metabolism ; Animals ; Brain/*metabolism ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic/*metabolism
    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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    The prevention of thymic lymphomas in transgenic mice by human O6-alkylguanine-DNA alkyltransferase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-08
    Description: Nitrosoureas form O6-alkylguanine-DNA adducts that are converted to G to A transitions, the mutation found in the activated ras oncogenes of nitrosourea-induced mouse lymphomas and rat mammary tumors. These adducts are removed by the DNA repair protein O6-alkylguanine-DNA alkyltransferase. Transgenic mice that express the human homolog of this protein in the thymus were found to be protected from developing thymic lymphomas after exposure to N-methyl-N-nitrosourea. Thus, transgenic expression of a single human DNA repair gene is sufficient to block chemical carcinogenesis. The transduction of DNA repair genes in vivo may unravel mechanisms of carcinogenesis and provide therapeutic protection from known carcinogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dumenco, L L -- Allay, E -- Norton, K -- Gerson, S L -- P01CA51183/CA/NCI NIH HHS/ -- P30CA43703/CA/NCI NIH HHS/ -- R01ES06288/ES/NIEHS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Jan 8;259(5092):219-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University Hospitals of Cleveland, OH.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8421782" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *DNA Repair/genetics ; Gene Expression ; Humans ; Lymphoma, T-Cell/chemically induced/*prevention & control ; Methylnitrosourea ; Methyltransferases/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; O(6)-Methylguanine-DNA Methyltransferase ; RNA, Messenger/analysis ; Thymus Neoplasms/chemically induced/*prevention & control
    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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    Activation-induced ubiquitination of the T cell antigen receptor (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-07
    Description: The zeta subunit of the T cell antigen receptor (TCR) exists primarily as a disulfide-linked homodimer. This receptor subunit is important in TCR-mediated signal transduction and is a substrate for a TCR-activated protein tyrosine kinase. The zeta chain was found to undergo ubiquitination in response to receptor engagement. This posttranslational modification occurred in normal T cells and tumor lines. Both nonphosphorylated and phosphorylated zeta molecules were modified, and at least one other TCR subunit, CD3 delta, was also ubiquitinated after activation of the receptor. These findings suggest an expanded role for ubiquitination in transmembrane receptor function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cenciarelli, C -- Hou, D -- Hsu, K C -- Rellahan, B L -- Wiest, D L -- Smith, H T -- Fried, V A -- Weissman, A M -- New York, N.Y. -- Science. 1992 Aug 7;257(5071):795-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1323144" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3 ; Antigens, Differentiation, T-Lymphocyte/immunology/metabolism ; Cells, Cultured ; Hybridomas/immunology ; Lymphocyte Activation/*physiology ; Macromolecular Substances ; Mice ; Mice, Inbred C57BL ; Molecular Weight ; *Protein Processing, Post-Translational ; Receptors, Antigen, T-Cell/immunology/isolation & purification/*metabolism ; Spleen/immunology ; T-Lymphocytes/*immunology ; Ubiquitins/isolation & purification/*metabolism
    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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    Multiple intestinal neoplasia caused by a mutation in the murine homolog of the APC gene (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-01
    Description: Germ-line mutations of the APC gene are responsible for familial adenomatous polyposis (FAP), an autosomal dominantly inherited disease in humans. Patients with FAP develop multiple benign colorectal tumors. Recently, a mouse lineage that exhibits an autosomal dominantly inherited predisposition to multiple intestinal neoplasia (Min) was described. Linkage analysis showed that the murine homolog of the APC gene (mApc) was tightly linked to the Min locus. Sequence comparison of mApc between normal and Min-affected mice identified a nonsense mutation, which cosegregated with the Min phenotype. This mutation is analogous to those found in FAP kindreds and in sporadic colorectal cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, L K -- Kinzler, K W -- Vogelstein, B -- Preisinger, A C -- Moser, A R -- Luongo, C -- Gould, K A -- Dove, W F -- CA-06973/CA/NCI NIH HHS/ -- CA-07175/CA/NCI NIH HHS/ -- CA-23076/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 May 1;256(5057):668-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics Laboratory, Johns Hopkins University School of Medicine, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1350108" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli/*genetics ; Animals ; Base Sequence ; Blotting, Southern ; Colorectal Neoplasms/genetics ; DNA, Neoplasm/chemistry/genetics ; *Genes, Tumor Suppressor ; Genetic Linkage ; Humans ; Intestinal Neoplasms/*genetics ; Mice ; Mice, Inbred AKR ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Molecular Sequence Data ; *Mutation ; Phenotype ; Polymorphism, Restriction Fragment Length ; Sequence Homology, Nucleic Acid
    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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  • 5
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Helper T cells without CD4: control of leishmaniasis in CD4-deficient mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: Expression of either the CD4 or CD8 glycoproteins discriminates two functionally distinct lineages of T lymphocytes. A null mutation in the gene encoding CD4 impairs the development of the helper cell lineage that is normally defined by CD4 expression. Infection of CD4-null mice with Leishmania has revealed a population of functional helper T cells that develops despite the absence of CD4. These CD8- alpha beta T cell receptor+ T cells are major histocompatibility complex class II-restricted and produce interferon-gamma when challenged with parasite antigens. These results indicate that T lymphocyte lineage commitment and peripheral function need not depend on the function of CD4.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Locksley, R M -- Reiner, S L -- Hatam, F -- Littman, D R -- Killeen, N -- AI30663/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1448-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco 94143-0654.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8367726" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/genetics/*immunology ; Antigens, CD8/immunology ; Antigens, Protozoan/immunology ; B-Lymphocytes/immunology ; Base Sequence ; CD4-CD8 Ratio ; Histocompatibility Antigens Class II/immunology ; Hypersensitivity, Delayed ; Interferon-gamma/biosynthesis/immunology ; Leishmania tropica/*immunology ; Leishmaniasis, Cutaneous/*immunology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Oligodeoxyribonucleotides ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; T-Lymphocytes/immunology ; T-Lymphocytes, Helper-Inducer/*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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  • 8
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    Atherosclerosis in transgenic mice overexpressing apolipoprotein A-II (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-23
    Description: Concentrations of plasma high density lipoprotein (HDL) are inversely correlated with atherosclerotic coronary artery disease. The two most abundant protein constituents of HDL are apolipoproteins A-I and A-II (apoA-I and apoA-II). ApoA-I is required for assembly of HDL and, when overexpressed in transgenic mice, confers resistance to early atherosclerosis. The present studies reveal that transgenic mice that overexpress mouse apoA-II had elevated HDL-cholesterol concentrations but, nevertheless, exhibited increased atherosclerotic lesion development as compared to normal mice. The HDL in the transgenic mice was larger and had an increased ratio of apoA-II to apoA-I. Thus, both the composition and amount of HDL appear to be important determinants of atherosclerosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warden, C H -- Hedrick, C C -- Qiao, J H -- Castellani, L W -- Lusis, A J -- HL-07386/HL/NHLBI NIH HHS/ -- HL-28481/HL/NHLBI NIH HHS/ -- HL-42488/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 23;261(5120):469-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8332912" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoprotein A-I/physiology ; Apolipoprotein A-II/genetics/*physiology ; Arteriosclerosis/*blood/genetics ; Cholesterol/blood ; Crosses, Genetic ; Female ; Lipoproteins, HDL/blood/chemistry ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Transgenic
    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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    LCMV-specific, class II-restricted cytotoxic T cells in beta 2-microglobulin-deficient mice (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-20
    Description: Intracranial infection of normal mice with lymphocytic choriomeningitis virus (LCMV) causes meningitis and death mediated by CD8+ major histocompatibility complex (MHC) class I-restricted cytotoxic T lymphocytes (CTLs). beta 2-Microglobulin-deficient mice (beta 2M-/-) do not express functional MHC class I proteins and do not produce significant numbers of CD8+ T cells. When beta 2M-/- mice were infected with LCMV, many died from LCMV disease and produced a specific response to LCMV mediated by CD4+ CTLs that were class II-restricted. In these mice, CD4+ CTLs may compensate for the lack of CD8+ CTLs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, D -- Koller, B H -- Whitton, J L -- LaPan, K E -- Brigman, K K -- Frelinger, J A -- AI-20288/AI/NIAID NIH HHS/ -- AI-29324/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 Mar 20;255(5051):1576-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of North Carolina, Chapel Hill 27599.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1347959" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD8/immunology ; CD4-Positive T-Lymphocytes/immunology ; Cytotoxicity, Immunologic ; H-2 Antigens/immunology ; Histocompatibility Antigens Class II/*immunology ; Lymphocyte Depletion ; Lymphocytic Choriomeningitis/*immunology ; Lymphocytic choriomeningitis virus ; Mice ; Mice, Inbred C57BL ; Spleen/immunology ; T-Lymphocytes, Cytotoxic/*immunology ; beta 2-Microglobulin/*deficiency
    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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  • 10
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    Transforming growth factor-beta in leishmanial infection: a parasite escape mechanism (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-24
    Description: The course of infection with the protozoan parasite Leishmania is determined in part by their early replication in macrophages, the exclusive host cells for these organisms. Although factors contributing to the survival of Leishmania are not well understood, cytokines influence the course of infection. Transforming growth factor-beta (TGF-beta) is a multipotential cytokine with diverse effects on cells of the immune system, including down-regulation of certain macrophage functions. Leishmanial infection induced the production of active TGF-beta, both in vitro and in vivo. TGF-beta was important for determining in vivo susceptibility to experimental leishmanial infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barral-Netto, M -- Barral, A -- Brownell, C E -- Skeiky, Y A -- Ellingsworth, L R -- Twardzik, D R -- Reed, S G -- AI-16282/AI/NIAID NIH HHS/ -- AI-25038/AI/NIAID NIH HHS/ -- TW-00018/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 24;257(5069):545-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Federal University of Bahia School of Medicine, Brazil.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1636092" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/genetics ; Animals ; Base Sequence ; Disease Susceptibility ; Interferon-gamma/genetics ; Interleukin-4/genetics ; Leishmania/pathogenicity/physiology ; Leishmaniasis, Cutaneous/immunology/pathology/*physiopathology ; Macrophages/drug effects/parasitology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction/methods ; Transforming Growth Factor beta/genetics/pharmacology/*physiology
    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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