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  • Mice  (9)
  • 1995-1999  (9)
  • 1965-1969
  • 1945-1949
  • 1940-1944
  • 1
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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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
    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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    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
    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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    Activation of RET as a dominant transforming gene by germline mutations of MEN2A and MEN2B (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-01-20
    Description: Multiple endocrine neoplasia types 2A and 2B (MEN2A and MEN2B) and familial medullary thyroid carcinoma are dominantly inherited cancer syndromes. All three syndromes are associated with mutations in RET, which encodes a receptor-like tyrosine kinase. The altered RET alleles were shown to be transforming genes in NIH 3T3 cells as a consequence of constitutive activation of the RET kinase. The MEN2A mutation resulted in RET dimerization at steady state, whereas the MEN2B mutation altered RET catalytic properties both quantitatively and qualitatively. Oncogenic conversion of RET in these neoplastic syndromes establishes germline transmission of dominant transforming genes in human cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santoro, M -- Carlomagno, F -- Romano, A -- Bottaro, D P -- Dathan, N A -- Grieco, M -- Fusco, A -- Vecchio, G -- Matoskova, B -- Kraus, M H -- New York, N.Y. -- Science. 1995 Jan 20;267(5196):381-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centro di Endocrinologia ed Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (CNR), Napoli, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7824936" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Alleles ; Animals ; Cell Transformation, Neoplastic/*genetics ; *Drosophila Proteins ; Genetic Vectors ; Humans ; Mice ; Multiple Endocrine Neoplasia Type 2a/*genetics ; Multiple Endocrine Neoplasia Type 2b/*genetics ; Mutation ; Phosphorylation ; Proto-Oncogene Proteins/chemistry/*genetics/metabolism ; Proto-Oncogene Proteins c-ret ; *Proto-Oncogenes ; Receptor Protein-Tyrosine Kinases/chemistry/*genetics/metabolism ; Substrate Specificity ; Transfection ; 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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  • 5
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    Fibroblasts as efficient antigen-presenting cells in lymphoid organs (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-02
    Description: Only so-called "professional" antigen-presenting cells (APCs) of hematopoietic origin are believed capable of inducing T lymphocyte responses. However, fibroblasts transfected with viral proteins directly induced antiviral cytotoxic T lymphocyte responses in vivo, without involvement of host APCs. Fibroblasts induced T cells only in the milieu of lymphoid organs. Thus, antigen localization affects self-nonself discrimination and cell-based vaccine strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kundig, T M -- Bachmann, M F -- DiPaolo, C -- Simard, J J -- Battegay, M -- Lother, H -- Gessner, A -- Kuhlcke, K -- Ohashi, P S -- Hengartner, H -- New York, N.Y. -- Science. 1995 Jun 2;268(5215):1343-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Experimental Immunology, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7761853" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/*immunology ; Cytotoxicity, Immunologic ; Fibroblasts/*immunology ; Glycoproteins/immunology ; Histocompatibility Antigens Class I/immunology ; L Cells (Cell Line) ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic choriomeningitis virus/*immunology ; Lymphoid Tissue/*immunology ; Mice ; Mice, Inbred C57BL ; Neoplasms/immunology ; T-Lymphocytes, Cytotoxic/*immunology ; Transfection ; Tumor Cells, Cultured ; Viral Proteins/*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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  • 6
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    Massive cell death of immature hematopoietic cells and neurons in Bcl-x-deficient mice (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-10
    Description: bcl-x is a member of the bcl-2 gene family, which may regulate programmed cell death. Mice were generated that lacked Bcl-x. The Bcl-x-deficient mice died around embryonic day 13. Extensive apoptotic cell death was evident in postmitotic immature neurons of the developing brain, spinal cord, and dorsal root ganglia. Hematopoietic cells in the liver were also apoptotic. Analyses of bcl-x double-knockout chimeric mice showed that the maturation of Bcl-x-deficient lymphocytes was diminished. The life-span of immature lymphocytes, but not mature lymphocytes, was shortened. Thus, Bcl-x functions to support the viability of immature cells during the development of the nervous and hematopoietic systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Motoyama, N -- Wang, F -- Roth, K A -- Sawa, H -- Nakayama, K -- Negishi, I -- Senju, S -- Zhang, Q -- Fujii, S -- New York, N.Y. -- Science. 1995 Mar 10;267(5203):1506-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, 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/7878471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Bone Marrow Cells ; Brain/cytology/embryology ; Cell Differentiation ; Cell Survival ; Cells, Cultured ; Ganglia, Spinal/cytology/embryology ; Hematopoietic Stem Cells/*cytology ; Liver/cytology/embryology ; Lymphocytes/*cytology ; Mice ; Mice, Knockout ; Nerve Degeneration ; Neurons/*cytology ; Proto-Oncogene Proteins/deficiency/*physiology ; *Proto-Oncogene Proteins c-bcl-2 ; Spinal Cord/cytology/embryology ; Transfection ; bcl-X Protein
    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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  • 7
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    Deregulated T cell activation and autoimmunity in mice lacking interleukin-2 receptor beta (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-09
    Description: In mice lacking the interleukin-2 receptor beta chain (IL-2R beta), T cells were shown to be spontaneously activated, resulting in exhaustive differentiation of B cells into plasma cells and the appearance of high serum concentrations of immunoglobulins G1 and E as well as autoantibodies that cause hemolytic anemia. Marked infiltrative granulocytopoiesis was also apparent, and the animals died after about 12 weeks. Depletion of CD4+ T cells in mutant mice rescued B cells without reversion of granulocyte abnormalities. T cells did not proliferate in response to polyclonal activators, nor could antigen-specific immune responses be elicited. Thus, IL-2R beta is required to keep the activation programs of T cells under control, to maintain homeostasis, and to prevent autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzuki, H -- Kundig, T M -- Furlonger, C -- Wakeham, A -- Timms, E -- Matsuyama, T -- Schmits, R -- Simard, J J -- Ohashi, P S -- Griesser, H -- New York, N.Y. -- Science. 1995 Jun 9;268(5216):1472-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen Institute, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7770771" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantibodies/blood ; *Autoimmunity ; B-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/immunology ; Female ; Heterozygote ; Homozygote ; Lymph Nodes/immunology ; *Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Nude ; Mutagenesis, Insertional ; Myeloproliferative Disorders/immunology ; Receptors, Interleukin-2/genetics/*physiology ; Signal Transduction ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/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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  • 8
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    Targeted disruption of mouse EGF receptor: effect of genetic background on mutant phenotype (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-07-14
    Description: Gene targeting was used to create a null allele at the epidermal growth factor receptor locus (Egfr). The phenotype was dependent on genetic background. EGFR deficiency on a CF-1 background resulted in peri-implantation death due to degeneration of the inner cell mass. On a 129/Sv background, homozygous mutants died at mid-gestation due to placental defects; on a CD-1 background, the mutants lived for up to 3 weeks and showed abnormalities in skin, kidney, brain, liver, and gastrointestinal tract. The multiple abnormalities associated with EGFR deficiency indicate that the receptor is involved in a wide range of cellular activities.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Threadgill, D W -- Dlugosz, A A -- Hansen, L A -- Tennenbaum, T -- Lichti, U -- Yee, D -- LaMantia, C -- Mourton, T -- Herrup, K -- Harris, R C -- GM14630/GM/NIGMS NIH HHS/ -- HD07104/HD/NICHD NIH HHS/ -- HD26722/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 Jul 14;269(5221):230-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Case Western Reserve University, Cleveland, OH 44106-4955, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7618084" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Multiple/*genetics ; Animals ; Base Sequence ; Brain/abnormalities/cytology ; Cell Division ; Digestive System/cytology ; Digestive System Abnormalities ; *Embryonic and Fetal Development ; Female ; *Gene Targeting ; Hair/abnormalities ; Homozygote ; Kidney/cytology ; Lung/cytology ; Male ; Mice ; Molecular Sequence Data ; Mutation ; Phenotype ; Receptor, Epidermal Growth Factor/deficiency/*genetics/*physiology ; Skin/cytology ; Skin Abnormalities
    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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  • 9
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    Inactivation of the type II TGF-beta receptor in colon cancer cells with microsatellite instability (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-02
    Description: Transforming growth factor-beta (TGF-beta) is a potent inhibitor of epithelial cell growth. Human colon cancer cell lines with high rates of microsatellite instability were found to harbor mutations in the type II TGF-beta receptor (RII) gene. Eight such examples, due to three different mutations, were identified. The mutations were clustered within small repeated sequences in the RII gene, were accompanied by the absence of cell surface RII receptors, and were usually associated with small amounts of RII transcript. RII mutation, by inducing the escape of cells from TGF-beta-mediated growth control, links DNA repair defects with a specific pathway of tumor progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Markowitz, S -- Wang, J -- Myeroff, L -- Parsons, R -- Sun, L -- Lutterbaugh, J -- Fan, R S -- Zborowska, E -- Kinzler, K W -- Vogelstein, B -- CA38173/CA/NCI NIH HHS/ -- CA50457/CA/NCI NIH HHS/ -- CA63480/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 Jun 2;268(5215):1336-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University Hospitals of Cleveland, OH, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7761852" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Colonic Neoplasms/*genetics/metabolism/pathology ; Colorectal Neoplasms, Hereditary Nonpolyposis/*genetics/metabolism/pathology ; DNA Repair ; DNA, Neoplasm/genetics ; DNA, Satellite/*genetics ; Disease Progression ; Frameshift Mutation ; Humans ; Mice ; Molecular Sequence Data ; Neoplasm Transplantation ; Phenotype ; RNA, Messenger/genetics ; Receptors, Transforming Growth Factor beta/*genetics/metabolism ; Repetitive Sequences, Nucleic Acid ; Sequence Deletion ; Transforming Growth Factor beta/metabolism ; 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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