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  • Mice  (184)
  • American Association for the Advancement of Science (AAAS)  (184)
  • American Institute of Physics (AIP)
  • MDPI Publishing
  • 1995-1999  (184)
  • 1996  (184)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (184)
  • American Institute of Physics (AIP)
  • MDPI Publishing
  • Springer  (1)
Years
  • 1995-1999  (184)
Year
  • 101
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    Presynaptic long-term depression at the hippocampal mossy fiber-CA3 synapse (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-02
    Description: Long-term potentiation (LTP) and long-term depression (LTD) of synaptic strength may underlie learning and memory in the brain. The induction of LTP occurs in postsynaptic cells in the hippocampal CA1 region but is presynaptic in CA3. LTD is also well characterized in CA1 but not in CA3. Low-frequency stimulation of mouse hippocampal slices caused homosynaptic LTD at the mossy fiber-CA3 synapse, which may be induced presynaptically by activation of metabotropic glutamate receptors. Thus, the efficacy of mossy fiber-CA3 synapses can be regulated bidirectionally, which may contribute to neuronal information processing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kobayashi, K -- Manabe, T -- Takahashi, T -- New York, N.Y. -- Science. 1996 Aug 2;273(5275):648-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Institute for Brain Research, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662556" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Axons/*physiology ; Benzoates/pharmacology ; Calcium Channel Blockers/pharmacology ; Calcium Channels/physiology ; Electric Stimulation ; Excitatory Amino Acid Antagonists/pharmacology ; Glycine/analogs & derivatives/pharmacology ; Hippocampus/*physiology ; In Vitro Techniques ; Long-Term Potentiation ; Mice ; Mice, Inbred ICR ; *Neuronal Plasticity/drug effects ; Nicardipine/pharmacology ; Pyramidal Cells/*physiology ; Receptors, Metabotropic Glutamate/antagonists & inhibitors/*physiology ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/physiology ; Synapses/*physiology ; Synaptic Transmission/drug effects
    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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  • 102
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    Ironing out the wrinkles in the prion strain problem (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grady, D -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2010.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8984659" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry ; Creutzfeldt-Jakob Syndrome/metabolism ; Humans ; Mice ; Mice, Transgenic ; Prion Diseases/*etiology/metabolism/transmission ; Prions/*chemistry/genetics ; *Protein Conformation ; *Protein Folding
    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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  • 103
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    Independent modes of natural killing distinguished in mice lacking Lag3 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-19
    Description: The LAG3 protein has several features in common with CD4, suggesting that it may be important in controlling T cell reactivity. However, mice with a Lag3 null mutation have now been shown to exhibit a defect in the natural killer cell, rather than the T cell, compartment. Killing of certain tumor targets by natural killer cells from these mice was inhibited or even abolished, whereas lysis of cells displaying major histocompatibility complex class I disparities remained intact. It appears that LAG3 is a receptor or coreceptor that defines different modes of natural killing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyazaki, T -- Dierich, A -- Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1996 Apr 19;272(5260):405-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire (INSERM, CNRS, ULP), Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8602528" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, CD ; B-Lymphocytes/immunology ; Base Sequence ; *Cytotoxicity, Immunologic ; Female ; Histocompatibility Antigens Class I/immunology ; Killer Cells, Natural/*immunology ; Male ; Membrane Proteins/genetics/*physiology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Phenotype ; T-Lymphocytes/immunology ; Tumor Cells, Cultured ; beta 2-Microglobulin/deficiency/physiology
    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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  • 104
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    Receptor tails unlock developmental checkpoints for B lymphocytes (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roth, P E -- DeFranco, A L -- New York, N.Y. -- Science. 1996 Jun 21;272(5269):1752-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of California, San Francisco-Hooper Foundation, 94143, USA. proth@itsa.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650572" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Formation ; Antigens, CD/*physiology ; Antigens, CD79 ; B-Lymphocytes/*cytology/*immunology ; Gene Rearrangement, B-Lymphocyte ; Gene Targeting ; Genes, Immunoglobulin ; Mice ; Receptors, Antigen, B-Cell/*physiology ; Signal Transduction
    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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  • 105
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    Mutant enzyme provides new insights into the cause of ALS (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1996 Jan 26;271(5248):446-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8560253" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/*enzymology/genetics/pathology ; Animals ; Apoptosis ; Cells, Cultured ; Free Radicals ; Humans ; Lipid Peroxidation ; Mice ; Mutation ; Neurons/cytology ; Nitrates/metabolism ; Peroxidases/metabolism ; Selenium/administration & dosage ; Superoxide Dismutase/genetics/*metabolism ; Vitamin E/administration & dosage/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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  • 106
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    Somatic mutation of immunoglobulin V genes in vitro (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: The molecular mechanism behind affinity maturation is the introduction of point mutations in immunoglobulin (Ig) V genes, followed by the selective proliferation of B cells expressing mutants with increased affinity for antigen. An in vitro culture system was developed in which somatic hypermutation of Ig V genes was sustained in primed B cells. Cognate T cell help and cross-linking of the surface Ig were required, whereas the addition of lipopolysaccharide or a CD40 ligand to drive proliferation was insufficient. This system should facilitate understanding of the molecular and cellular mechanisms that regulate somatic mutation and B cell selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kallberg, E -- Jainandunsing, S -- Gray, D -- Leanderson, T -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1285-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Unit, Lund University, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638111" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD40 ; B-Lymphocytes/*immunology ; Base Sequence ; CD40 Ligand ; Cells, Cultured ; Coculture Techniques ; *Genes, Immunoglobulin ; Haptens/immunology ; Hybridomas ; Immunoglobulin Variable Region/*genetics ; Lipopolysaccharides/pharmacology ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; *Mutation ; Ovalbumin/immunology ; Oxazolone/analogs & derivatives/immunology ; Receptors, Antigen, B-Cell/immunology ; Th2 Cells/immunology ; Transfection
    Print ISSN: 0036-8075
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  • 107
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    Impaired defense of intestinal mucosa in mice lacking intestinal trefoil factor (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-11
    Description: The mechanisms that maintain the epithelial integrity of the gastrointestinal tract remain largely undefined. The gene encoding intestinal trefoil factor (ITF), a protein secreted throughout the small intestine and colon, was rendered nonfunctional in mice by targeted disruption. Mice lacking ITF had impaired mucosal healing and died from extensive colitis after oral administration of dextran sulfate sodium, an agent that causes mild epithelial injury in wild-type mice. ITF-deficient mice manifested poor epithelial regeneration after injury. These findings reveal a central role for ITF in the maintenance and repair of the intestinal mucosa.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mashimo, H -- Wu, D C -- Podolsky, D K -- Fishman, M C -- P30DK43351/DK/NIDDK NIH HHS/ -- R01DK46906/DK/NIDDK NIH HHS/ -- T32DK07191/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Oct 11;274(5285):262-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Jackson 7, Massachusetts General Hospital, Fruit Street, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8824194" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Movement ; Colitis/etiology/pathology ; Colon/drug effects/pathology/physiology ; Dextran Sulfate/pharmacology ; Gene Targeting ; Growth Substances/genetics/pharmacology/*physiology ; Intestinal Mucosa/drug effects/pathology/*physiology ; Mice ; Molecular Sequence Data ; *Mucins ; *Muscle Proteins ; *Neuropeptides ; Peptides/genetics/pharmacology/*physiology ; Recombinant Proteins/pharmacology
    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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  • 108
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    Trefoil peptides: less clandestine in the intestine (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chinery, R -- Coffey, R J -- New York, N.Y. -- Science. 1996 Oct 11;274(5285):204.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Vanderbilt University, Nashville, TN 37232-2279, USA. coffeyrj@ctrvax.vanderbilt.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8927980" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gastric Mucosa/*physiology ; Gene Deletion ; Gene Targeting ; Growth Substances/chemistry/genetics/*physiology ; Humans ; Intestinal Mucosa/*physiology ; Mice ; *Mucins ; *Muscle Proteins ; Neoplasm Proteins/chemistry/genetics/*physiology ; *Neuropeptides ; Peptides/chemistry/genetics/*physiology ; *Proteins ; Tumor Suppressor Proteins
    Print ISSN: 0036-8075
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  • 109
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    A role for endothelial NO synthase in LTP revealed by adenovirus-mediated inhibition and rescue (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-06
    Description: Pharmacological studies support the idea that nitric oxide (NO) serves as a retrograde messenger during long-term potentiation (LTP) in area CA1 of the hippocampus. Mice with a defective form of the gene for neuronal NO synthase (nNOS), however, exhibit normal LTP. The myristoyl protein endothelial NOS (eNOS) is present in the dendrites of CA1 neurons. Recombinant adenovirus vectors containing either a truncated eNOS (a putative dominant negative) or an eNOS fused to a transmembrane protein were used to demonstrate that membrane-targeted eNOS is required for LTP. The membrane localization of eNOS may optimally position the enzyme both to respond to Ca2+ influx and to release NO into the extracellular space during LTP induction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kantor, D B -- Lanzrein, M -- Stary, S J -- Sandoval, G M -- Smith, W B -- Sullivan, B M -- Davidson, N -- Schuman, E M -- 49176/PHS HHS/ -- NS37292/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 6;274(5293):1744-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology 216-76, California Institute of Technology, Pasadena, CA 91125, USA. schumane@cco.caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8939872" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Animals ; CHO Cells ; Cell Membrane/enzymology ; Cricetinae ; Cytosol/enzymology ; Endothelium/*enzymology ; Genetic Vectors ; Hippocampus/*physiology ; In Vitro Techniques ; *Long-Term Potentiation/drug effects ; Mice ; Myristic Acid ; Myristic Acids/metabolism/pharmacology ; Neurons/*physiology ; Nitric Oxide Synthase/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Synaptic Transmission ; 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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  • 110
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    Molecular mimicry of human cytokine and cytokine response pathway genes by KSHV (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-06
    Description: Four virus proteins similar to two human macrophage inflammatory protein (MIP) chemokines, interleukin-6 (IL-6), and interferon regulatory factor (IRF) are encoded by the Kaposi's sarcoma-associated herpesvirus (KSHV) genome. vIL-6 was functional in B9 proliferation assays and primarily expressed in KSHV-infected hematopoietic cells rather than KS lesions. HIV-1 transmission studies showed that vMIP-I is similar to human MIP chemokines in its ability to inhibit replication of HIV-1 strains dependent on the CCR5 co-receptor. These viral genes may form part of the response to host defenses contributing to virus-induced neoplasia and may have relevance to KSHV and HIV-I interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, P S -- Boshoff, C -- Weiss, R A -- Chang, Y -- CA67391/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 6;274(5293):1739-44.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Public Health, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8939871" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Division ; Cell Line ; Chemokine CCL4 ; Gene Expression ; Genes, Viral ; HIV-1/physiology ; Herpesvirus 4, Human/physiology ; Herpesvirus 8, Human/*genetics/physiology ; Humans ; Interleukin-6/chemistry/genetics ; Lymph Nodes/virology ; Lymphoma, B-Cell/virology ; Macrophage Inflammatory Proteins/chemistry/genetics ; Mice ; *Molecular Mimicry ; Molecular Sequence Data ; Receptors, CCR5 ; Receptors, Cytokine/metabolism ; Receptors, HIV/metabolism ; Sarcoma, Kaposi/virology ; Sequence Alignment ; Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; Tumor Cells, Cultured ; Viral Nonstructural Proteins/chemistry/*genetics/physiology ; Virus Replication
    Print ISSN: 0036-8075
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  • 111
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    Markers on distal chromosome 2q linked to insulin-dependent diabetes mellitus (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-21
    Description: Insulin-dependent diabetes mellitus (IDDM) is a multigenic autoimmune disease. An IDDM susceptibility gene was mapped to chromosome 2q34. This gene may act early in diabetogenesis, because "preclinical" individuals also showed linkage. Human leukocyte antigen (HLA)-disparate, but not HLA-identical, sibs showed linkage, which was even stronger in families with affected females. The genes encoding insulin-like growth factor-binding proteins 2 and 5 were mapped to a 4-megabase pair interval near this locus. These results indicate the existence of a gene that acts at an early stage in IDDM development, screening for which may identify a specific subset of at-risk individuals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morahan, G -- Huang, D -- Tait, B D -- Colman, P G -- Harrison, L C -- New York, N.Y. -- Science. 1996 Jun 21;272(5269):1811-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia. morahan@wehi.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650584" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Autoantibodies/analysis ; Chromosome Mapping ; Chromosomes, Human, Pair 2/*genetics ; Diabetes Mellitus, Type 1/*genetics ; Female ; Gene Frequency ; *Genetic Linkage ; *Genetic Markers ; Genetic Predisposition to Disease ; HLA Antigens/genetics ; Humans ; Insulin-Like Growth Factor Binding Protein 2/genetics ; Insulin-Like Growth Factor Binding Protein 5/genetics ; Islets of Langerhans/immunology ; Male ; Mice ; Mice, Inbred NOD/genetics ; Microsatellite Repeats
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  • 112
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    Induction of bystander T cell proliferation by viruses and type I interferon in vivo (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-28
    Description: T cell proliferation in vivo is presumed to reflect a T cell receptor (TCR)-mediated polyclonal response directed to various environmental antigens. However, the massive proliferation of T cells seen in viral infections is suggestive of a bystander reaction driven by cytokines instead of the TCR. In mice, T cell proliferation in viral infections preferentially affected the CD44hi subset of CD8+ cells and was mimicked by injection of polyinosinic-polycytidylic acid [poly(I:C)], an inducer of type I interferon (IFN I), and also by purified IFN I; such proliferation was not associated with up-regulation of CD69 or CD25 expression, which implies that TCR signaling was not involved. IFN I [poly(I:C)]-stimulated CD8+ cells survived for prolonged periods in vivo and displayed the same phenotype as did long-lived antigen-specific CD8+ cells. IFN I also potentiated the clonal expansion and survival of CD8+ cells responding to specific antigen. Production of IFN I may thus play an important role in the generation and maintenance of specific memory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tough, D F -- Borrow, P -- Sprent, J -- AI21487/AI/NIAID NIH HHS/ -- CA25803/CA/NCI NIH HHS/ -- CA38355/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Jun 28;272(5270):1947-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658169" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/analysis ; Antigens, CD44/analysis ; Antigens, Differentiation, T-Lymphocyte/analysis ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/cytology/*immunology ; Cell Division ; Cell Survival ; Immunologic Memory ; Immunophenotyping ; Interferon Type I/*immunology/pharmacology ; Lectins, C-Type ; *Lymphocyte Activation ; Lymphocytic Choriomeningitis/*immunology ; Lymphocytic choriomeningitis virus/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Poly I-C/pharmacology ; Receptors, Antigen, T-Cell/immunology ; Receptors, Interleukin-2/analysis
    Print ISSN: 0036-8075
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  • 113
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    Aberrant B cell development and immune response in mice with a compromised BCR complex (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-21
    Description: The immunoglobulin alpha (Ig-alpha)-Ig-beta heterodimer is the signaling component of the antigen receptor complex on B cells (BCR) and B cell progenitors (pre-BCR). A mouse mutant that lacks most of the Ig-alpha cytoplasmic tail exhibits only a small impairment in early B cell development but a severe block in the generation of the peripheral B cell pool, revealing a checkpoint in B cell maturation that ensures the expression of a functional BCR on mature B cells. B cells that do develop demonstrate a differential dependence on Ig-alpha signaling in antibody responses such that a signaling-competent Ig-alpha appears to be critical for the response to T-independent, but not T-dependent, antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Torres, R M -- Flaswinkel, H -- Reth, M -- Rajewsky, K -- New York, N.Y. -- Science. 1996 Jun 21;272(5269):1804-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650582" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Formation ; Antigens/immunology ; Antigens, CD/chemistry/immunology/*physiology ; Antigens, CD79 ; Antigens, T-Independent/immunology ; B-Lymphocytes/*cytology/*immunology ; Bone Marrow Cells ; Cell Lineage ; Gene Rearrangement, B-Lymphocyte ; Gene Targeting ; Genes, Immunoglobulin ; Hematopoietic Stem Cells/cytology/immunology ; Lymphoid Tissue/cytology/immunology ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, B-Cell/chemistry/immunology/*physiology ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 114
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    Genetic susceptibility to Leishmania: IL-12 responsiveness in TH1 cell development (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-16
    Description: The genetic background of T lymphocytes influences development of the T helper (TH) phenotype, resulting in either resistance or susceptibility of certain mouse strains to pathogens such as Leishmania major. With an in vitro model system, a difference in maintenance of responsiveness of T cells to interleukin-12 (IL-12) was detected between BALB/c and B10.D2 mice. Although naive T cells from both strains initially responded to IL-12, BALB/c T cells lost IL-12 responsiveness after stimulation with antigen in vitro, even when cocultured with B10.D2 T cells. Thus, susceptibility of BALB/c mice to infection with L. major may derive from the loss of the ability to generate IL-12-induced TH1 responses rather than from an IL-4-induced TH2 response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guler, M L -- Gorham, J D -- Hsieh, C S -- Mackey, A J -- Steen, R G -- Dietrich, W F -- Murphy, K M -- AI31238/AI/NIAID NIH HHS/ -- AI34580/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 16;271(5251):984-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8584935" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Coculture Techniques ; Genetic Predisposition to Disease ; Immunity, Innate/genetics ; Interferon-gamma/biosynthesis ; Interleukin-12/*pharmacology ; Interleukin-4/biosynthesis ; Leishmania major/*immunology ; Leishmaniasis, Cutaneous/*immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Phenotype ; Receptors, Interleukin-2/biosynthesis ; Signal Transduction ; Th1 Cells/*immunology ; Th2 Cells/immunology
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    Mouse model for pregnancy problem? (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gura, T -- New York, N.Y. -- Science. 1996 Nov 8;274(5289):922.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966572" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/metabolism ; Angiotensinogen/genetics/metabolism ; Animals ; Blood Pressure ; Crosses, Genetic ; *Disease Models, Animal ; Female ; Humans ; *Hypertension/physiopathology ; Male ; Mice ; Mice, Transgenic ; Placenta/metabolism ; Pregnancy ; *Pregnancy Complications, Cardiovascular/physiopathology ; Renin/genetics/metabolism
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    The cytolytic P2Z receptor for extracellular ATP identified as a P2X receptor (P2X7) (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-03
    Description: The P2Z receptor is responsible for adenosine triphosphate (ATP)-dependent lysis of macrophages through the formation of membrane pores permeable to large molecules. Other ATP-gated channels, the P2X receptors, are permeable only to small cations. Here, an ATP receptor, the P2X7 receptor, was cloned from rat brain and exhibited both these properties. This protein is homologous to other P2X receptors but has a unique carboxyl-terminal domain that was required for the lytic actions of ATP. Thus, the P2X7 (or P2Z) receptor is a bifunctional molecule that could function in both fast synaptic transmission and the ATP-mediated lysis of antigen-presenting cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Surprenant, A -- Rassendren, F -- Kawashima, E -- North, R A -- Buell, G -- New York, N.Y. -- Science. 1996 May 3;272(5262):735-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Glaxo Institute for Molecular Biology, Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614837" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/analogs & derivatives/*metabolism/pharmacology ; Amino Acid Sequence ; Animals ; Base Sequence ; Cations, Divalent/pharmacology ; Cell Death ; Cell Line ; Cloning, Molecular ; DNA, Complementary/genetics ; Electric Conductivity ; Humans ; Ion Channels/physiology ; Mice ; Molecular Sequence Data ; Patch-Clamp Techniques ; Rats ; Receptors, Purinergic P2/chemistry/genetics/*physiology ; Receptors, Purinergic P2X7 ; Transfection
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    CNS gene encoding astrotactin, which supports neuronal migration along glial fibers (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-04-19
    Description: Vertebrate central nervous system (CNS) histogenesis depends on glia-guided migration of postmitotic neurons to form neuronal laminae. Previous studies have established that the neuronal protein astrotactin functions in murine cerebellar granule cell migration in vitro. The gene encoding astrotactin predicts a protein with three epidermal growth factor repeats and two fibronectin type III repeats. Astrotactin messenger RNA is expressed in postmitotic neuronal precursors in the cerebellum, hippocampus, cerebrum, and olfactory bulb, where migration establishes laminar structures. Fab fragments of antibodies to a recombinant astrotactin peptide blocked migration of cerebellar granule neurons in vitro along astroglial fibers. Transfection of astrotactin complementary DNA into 3T3 cells indicated that astrotactin acts as a ligand for neuron-glia binding during neuronal migration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zheng, C -- Heintz, N -- Hatten, M E -- NS15429/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Apr 19;272(5260):417-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rockefeller University, New York, NY 10021-6399, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8602532" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Astrocytes/metabolism ; Blotting, Northern ; Brain/*metabolism ; Cell Movement ; Cerebellum/cytology/metabolism ; Gene Expression ; Glycoproteins/chemistry/*genetics/*physiology ; Hippocampus/metabolism ; Ligands ; Mice ; Molecular Sequence Data ; Nerve Tissue Proteins/chemistry/*genetics/*physiology ; Neuroglia/*metabolism ; Neurons/cytology/*physiology ; Olfactory Bulb/metabolism ; Transfection
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    Life-death balance within the cell (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1996 Nov 1;274(5288):724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966553" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cells, Cultured ; Humans ; Mice ; Mice, Knockout ; NF-kappa B/antagonists & inhibitors/metabolism/*physiology ; Neoplasms/metabolism/*pathology/therapy ; Proto-Oncogene Proteins/metabolism/pharmacology ; Transcription Factor RelB ; *Transcription Factors ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/pharmacology/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Melanoma cell expression of Fas(Apo-1/CD95) ligand: implications for tumor immune escape (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-22
    Description: Malignant melanoma accounts for most of the increasing mortality from skin cancer. Melanoma cells were found to express Fas (also called Apo-1 or CD95) ligand (FasL). In metastatic lesions, Fas-expressing T cell infiltrates were proximal to FasL+ tumor cells. In vitro, apoptosis of Fas-sensitive target cells occurred upon incubation with melanoma tumor cells; and in vivo, injection of FasL+ mouse melanoma cells in mice led to rapid tumor formation. In contrast, tumorigenesis was delayed in Fas-deficient lpr mutant mice in which immune effector cells cannot be killed by FasL. Thus, FasL may contribute to the immune privilege of tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hahne, M -- Rimoldi, D -- Schroter, M -- Romero, P -- Schreier, M -- French, L E -- Schneider, P -- Bornand, T -- Fontana, A -- Lienard, D -- Cerottini, J -- Tschopp, J -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1363-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Biochemistry, University of Lausanne, CH-1066 Epalinges, Switzerland. jurg.tschopp@ib.unil.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8910274" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/biosynthesis/*physiology ; *Apoptosis ; Fas Ligand Protein ; Humans ; Ligands ; Lymphocytes, Tumor-Infiltrating/cytology/immunology ; Melanoma/*immunology/metabolism/pathology/secondary ; Membrane Glycoproteins/analysis/biosynthesis/*physiology ; Mice ; Mice, Inbred C57BL ; T-Lymphocytes, Cytotoxic/*cytology/immunology ; Tumor Cells, Cultured ; *Tumor Escape
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    Signaling inside neurons takes some new twists (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1996 Jun 21;272(5269):1742-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650570" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Chick Embryo ; Membrane Glycoproteins/metabolism ; Mice ; Nerve Growth Factors/*metabolism ; Neurons/cytology/*physiology ; Receptor, Nerve Growth Factor ; Receptors, Nerve Growth Factor/metabolism ; *Signal Transduction ; Taste/*physiology ; Transducin/*physiology
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    Platelet-mediated lymphocyte delivery to high endothelial venules (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-12
    Description: Circulating lymphocytes gain access to lymph nodes owing to their ability to initiate rolling along specialized high endothelial venules (HEVs). One mechanism of rolling involves L-selectin binding to peripheral node addressin (PNAd) on HEVs. Activated platelets are shown to bind to circulating lymphocytes and to mediate rolling in HEVs, in vivo, through another molecule, P-selectin, which also interacts with PNAd. In vitro, activated platelets enhanced tethering of lymphocytes to PNAd and sustained lymphocyte rolling, even in the absence of functional L-selectin. Thus, a platelet pathway operating through P-selectin provides a second mechanism for lymphocyte delivery to HEVs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diacovo, T G -- Puri, K D -- Warnock, R A -- Springer, T A -- von Andrian, U H -- HL48675/HL/NHLBI NIH HHS/ -- HL54936/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Jul 12;273(5272):252-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Blood Research, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662511" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/*metabolism ; Blood Platelets/*physiology ; Cell Adhesion ; Cell Movement ; Endothelium, Vascular/cytology ; Humans ; L-Selectin/physiology ; Ligands ; Lymph Nodes/*blood supply/cytology ; Lymphocytes/cytology/*physiology ; Membrane Glycoproteins/metabolism ; Membrane Proteins ; Mice ; P-Selectin/metabolism ; Platelet Activation ; Receptors, Lymphocyte Homing/metabolism ; Transfection ; Tumor Cells, Cultured ; Venules/cytology
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    Exclusion of Int-6 from PML nuclear bodies by binding to the HTLV-I Tax oncoprotein (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-16
    Description: The Tax transactivator of the human T cell leukemia virus type I (HTLV-I) exhibits oncogenic properties. A screen for proteins interacting with Tax yielded a complementary DNA (cDNA) encoding the human Int-6 protein. In mice, the Int-6 gene can be converted into a putative dominant negative oncogene after retroviral insertion. Here, Int-6 was localized in the cell nucleus to give a speckled staining pattern superposed to that of the promyelocytic leukemia (PML) protein. The binding of Tax to Int-6 caused its redistribution from the nuclear domains to the cytoplasm. Thus, Int-6 is a component of the PML nuclear bodies and Tax disrupts its normal cellular localization by binding to it.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Desbois, C -- Rousset, R -- Bantignies, F -- Jalinot, P -- New York, N.Y. -- Science. 1996 Aug 16;273(5277):951-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre National de la Recherche Scientifique UMR49, Ecole Normale Superieure de Lyon, 69364 Lyon Cedex 07, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8688078" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Nucleus/*chemistry ; Cytoplasm/chemistry ; Eukaryotic Initiation Factor-3 ; Gene Products, tax/analysis/*metabolism ; HeLa Cells ; Humans ; Mice ; *Neoplasm Proteins ; *Nuclear Proteins ; Proto-Oncogene Proteins/analysis/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Transcription Factors/*analysis ; Transfection ; Tumor Suppressor Proteins
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    Survival of cholinergic forebrain neurons in developing p75NGFR-deficient mice (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-06
    Description: The functions of the low-affinity p75 nerve growth factor receptor (p75(NGFR)) in the central nervous system were explored in vivo. In normal mice, approximately 25 percent of the cholinergic basal forebrain neurons did not express TrkA and died between postnatal day 6 and 15. This loss did not occur in p75(NGFR)-deficient mice or in normal mice systemically injected with a p75(NGFR)-inhibiting peptide. Control, but not p75(NGFR)-deficient, mice also had fewer cholinergic striatal interneurons. Apparently, p75(NGFR) mediates apoptosis of these developing neurons in the absence of TrkA, and modulation of p75(NGFR) can promote neuronal survival. Cholinergic basal forebrain neurons are involved in learning and memory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van der Zee, C E -- Ross, G M -- Riopelle, R J -- Hagg, T -- New York, N.Y. -- Science. 1996 Dec 6;274(5293):1729-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Tupper Building, Dalhousie University, Halifax, Nova Scotia B3H 4H7, Canada. thagg@is.dal.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8939868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cell Survival ; Choline O-Acetyltransferase/metabolism ; DNA Fragmentation ; Interneurons/cytology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neostriatum/cytology ; Neurons/*cytology/enzymology ; Oligopeptides/pharmacology ; Parasympathetic Nervous System/*cytology ; Phosphorylation ; Prosencephalon/*cytology ; Proto-Oncogene Proteins/metabolism ; Purkinje Cells/cytology ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Nerve Growth Factor ; Receptor, trkA ; Receptors, Nerve Growth Factor/deficiency/metabolism/*physiology
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    Prevention of islet allograft rejection with engineered myoblasts expressing FasL in mice (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-07-05
    Description: Allogeneic transplantation of islets of Langerhans was facilitated by the cotransplantation of syngeneic myoblasts genetically engineered to express the Fas ligand (FasL). Composite grafting of allogeneic islets with syngeneic myoblasts expressing FasL protected the islet graft from immune rejection and maintained normoglycemia for more than 80 days in mice with streptozotocin-induced diabetes. Graft survival was not prolonged with composite grafts of unmodified myoblasts or Fas-expressing myoblasts. Islet allografts transplanted separately from FasL-expressing myoblasts into the contralateral kidney were rejected, as were similarly transplanted third-party thyroid allografts. Thus, the FasL signal provided site- and immune-specific protection of islet allografts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lau, H T -- Yu, M -- Fontana, A -- Stoeckert, C J Jr -- New York, N.Y. -- Science. 1996 Jul 5;273(5271):109-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Surgery, Children's Hospital of Philadelphia, University of Pennsylvania, 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658177" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Transplantation ; Coculture Techniques ; Diabetes Mellitus, Experimental/surgery ; Fas Ligand Protein ; Genetic Engineering ; Graft Rejection/*prevention & control ; Graft Survival ; *Islets of Langerhans Transplantation ; Ligands ; Membrane Glycoproteins/*biosynthesis ; Mice ; Mice, Inbred A ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Muscle Fibers, Skeletal/*cytology/*metabolism/transplantation ; Recombinant Proteins/biosynthesis ; T-Lymphocytes/cytology/immunology ; Transfection ; Transplantation, Heterotopic ; Transplantation, Homologous
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    Role of Rho in chemoattractant-activated leukocyte adhesion through integrins (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-02-16
    Description: Heterotrimeric guanine nucleotide binding protein (G protein)-linked receptors of the chemoattractant subfamily can trigger adhesion through leukocyte integrins, and in this role they are thought to regulate immune cell-cell interactions and trafficking. In lymphoid cells transfected with formyl peptide or interleukin-8 receptors, agonist stimulation activated nucleotide exchange on the small guanosine triphosphate-binding protein RhoA in seconds. Inactivation of Rho by C3 transferase exoenzyme blocked agonist-induced lymphocyte alpha4beta1 adhesion to vascular cell adhesion molecule-1 and neutrophil beta2 integrin adhesion to fibrinogen. These findings suggest that Rho participates in signaling from chemoattractant receptors to trigger rapid adhesion in leukocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laudanna, C -- Campbell, J J -- Butcher, E C -- 1F32 AI08930/AI/NIAID NIH HHS/ -- 5T32 CA09302/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 16;271(5251):981-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8584934" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD/genetics ; B-Lymphocytes/*physiology ; *Cell Adhesion ; Cells, Cultured ; Chemotactic Factors/*pharmacology ; GTP-Binding Proteins/metabolism/*physiology ; Guanosine 5'-O-(3-Thiotriphosphate)/metabolism ; Guanosine Diphosphate/metabolism ; Integrin alpha4beta1 ; Integrins/*physiology ; Interleukin-8/pharmacology ; Mice ; Molecular Sequence Data ; N-Formylmethionine Leucyl-Phenylalanine/pharmacology ; Receptors, Formyl Peptide ; Receptors, Immunologic/genetics ; Receptors, Interleukin/genetics ; Receptors, Interleukin-8A ; Receptors, Lymphocyte Homing/*physiology ; Receptors, Peptide/genetics ; Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; Transfection ; Vascular Cell Adhesion Molecule-1/*physiology ; rhoA GTP-Binding Protein
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    Correlative memory deficits, Abeta elevation, and amyloid plaques in transgenic mice (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-10-04
    Description: Transgenic mice overexpressing the 695-amino acid isoform of human Alzheimer beta-amyloid (Abeta) precursor protein containing a Lys670 --〉 Asn, Met671 --〉 Leu mutation had normal learning and memory in spatial reference and alternation tasks at 3 months of age but showed impairment by 9 to 10 months of age. A fivefold increase in Abeta(1-40) and a 14-fold increase in Abeta(1-42/43) accompanied the appearance of these behavioral deficits. Numerous Abeta plaques that stained with Congo red dye were present in cortical and limbic structures of mice with elevated amounts of Abeta. The correlative appearance of behavioral, biochemical, and pathological abnormalities reminiscent of Alzheimer's disease in these transgenic mice suggests new opportunities for exploring the pathophysiology and neurobiology of this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsiao, K -- Chapman, P -- Nilsen, S -- Eckman, C -- Harigaya, Y -- Younkin, S -- Yang, F -- Cole, G -- AG06656/AG/NIA NIH HHS/ -- AG9009/AG/NIA NIH HHS/ -- NS33249/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Oct 4;274(5284):99-102.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, UMHC Box 295, 420 Delaware Street, University of Minnesota, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8810256" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Alzheimer Disease/metabolism/pathology ; Amyloid beta-Peptides/*analysis ; Amyloid beta-Protein Precursor/*analysis/genetics ; Animals ; Brain/*pathology ; *Brain Chemistry ; Learning Disorders/*metabolism/pathology ; Maze Learning ; Memory Disorders/*metabolism/pathology ; Mice ; Mice, Transgenic ; Peptide Fragments/*analysis ; Psychomotor Performance
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    PKC-dependent stimulation of exocytosis by sulfonylureas in pancreatic beta cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-09
    Description: Hypoglycemic sulfonylureas represent a group of clinically useful antidiabetic compounds that stimulate insulin secretion from pancreatic beta cells. The molecular mechanisms involved are not fully understood but are believed to involve inhibition of potassium channels sensitive to adenosine triphosphate (KATP channels) in the beta cell membrane, causing membrane depolarization, calcium influx, and activation of the secretory machinery. In addition to these effects, sulfonylureas also promoted exocytosis by direct interaction with the secretory machinery not involving closure of the plasma membrane KATP channels. This effect was dependent on protein kinase C (PKC) and was observed at therapeutic concentrations of sulfonylureas, which suggests that it contributes to their hypoglycemic action in diabetics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eliasson, L -- Renstrom, E -- Ammala, C -- Berggren, P O -- Bertorello, A M -- Bokvist, K -- Chibalin, A -- Deeney, J T -- Flatt, P R -- Gabel, J -- Gromada, J -- Larsson, O -- Lindstrom, P -- Rhodes, C J -- Rorsman, P -- New York, N.Y. -- Science. 1996 Feb 9;271(5250):813-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Pharmacology, University of Goteborg, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8628999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Cells, Cultured ; Cytoplasmic Granules/metabolism ; Electric Conductivity ; Exocytosis/*drug effects ; Glipizide/pharmacology ; Glyburide/pharmacology ; Hypoglycemic Agents/*pharmacology ; Insulin/secretion ; Islets of Langerhans/drug effects/*physiology ; Membrane Potentials/drug effects ; Mice ; Patch-Clamp Techniques ; Protein Kinase C/*metabolism ; Sulfonylurea Compounds/*pharmacology ; Tolbutamide/*pharmacology
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    Neurogenic amplification of immune complex inflammation (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-09-20
    Description: The formation of intrapulmonary immune complexes in mice generates a vigorous inflammatory response characterized by microvascular permeability and polymorphonuclear neutrophil influx. Gene-targeted disruption of the substance P receptor (NK-1R) protected the lung from immune complex injury, as did disruption of the C5a anaphylatoxin receptor. Immunoreactive substance P was measurable in fluids lining the lung at time points before neutrophil influx and may thus be involved in an early step in the inflammatory response to immune complexes in the lung.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bozic, C R -- Lu, B -- Hopken, U E -- Gerard, C -- Gerard, N P -- HL36162/HL/NHLBI NIH HHS/ -- HL51366/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Sep 20;273(5282):1722-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Perlmutter Laboratory, Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8781237" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Antibody Complex/*immunology ; Antigens, CD/genetics/physiology ; Bronchoalveolar Lavage Fluid/chemistry ; Capillary Permeability ; Complement C5a/*physiology ; Female ; Gene Targeting ; Immune Complex Diseases/immunology/*metabolism/pathology ; Inflammation/immunology/metabolism/pathology ; Lung/chemistry/pathology ; Lung Diseases/immunology/*metabolism/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Neutrophils ; Receptor, Anaphylatoxin C5a ; Receptors, Complement/genetics/physiology ; Receptors, Neurokinin-1/genetics/physiology ; Substance P/analysis/*physiology ; Tumor Necrosis Factor-alpha/analysis
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    TAB1: an activator of the TAK1 MAPKKK in TGF-beta signal transduction (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-24
    Description: Transforming growth factor-beta (TGF-beta) regulates many aspects of cellular function. A member of the mitogen-activated protein kinase kinase kinase (MAPKKK) family, TAK1, was previously identified as a mediator in the signaling pathway of TGF-beta superfamily members. The yeast two-hybrid system has now revealed two human proteins, termed TAB1 and TAB2 (for TAK1 binding protein), that interact with TAK1. TAB1 and TAK1 were co-immunoprecipitated from mammalian cells. Overproduction of TAB1 enhanced activity of the plasminogen activator inhibitor 1 gene promoter, which is regulated by TGF-beta, and increased the kinase activity of TAK1. TAB1 may function as an activator of the TAK1 MAPKKK in TGF-beta signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shibuya, H -- Yamaguchi, K -- Shirakabe, K -- Tonegawa, A -- Gotoh, Y -- Ueno, N -- Irie, K -- Nishida, E -- Matsumoto, K -- New York, N.Y. -- Science. 1996 May 24;272(5265):1179-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638164" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Base Sequence ; Carrier Proteins/chemistry/*metabolism ; Cell Line ; Cloning, Molecular ; Enzyme Activation ; Genes, Reporter ; Humans ; *Intracellular Signaling Peptides and Proteins ; *MAP Kinase Kinase Kinases ; Mice ; Molecular Sequence Data ; Plasminogen Activator Inhibitor 1/genetics ; Promoter Regions, Genetic ; Protein-Serine-Threonine Kinases/*metabolism ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/genetics/metabolism ; *Signal Transduction ; Transfection ; Transformation, Genetic ; Transforming Growth Factor beta/*metabolism
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    Specification of pituitary cell lineages by the LIM homeobox gene Lhx3 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-17
    Description: During pituitary organogenesis, the progressive differentiation of distinct pituitary-specific cell lineages from a common primordium involves a series of developmental decisions and inductive interactions. Targeted gene disruption in mice showed that Lhx3, a LIM homeobox gene expressed in the pituitary throughout development, is essential for differentiation and proliferation of pituitary cell lineages. In mice homozygous for the Lhx3 mutation, Rathke's pouch formed but failed to grow and differentiate; such mice lacked both the anterior and intermediate lobes of the pituitary. The determination of all pituitary cell lineages, except the corticotrophs, was affected, suggesting that a distinct, Lhx3-independent ontogenetic pathway exists for the initial specification of this lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheng, H Z -- Zhadanov, A B -- Mosinger, B Jr -- Fujii, T -- Bertuzzi, S -- Grinberg, A -- Lee, E J -- Huang, S P -- Mahon, K A -- Westphal, H -- New York, N.Y. -- Science. 1996 May 17;272(5264):1004-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638120" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/genetics ; Cell Differentiation ; Cell Lineage ; Embryonic and Fetal Development ; *Gene Expression Regulation, Developmental ; Gene Targeting ; *Genes, Homeobox ; Glycoprotein Hormones, alpha Subunit/biosynthesis/genetics ; Homeodomain Proteins/*genetics ; LIM-Homeodomain Proteins ; *Membrane Proteins ; Mice ; Mutation ; Phospholipid Transfer Proteins ; Pituitary Gland/abnormalities/*cytology/embryology ; Pituitary Gland, Anterior/abnormalities/*cytology/embryology ; Pro-Opiomelanocortin/biosynthesis/genetics ; Transcription Factors
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    Receptor-ligand interaction between CD44 and osteopontin (Eta-1) (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-26
    Description: The CD44 family of surface receptors regulates adhesion, movement, and activation of normal and neoplastic cells. The cytokine osteopontin (Eta-1), which regulates similar cellular functions, was found to be a protein ligand of CD44. Osteopontin induces cellular chemotaxis but not homotypic aggregation, whereas the inverse is true for the interaction between CD44 and a carbohydrate ligand, hyaluronate. The different responses of cells after CD44 ligation by either osteopontin or hyaluronate may account for the independent effects of CD44 on cell migration and growth. This mechanism may also be exploited by tumor cells to promote metastasis formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weber, G F -- Ashkar, S -- Glimcher, M J -- Cantor, H -- AI12184/AI/NIAID NIH HHS/ -- AI13600/AI/NIAID NIH HHS/ -- P01 AR34078/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 26;271(5248):509-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8560266" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD44/*metabolism ; Base Sequence ; *Cell Adhesion ; Cell Aggregation ; Cell Line ; *Chemotaxis ; Cytokines/*metabolism/pharmacology ; Hyaluronic Acid/metabolism/pharmacology ; Ligands ; Mice ; Molecular Sequence Data ; Monocytes/metabolism ; Oligopeptides/pharmacology ; Osteopontin ; Sialoglycoproteins/*metabolism/pharmacology ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Simple mice test antibody complexity (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, N -- New York, N.Y. -- Science. 1996 Jun 14;272(5268):1585.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658129" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/genetics/immunology ; Immunoglobulin Heavy Chains/*genetics/immunology ; Immunoglobulin Light Chains/genetics ; Mice ; Mice, Knockout/*genetics/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Genes, junctions, and disease at cell biology meeting (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2008-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8984657" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cataract/etiology ; Chromosomes, Human, Pair 21 ; Connexins/genetics/*physiology ; Down Syndrome/*genetics ; Female ; Gap Junctions/*physiology ; Gene Dosage ; Heart Defects, Congenital/etiology ; Humans ; Infertility, Female/etiology ; Mice ; Protein Kinases/*genetics/metabolism ; *Protein-Serine-Threonine Kinases ; *Protein-Tyrosine Kinases
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    An adenovirus mutant that replicates selectively in p53-deficient human tumor cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-18
    Description: The human adenovirus E1B gene encodes a 55-kilodalton protein that inactivates the cellular tumor suppressor protein p53. Here it is shown that a mutant adenovirus that does not express this viral protein can replicate in and lyse p53-deficient human tumor cells but not cells with functional p53. Ectopic expression of the 55-kilodalton EIB protein in the latter cells rendered them sensitive to infection with the mutant virus. Injection of the mutant virus into p53-deficient human cervical carcinomas grown in nude mice caused a significant reduction in tumor size and caused complete regression of 60 percent of the tumors. These data raise the possibility that mutant adenoviruses can be used to treat certain human tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bischoff, J R -- Kirn, D H -- Williams, A -- Heise, C -- Horn, S -- Muna, M -- Ng, L -- Nye, J A -- Sampson-Johannes, A -- Fattaey, A -- McCormick, F -- New York, N.Y. -- Science. 1996 Oct 18;274(5286):373-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ONYX Pharmaceuticals, 3031 Research Drive, Richmond, CA 94806, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8832876" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus E1B Proteins/*genetics/metabolism ; Adenoviruses, Human/genetics/*physiology ; Animals ; Cytopathogenic Effect, Viral ; Gene Deletion ; *Genes, p53 ; Head and Neck Neoplasms/*therapy/virology ; Humans ; Mice ; Mice, Nude ; Mutation ; Neoplasm Transplantation ; Neoplasms, Experimental/pathology/*therapy/virology ; Sigmodontinae ; Transplantation, Heterologous ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/metabolism ; Virus Replication
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    Induction of TH1 and TH2 immunity in neonatal mice (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-22
    Description: The neonatal period has been thought of as a window in ontogeny, during which the developing immune system is particularly susceptible to tolerization. In the present study, the classic system for induction of neonatal tolerance to protein antigens was reexamined in mice. The presumably tolerogenic protocol was found to trigger a vigorous T helper cell type 2 (TH2) immune response. Thus, neonatal "tolerization" induces immune deviation, not tolerance in the immunological sense. Neonates are not immune privileged but generate TH2 or TH1 responses, depending on the mode of immunization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Forsthuber, T -- Yip, H C -- Lehmann, P V -- AI36219-02/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1728-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Case Western Reserve University, Cleveland, OH 44106-4943, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596934" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn/*immunology ; Antibody Formation ; Freund's Adjuvant ; *Immune Tolerance ; Immunization ; Immunoglobulin G/biosynthesis ; Immunologic Memory ; Lymph Nodes/immunology ; Mice ; Mice, Inbred BALB C ; Muramidase/immunology ; Spleen/immunology ; Th1 Cells/*immunology ; Th2 Cells/*immunology
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    An orphan nuclear hormone receptor that lacks a DNA binding domain and heterodimerizes with other receptors (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-31
    Description: SHP is an orphan member of the nuclear hormone receptor superfamily that contains the dimerization and ligand-binding domain found in other family members but lacks the conserved DNA binding domain. In the yeast two-hybrid system, SHP interacted with several conventional and orphan members of the receptor superfamily, including retinoid receptors, the thyroid hormone receptor, and the orphan receptor MB67. SHP also interacted directly with these receptors in vitro. In mammalian cells, SHP specifically inhibited transactivation by the superfamily members with which it interacted. These results suggest that SHP functions as a negative regulator of receptor-dependent signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seol, W -- Choi, H S -- Moore, D D -- DK46546/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 May 31;272(5266):1336-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital, Boston, 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650544" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; DAX-1 Orphan Nuclear Receptor ; DNA/*metabolism ; DNA-Binding Proteins/chemistry/metabolism ; Humans ; Mice ; Molecular Sequence Data ; Receptors, Cytoplasmic and Nuclear/chemistry/*metabolism ; Receptors, Retinoic Acid/chemistry/metabolism ; Receptors, Thyroid Hormone/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; *Repressor Proteins ; Retinoid X Receptors ; Signal Transduction ; Transcription Factors/chemistry/metabolism ; Transcriptional Activation/drug effects ; Tumor Cells, Cultured
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    Decreased resistance to bacterial infection and granulocyte defects in IAP-deficient mice (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-01
    Description: Granulocyte [polymorphonuclear leucocyte (PMN)] migration to sites of infection and subsequent activation is essential for host defense. Gene-targeted mice deficient for integrin-associated protein (IAP, also termed CD47) succumbed to Escherichia coli peritonitis at inoccula survived by heterozygous littermates. In vivo, they had an early defect in PMN accumulation at the site of infection. In vitro, IAP-/- PMNs were deficient in beta3 integrin-dependent ligand binding, activation of an oxidative burst, and Fc receptor-mediated phagocytosis. Thus, IAP plays a key role in host defense by participating both in PMN migration in response to bacterial infection and in PMN activation at extravascular sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lindberg, F P -- Bullard, D C -- Caver, T E -- Gresham, H D -- Beaudet, A L -- Brown, E J -- AI32177/AI/NIAID NIH HHS/ -- GM15483/GM/NIGMS NIH HHS/ -- GM38330/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Nov 1;274(5288):795-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectious Diseases, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8864123" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD/genetics/*immunology/physiology ; Antigens, CD47 ; Carrier Proteins/genetics/*immunology ; Cell Movement ; Escherichia coli Infections/*immunology ; Female ; Gene Targeting ; Heterozygote ; Immunity, Innate ; Integrin beta3 ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; *Neutrophil Activation ; Neutrophils/*immunology/physiology ; Peptide Fragments/pharmacology ; Peritonitis/immunology ; Phagocytosis ; Phenotype ; Platelet Membrane Glycoproteins/physiology ; Respiratory Burst
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    Altered sensory processing in the somatosensory cortex of the mouse mutant barrelless (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-03-29
    Description: Mice homozygous for the barrelless (brl) mutation, mapped here to chromosome 11, lack barrel-shaped arrays of cell clusters termed "barrels" in the primary somatosensory cortex. Deoxyglucose uptake demonstrated that the topology of the cortical whisker representation is nevertheless preserved. Anterograde tracers revealed a lack of spatial segregation of thalamic afferents into individual barrel territories, and single-cell recordings demonstrated a lack of temporal discrimination of center from surround information. Thus, structural segregation of thalamic inputs is not essential to generate topological order in the somatosensory cortex, but it is required for discrete spatiotemporal relay of sensory information to the cortex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Welker, E -- Armstrong-James, M -- Bronchti, G -- Ourednik, W -- Gheorghita-Baechler, F -- Dubois, R -- Guernsey, D L -- Van der Loos, H -- Neumann, P E -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1996 Mar 29;271(5257):1864-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Anatomy, University of Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596955" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/ultrastructure ; Brain/cytology/metabolism ; Chromosome Mapping ; Deoxyglucose/metabolism ; Mice ; Mice, Mutant Strains ; Neural Pathways ; Neurons/cytology/physiology ; Phenotype ; Somatosensory Cortex/cytology/metabolism/*physiology ; Thalamus/cytology/physiology ; Vibrissae/*innervation/physiology
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    Time-sensitive reversal of hyperplasia in transgenic mice expressing SV40 T antigen (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-09-06
    Description: The role of viral oncoprotein expression in the maintenance of cellular transformation was examined as a function of time through controlled expression of simian virus 40 T antigen (TAg). Expression of TAg in the submandibular gland of transgenic mice from the time of birth induced cellular transformation and extensive ductal hyperplasia by 4 months of age. The hyperplasia was reversed when TAg expression was silenced for 3 weeks. When TAg expression was silenced after 7 months, however, the hyperplasia persisted even though TAg was absent. Although the polyploidy of ductal cells could be reversed at 4 months of age, cells at 7 months of age remained polyploid even in the absence of TAg. These results support a model of time-dependent multistep tumorigenesis, in which virally transformed cells eventually lose their dependence on the viral oncoprotein for maintenance of the transformed state.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ewald, D -- Li, M -- Efrat, S -- Auer, G -- Wall, R J -- Furth, P A -- Hennighausen, L -- New York, N.Y. -- Science. 1996 Sep 6;273(5280):1384-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biochemistry and Metabolism, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8703072" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Polyomavirus Transforming/genetics/*physiology ; *Cell Transformation, Neoplastic ; *Cell Transformation, Viral ; Gene Expression ; Hyperplasia ; Mice ; Mice, Transgenic ; Polyploidy ; Submandibular Gland/*pathology ; Tetracycline/pharmacology ; Time Factors ; Trans-Activators/genetics
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    Long-term lymphohematopoietic reconstitution by a single CD34-low/negative hematopoietic stem cell (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-12
    Description: Hematopoietic stem cells (HSCs) supply all blood cells throughout life by making use of their self-renewal and multilineage differentiation capabilities. A monoclonal antibody raised to the mouse homolog of CD34 (mCD34) was used to purify mouse HSCs to near homogeneity. Unlike in humans, primitive adult mouse bone marrow HSCs were detected in the mCD34 low to negative fraction. Injection of a single mCD34(lo/-), c-Kit+, Sca-1(+), lineage markers negative (Lin-) cell resulted in long-term reconstitution of the lymphohematopoietic system in 21 percent of recipients. Thus, the purified HSC population should enable analysis of the self-renewal and multilineage differentiation of individual HSCs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Osawa, M -- Hanada, K -- Hamada, H -- Nakauchi, H -- New York, N.Y. -- Science. 1996 Jul 12;273(5272):242-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Institute of Basic Medical Sciences and Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba Science-City, Ibaraki 305, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662508" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/*analysis ; Base Sequence ; *Bone Marrow Cells ; Cell Differentiation ; Cell Lineage ; Cell Separation ; DNA Primers ; *Hematopoiesis ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*cytology/immunology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Time Factors
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  • 141
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    A role for CD81 in early T cell development (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-12
    Description: Early stages of T cell development are thought to include a series of coordinated interactions between thymocytes and other cells of the thymus. A monoclonal antibody specific for mouse CD81 was identified that blocked the appearance of alpha beta but not gamma delta T cells in fetal organ cultures initiated with day 14.5 thymus lobes. In reaggregation cultures with CD81-transfected fibroblasts, CD4-CD8- thymocytes differentiated into CD4+CD8+ T cells. Thus, interactions between immature thymocytes and stromal cells expressing CD81 are required and may be sufficient to induce early events associated with T cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boismenu, R -- Rhein, M -- Fischer, W H -- Havran, W L -- AI32751/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 12;271(5246):198-200.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8539618" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/immunology ; Antigens, CD/genetics/immunology/*physiology ; Antigens, CD4/analysis ; Antigens, CD8/analysis ; Antigens, CD81 ; Base Sequence ; CHO Cells ; Cell Differentiation ; Cricetinae ; Membrane Proteins/immunology/*physiology ; Mice ; Molecular Sequence Data ; Organ Culture Techniques ; Receptors, Antigen, T-Cell, alpha-beta/*analysis ; Receptors, Antigen, T-Cell, gamma-delta/analysis ; Stromal Cells/immunology ; T-Lymphocyte Subsets/cytology/*immunology ; Thymus Gland/cytology/*immunology ; Transfection
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  • 142
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    Uncoupling of obesity from insulin resistance through a targeted mutation in aP2, the adipocyte fatty acid binding protein (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-22
    Description: Fatty acid binding proteins (FABPs) are small cytoplasmic proteins that are expressed in a highly tissue-specific manner and bind to fatty acids such as oleic and retinoic acid. Mice with a null mutation in aP2, the gene encoding the adipocyte FABP, were developmentally and metabolically normal. The aP2-deficient mice developed dietary obesity but, unlike control mice, they did not develop insulin resistance or diabetes. Also unlike their obese wild-type counterparts, obese aP2-/- animals failed to express in adipose tissue tumor necrosis factor-alpha (TNF-alpha), a molecule implicated in obesity-related insulin resistance. These results indicate that aP2 is central to the pathway that links obesity to insulin resistance, possibly by linking fatty acid metabolism to expression of TNF-alpha.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hotamisligil, G S -- Johnson, R S -- Distel, R J -- Ellis, R -- Papaioannou, V E -- Spiegelman, B M -- DK31405/DK/NIDDK NIH HHS/ -- HD27295/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1377-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA. CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8910278" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*metabolism ; Animals ; Blood Glucose/metabolism ; Carrier Proteins/genetics/metabolism/*physiology ; Dietary Fats/administration & dosage ; Fatty Acid-Binding Proteins ; Fatty Acids/*metabolism ; Female ; Gene Expression Regulation ; Gene Targeting ; Glucose Tolerance Test ; Homeostasis ; Insulin/blood ; *Insulin Resistance ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Myelin P2 Protein/genetics/metabolism/*physiology ; *Neoplasm Proteins ; *Nerve Tissue Proteins ; Obesity/*metabolism ; Triglycerides/blood ; Tumor Necrosis Factor-alpha/*biosynthesis/genetics
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  • 143
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    An alphabeta T cell receptor structure at 2.5 A and its orientation in the TCR-MHC complex (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-11
    Description: The central event in the cellular immune response to invading microorganisms is the specific recognition of foreign peptides bound to major histocompatibility complex (MHC) molecules by the alphabeta T cell receptor (TCR). The x-ray structure of the complete extracellular fragment of a glycosylated alphabeta TCR was determined at 2.5 angstroms, and its orientation bound to a class I MHC-peptide (pMHC) complex was elucidated from crystals of the TCR-pMHC complex. The TCR resembles an antibody in the variable Valpha and Vbeta domains but deviates in the constant Calpha domain and in the interdomain pairing of Calpha with Cbeta. Four of seven possible asparagine-linked glycosylation sites have ordered carbohydrate moieties, one of which lies in the Calpha-Cbeta interface. The TCR combining site is relatively flat except for a deep hydrophobic cavity between the hypervariable CDR3s (complementarity-determining regions) of the alpha and beta chains. The 2C TCR covers the class I MHC H-2Kb binding groove so that the Valpha CDRs 1 and 2 are positioned over the amino-terminal region of the bound dEV8 peptide, the Vbeta chain CDRs 1 and 2 are over the carboxyl-terminal region of the peptide, and the Valpha and Vbeta CDR3s straddle the peptide between the helices around the central position of the peptide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garcia, K C -- Degano, M -- Stanfield, R L -- Brunmark, A -- Jackson, M R -- Peterson, P A -- Teyton, L -- Wilson, I A -- R01 CA58896/CA/NCI NIH HHS/ -- T32-A107244/PHS HHS/ -- New York, N.Y. -- Science. 1996 Oct 11;274(5285):209-19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and the Skaggs Institute of Chemical Biology, Scripps Research Institute, 10550 N. Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8824178" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbohydrate Sequence ; Cells, Cultured ; Crystallization ; Crystallography, X-Ray ; Drosophila melanogaster ; Glycosylation ; H-2 Antigens/*chemistry/immunology/metabolism ; Hydrogen Bonding ; Major Histocompatibility Complex ; Mice ; Models, Molecular ; Molecular Sequence Data ; Peptides/*chemistry/immunology/metabolism ; *Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Receptors, Antigen, T-Cell, alpha-beta/*chemistry/immunology/metabolism ; Recombinant Proteins ; T-Lymphocytes, Cytotoxic/*immunology
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    Impairment of hippocampal mossy fiber LTD in mice lacking mGluR2 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-02
    Description: Subtype 2 of the metabotropic glutamate receptor (mGluR2) is expressed in the presynaptic elements of hippocampal mossy fiber-CA3 synapses. Knockout mice deficient in mGluR2 showed no histological changes and no alterations in basal synaptic transmission, paired-pulse facilitation, or tetanus-induced long-term potentiation (LTP) at the mossy fiber-CA3 synapses. Long-term depression (LTD) induced by low-frequency stimulation, however, was almost fully abolished. The mutant mice performed normally in water maze learning tasks. Thus, the presynaptic mGluR2 is essential for inducing LTD at the mossy fiber-CA3 synapses, but this hippocampal LTD does not seem to be required for spatial learning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yokoi, M -- Kobayashi, K -- Manabe, T -- Takahashi, T -- Sakaguchi, I -- Katsuura, G -- Shigemoto, R -- Ohishi, H -- Nomura, S -- Nakamura, K -- Nakao, K -- Katsuki, M -- Nakanishi, S -- New York, N.Y. -- Science. 1996 Aug 2;273(5275):645-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Kyoto University Faculty of Medicine, Kyoto 606, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662555" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Cyclopropanes/pharmacology ; Electric Stimulation ; Gene Targeting ; Glycine/analogs & derivatives/pharmacology ; Hippocampus/cytology/*physiology ; In Vitro Techniques ; Long-Term Potentiation ; Maze Learning ; Mice ; Mice, Knockout ; *Neuronal Plasticity ; Pyramidal Cells/*physiology ; Receptors, Metabotropic Glutamate/genetics/*physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Synapses/drug effects/*physiology ; Synaptic Transmission/drug effects
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  • 145
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    Requirement for alpha-CaMKII in experience-dependent plasticity of the barrel cortex (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-19
    Description: The mammalian sensory neocortex exhibits experience-dependent plasticity such that neurons modify their response properties according to changes in sensory experience. The synaptic plasticity mechanism of long-term potentiation requiring calcium-calmodulin-dependent kinase type II (CaMKII) could underlie experience-dependent plasticity. Plasticity in adult mice can be induced by changes in the patterns of tactile input to the barrel cortex. This response is strongly depressed in adult mice that lack the gene encoding alpha-CaMKII, although adolescent animals are unaffected. Thus, alpha-CaMKII is necessary either for the induction or for the expression of plasticity in adult mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glazewski, S -- Chen, C M -- Silva, A -- Fox, K -- 27759/PHS HHS/ -- New York, N.Y. -- Science. 1996 Apr 19;272(5260):421-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Minnesota, Minneapolis 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8602534" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/genetics/*metabolism ; Electric Stimulation ; Heterozygote ; Homozygote ; *Long-Term Potentiation ; Mice ; Mutation ; *Neuronal Plasticity ; Somatosensory Cortex/*physiology ; Vibrissae/*physiology
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  • 146
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    Hepatic fibrosis in Ahr-/- mice (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-01-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonnell, W M -- Chensue, S W -- Askari, F K -- Moseley, R H -- New York, N.Y. -- Science. 1996 Jan 12;271(5246):223-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8539627" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Ducts, Intrahepatic/pathology ; Collagen/analysis ; Liver/chemistry/*pathology ; Liver Cirrhosis, Experimental/*pathology ; Mice ; Mice, Inbred CBA ; Mice, Knockout ; Receptors, Aryl Hydrocarbon/*genetics
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  • 147
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    Cell cycle regulation of E2F site occupation in vivo (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-15
    Description: DNA-binding E2F complexes have been identified throughout the mammalian cell cycle, including the transcriptionally inactive complexes with pocket proteins, which occur early in the prereplicative G1 phase of the cycle, and the transactivating free E2F, which increases in late G1. Here, a regulatory B-myb promoter site was shown to bind with high affinity to free E2F and to E2F-pocket protein complexes in an indistinguishable way in vitro. In contrast, in vivo footprinting with NIH 3T3 cells demonstrated E2F site occupation specifically in early G1, when the B-myb promoter is inactive. These observations indicate that a novel mechanism governs E2F-DNA interactions during the cell cycle and emphasize the relevance of E2F site-directed transcriptional repression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zwicker, J -- Liu, N -- Engeland, K -- Lucibello, F C -- Muller, R -- New York, N.Y. -- Science. 1996 Mar 15;271(5255):1595-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Molekularbiologie und Tumorforschung, Philipps-Universitat Marburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8599118" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Base Sequence ; *Carrier Proteins ; *Cell Cycle Proteins ; DNA/*metabolism ; DNA-Binding Proteins/*genetics/metabolism ; E2F Transcription Factors ; *G1 Phase ; Mice ; Molecular Sequence Data ; Nuclear Proteins/metabolism ; *Promoter Regions, Genetic ; Retinoblastoma-Binding Protein 1 ; Retinoblastoma-Like Protein p107 ; *S Phase ; *Trans-Activators ; Transcription Factor DP1 ; Transcription Factors/*genetics/*metabolism ; Transcription, Genetic
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  • 148
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    Dissecting how presinilins function--and malfunction (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1996 Dec 13;274(5294):1838-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8984642" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*etiology/genetics/metabolism/pathology ; Amyloid beta-Peptides/*metabolism ; Amyloid beta-Protein Precursor/chemistry/*metabolism ; Animals ; Apoptosis ; Brain/pathology ; Caenorhabditis elegans ; Endoplasmic Reticulum/metabolism ; Humans ; Membrane Proteins/genetics/metabolism/*physiology ; Mice ; Mutation ; Neurons/pathology ; Peptide Fragments/*metabolism ; Presenilin-1 ; Presenilin-2 ; Protein Folding ; Receptors, Notch ; Signal Transduction
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  • 149
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    Bone morphogenetic protein-1: the type I procollagen C-proteinase (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-19
    Description: Bone morphogenetic proteins (BMPs) are bone-derived factors capable of inducing ectopic bone formation. Unlike other BMPs, BMP-1 is not like transforming growth factor-beta (TGF-beta), but it is the prototype of a family of putative proteases implicated in pattern formation during development in diverse organisms. Although some members of this group, such as Drosophila tolloid (TLD), are postulated to activate TGF-beta-like proteins, actual substrates are unknown. Procollagen C-proteinase (PCP) cleaves the COOH-propeptides of procollagens I, II, and III to yield the major fibrous components of vertebrate extracellular matrix. Here it is shown that BMP-1 and PCP are identical. This demonstration of enzymatic activity for a BMP-1/TLD-like protein links an enzyme involved in matrix deposition to genes involved in pattern formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kessler, E -- Takahara, K -- Biniaminov, L -- Brusel, M -- Greenspan, D S -- GM46846/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 19;271(5247):360-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Maurice and Gabriela Goldschleger Eye Research Institute, Tel Aviv University Sackler Faculty of Medicine, Sheba Medical Center, Tel Hashomer, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8553073" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bone Morphogenetic Protein 1 ; Bone Morphogenetic Proteins ; Humans ; Metalloendopeptidases/chemistry/*metabolism ; Mice ; Molecular Sequence Data ; Molecular Weight ; Peptide Fragments/metabolism ; Procollagen/metabolism ; Proteins/chemistry/*metabolism ; Recombinant Proteins/chemistry/metabolism
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  • 150
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    CC CKR5: a RANTES, MIP-1alpha, MIP-1beta receptor as a fusion cofactor for macrophage-tropic HIV-1 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-28
    Description: Human immunodeficiency virus-type 1 (HIV-1) entry requires fusion cofactors on the CD4+ target cell. Fusin, a heterotrimeric GTP-binding protein (G protein)-coupled receptor, serves as a cofactor for T cell line-tropic isolates. The chemokines RANTES, MIP-1alpha, and MIP-1beta, which suppress infection by macrophage-tropic isolates, selectively inhibited cell fusion mediated by the corresponding envelope glycoproteins (Envs). Recombinant CC CKR5, a G protein-coupled receptor for these chemokines, rendered CD4-expressing nonhuman cells fusion-competent preferentially with macrophage-tropic Envs. CC CKR5 messenger RNA was detected selectively in cell types susceptible to macrophage-tropic isolates. CC CKR5 is thus a fusion cofactor for macrophage-tropic HIV-1 strains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alkhatib, G -- Combadiere, C -- Broder, C C -- Feng, Y -- Kennedy, P E -- Murphy, P M -- Berger, E A -- New York, N.Y. -- Science. 1996 Jun 28;272(5270):1955-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658171" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Antigens, CD4/physiology ; Cell Fusion ; Chemokine CCL3 ; Chemokine CCL4 ; Chemokine CCL5/metabolism/pharmacology ; Chemokines/*metabolism/pharmacology ; Gene Products, env/physiology ; Giant Cells/metabolism ; HIV-1/pathogenicity/*physiology ; HeLa Cells ; Humans ; Macrophage Inflammatory Proteins ; Macrophages/*virology ; Membrane Fusion ; Mice ; Monokines/metabolism/pharmacology ; Receptors, CCR5 ; Receptors, Cytokine/*physiology ; Receptors, HIV/*physiology ; Recombinant Proteins/pharmacology ; T-Lymphocytes/virology ; Tumor Cells, Cultured
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  • 151
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    Evidence for the conformation of the pathologic isoform of the prion protein enciphering and propagating prion diversity (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: The fundamental event in prion diseases seems to be a conformational change in cellular prion protein (PrPC) whereby it is converted into the pathologic isoform PrPSc. In fatal familial insomnia (FFI), the protease-resistant fragment of PrPSc after deglycosylation has a size of 19 kilodaltons, whereas that from other inherited and sporadic prion diseases is 21 kilodaltons. Extracts from the brains of FFI patients transmitted disease to transgenic mice expressing a chimeric human-mouse PrP gene about 200 days after inoculation and induced formation of the 19-kilodalton PrPSc fragment, whereas extracts from the brains of familial and sporadic Creutzfeldt-Jakob disease patients produced the 21-kilodalton PrPSc fragment in these mice. The results presented indicate that the conformation of PrPSc functions as a template in directing the formation of nascent PrPSc and suggest a mechanism to explain strains of prions where diversity is encrypted in the conformation of PrPSc.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Telling, G C -- Parchi, P -- DeArmond, S J -- Cortelli, P -- Montagna, P -- Gabizon, R -- Mastrianni, J -- Lugaresi, E -- Gambetti, P -- Prusiner, S B -- NS07219/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2079-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953038" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*pathology ; *Brain Chemistry ; Creutzfeldt-Jakob Syndrome/metabolism/pathology ; Humans ; Mice ; Mice, Transgenic ; PrPSc Proteins/analysis/*chemistry ; Prion Diseases/*etiology/metabolism/pathology/transmission ; Prions/*chemistry ; *Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Protein Structure, Tertiary
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  • 152
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    Leishmania susceptibility puzzle gets another twist (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1996 Feb 16;271(5251):912-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8584928" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Disease Susceptibility ; Immunity, Innate ; Interleukin-12/immunology ; Interleukin-4/genetics/*immunology ; Leishmania major/*immunology ; Leishmaniasis, Cutaneous/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Th1 Cells/immunology ; Th2 Cells/immunology
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  • 153
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    Med schools receive Hughes windfall (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, J -- New York, N.Y. -- Science. 1996 Jan 12;271(5246):138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8539609" target="_blank"〉PubMed〈/a〉
    Keywords: Academies and Institutes/*economics ; Animals ; Financial Support ; Mice ; Mice, Transgenic ; *Research Support as Topic ; Schools, Medical/*economics ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 154
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    Multiple extracellular elements of CCR5 and HIV-1 entry: dissociation from response to chemokines (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-13
    Description: The human beta-chemokine receptor CCR5 is an important cofactor for entry of human immunodeficiency virus-type 1 (HIV-1). The murine form of CCR5, despite its 82 percent identity to the human form, was not functional as an HIV-1 coreceptor. HIV-1 entry function could be reconstituted by fusion of various individual elements derived from the extracellular region of human CCR5 onto murine CCR5. Analysis of chimeras containing elements from human CCR5 and human CCR2B suggested that a complex structure rather than single contact sites is responsible for facilitation of viral entry. Further, certain chimeras lacking the domains necessary to signal in response to their natural chemokine ligands retained vigorous HIV-1 coreceptor activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atchison, R E -- Gosling, J -- Monteclaro, F S -- Franci, C -- Digilio, L -- Charo, I F -- Goldsmith, M A -- HL52773/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 13;274(5294):1924-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Virology and Immunology, School of Medicine, University of California, San Francisco, Post Office Box 419100, San Francisco, CA 94141-9100, USA. mark_goldsmith@quickmail.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8943208" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/metabolism ; COS Cells ; HIV-1/*metabolism ; Humans ; Inositol Phosphates/metabolism ; Ligands ; Mice ; Receptors, CCR2 ; Receptors, CCR5 ; *Receptors, Chemokine ; Receptors, Cytokine/chemistry/genetics/*metabolism ; Receptors, HIV/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 155
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    Requirement for CD40 ligand in costimulation induction, T cell activation, and experimental allergic encephalomyelitis (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-09-27
    Description: The mechanism of CD40 ligand (CD40L)-mediated in vivo activation of CD4(+) T cells was examined by investigation of the development of experimental allergic encephalomyelitis (EAE) in CD40L-deficient mice that carried a transgenic T cell receptor specific for myelin basic protein. These mice failed to develop EAE after priming with antigen, and CD4(+) T cells remained quiescent and produced no interferon-gamma (IFN-gamma). T cells were primed to make IFN-gamma and induce EAE by providing these mice with B7.1(+) antigen-presenting cells (APCs). Thus, CD40L is required to induce costimulatory activity on APCs for in vivo activation of CD4(+) T cells to produce IFN-gamma and to evoke autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grewal, I S -- Foellmer, H G -- Grewal, K D -- Xu, J -- Hardardottir, F -- Baron, J L -- Janeway, C A Jr -- Flavell, R A -- New York, N.Y. -- Science. 1996 Sep 27;273(5283):1864-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, and Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8791592" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/*immunology ; Antigens, CD/biosynthesis ; Antigens, CD80/biosynthesis/immunology ; Antigens, CD86 ; Brain/immunology/pathology ; CD4-Positive T-Lymphocytes/*immunology ; CD40 Ligand ; Encephalomyelitis, Autoimmune, Experimental/*immunology/pathology ; Interferon-gamma/biosynthesis ; Interleukin-4/biosynthesis ; *Lymphocyte Activation ; Membrane Glycoproteins/biosynthesis/*immunology ; Mice ; Mice, Transgenic ; Myelin Basic Protein/immunology ; Receptors, Antigen, T-Cell/immunology ; Spinal Cord/immunology/pathology ; Up-Regulation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 156
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    Putting the brakes on bone growth (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roush, W -- New York, N.Y. -- Science. 1996 Aug 2;273(5275):579.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8701309" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Development ; Cartilage/*cytology/metabolism ; Cell Differentiation ; Cell Division ; Chick Embryo ; Feedback ; Growth Plate/*cytology/metabolism ; Hedgehog Proteins ; Humans ; Mice ; *Osteogenesis ; Parathyroid Hormone ; Parathyroid Hormone-Related Protein ; Proteins/*metabolism/pharmacology/*physiology ; Signal Transduction ; *Trans-Activators
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  • 157
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    Phenotypes of mouse diabetes and rat fatty due to mutations in the OB (leptin) receptor (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-16
    Description: Mice harboring mutations in the obese (ob) and diabetes (db) genes display similar phenotypes, and it has been proposed that these genes encode the ligand and receptor, respectively, for a physiologic pathway that regulates body weight. The cloning of ob, and the demonstration that it encodes a secreted protein (leptin) that binds specifically to a receptor (OB-R) in the brain, have validated critical aspects of this hypothesis. Here it is shown by genetic mapping and genomic analysis that mouse db, rat fatty (a homolog of db), and the gene encoding the OB-R are the same gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chua, S C Jr -- Chung, W K -- Wu-Peng, X S -- Zhang, Y -- Liu, S M -- Tartaglia, L -- Leibel, R L -- DK26687/DK/NIDDK NIH HHS/ -- DK47473/DK/NIDDK NIH HHS/ -- HD28047/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 16;271(5251):994-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Human Behavior and Metabolism, Rockefeller University, New York 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8584938" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Blotting, Southern ; Carrier Proteins/*genetics ; Chromosome Mapping ; Cloning, Molecular ; DNA Mutational Analysis ; Diabetes Mellitus/*genetics ; Genetic Markers ; Leptin ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Molecular Sequence Data ; Obesity/*genetics ; Phenotype ; Polymerase Chain Reaction ; Proteins/genetics ; Rats ; Rats, Inbred Strains ; *Receptors, Cell Surface ; Receptors, Cytokine/*genetics ; Receptors, Leptin
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 158
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    New clues to brain dopamine control, cocaine addiction (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, M -- New York, N.Y. -- Science. 1996 Feb 16;271(5251):909.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8584927" target="_blank"〉PubMed〈/a〉
    Keywords: Amphetamines/pharmacology ; Animals ; Brain/*metabolism ; Carrier Proteins/genetics/*physiology ; *Cocaine ; Dopamine/*metabolism ; Dopamine Plasma Membrane Transport Proteins ; *Membrane Glycoproteins ; *Membrane Transport Proteins ; Mice ; Mice, Knockout ; *Nerve Tissue Proteins ; Receptors, Dopamine/metabolism ; *Substance-Related Disorders ; Synapses/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 159
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    Sperm-egg binding protein or proto-oncogene? (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, J Y -- Silver, L M -- New York, N.Y. -- Science. 1996 Mar 8;271(5254):1432-4; author reply 1434-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596919" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Evolution, Molecular ; Female ; Humans ; Male ; Mice ; Molecular Sequence Data ; Protein-Tyrosine Kinases/*chemistry/genetics ; Proto-Oncogene Proteins/*chemistry/genetics ; Receptor Protein-Tyrosine Kinases/*chemistry/genetics ; Sequence Alignment ; Sperm-Ovum Interactions ; Spermatozoa/*chemistry
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 160
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    Retinal degeneration in mice lacking the gamma subunit of the rod cGMP phosphodiesterase (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-17
    Description: The retinal cyclic guanosine 3',5'-monophosphate (cGMP) phosphodiesterase (PDE) is a key regulator of phototransduction in the vertebrate visual system. PDE consists of a catalytic core of alpha and beta subunits associated with two inhibitory gamma subunits. A gene-targeting approach was used to disrupt the mouse PDEgamma gene. This mutation resulted in a rapid retinal degeneration resembling human retinitis pigmentosa. In homozygous mutant mice, reduced rather than increased PDE activity was apparent; the PDEalphabeta dimer was formed but lacked hydrolytic activity. Thus, the inhibitory gamma subunit appears to be necessary for integrity of the photoreceptors and expression of PDE activity in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757426/" 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/PMC2757426/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsang, S H -- Gouras, P -- Yamashita, C K -- Kjeldbye, H -- Fisher, J -- Farber, D B -- Goff, S P -- EY08285/EY/NEI NIH HHS/ -- K08 EY000408/EY/NEI NIH HHS/ -- K08 EY000408-01/EY/NEI NIH HHS/ -- T32 GM 073667-14/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 May 17;272(5264):1026-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry and Molecular Biophysics, Columbia University, College of Physicians and Surgeons, New York 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638127" target="_blank"〉PubMed〈/a〉
    Keywords: 3',5'-Cyclic-GMP Phosphodiesterases/deficiency/genetics/*metabolism ; Animals ; Base Sequence ; Chimera ; Crosses, Genetic ; Cyclic GMP/*metabolism ; Electroretinography ; Enzyme Activation ; Female ; Gene Targeting ; Humans ; Light ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Phenotype ; Retina/metabolism/*pathology/physiopathology ; Retinal Degeneration/*enzymology/pathology/physiopathology ; Retinal Rod Photoreceptor Cells/*enzymology/metabolism/pathology ; Retinitis Pigmentosa/pathology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 161
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    Binding of GSK3beta to the APC-beta-catenin complex and regulation of complex assembly (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-17
    Description: The adenomatous polyposis coli gene (APC) is mutated in most colon cancers. The APC protein binds to the cellular adhesion molecule beta-catenin, which is a mammalian homolog of ARMADILLO, a component of the WINGLESS signaling pathway in Drosophila development. Here it is shown that when beta-catenin is present in excess, APC binds to another component of the WINGLESS pathway, glycogen synthase kinase 3beta (GSK3beta), a mammalian homolog of Drosophila ZESTE WHITE 3. APC was a good substrate for GSK3 beta in vitro, and the phosphorylation sites were mapped to the central region of APC. Binding of beta-catenin to this region was dependent on phosphorylation by GSK3 beta.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rubinfeld, B -- Albert, I -- Porfiri, E -- Fiol, C -- Munemitsu, S -- Polakis, P -- New York, N.Y. -- Science. 1996 May 17;272(5264):1023-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Onyx Pharmaceuticals, Richmond, CA 94806, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638126" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Line ; Cytoskeletal Proteins/*metabolism ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinases ; Humans ; Mice ; Mutation ; Phosphorylation ; Protein Binding ; *Trans-Activators ; Tumor Cells, Cultured ; beta Catenin
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  • 162
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    Evidence for cell-surface association between fusin and the CD4-gp120 complex in human cell lines (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-25
    Description: Accessory cell-surface molecules involved in the entry of human immunodeficiency virus-type 1 into cells have recently been identified and shown to belong to the family of chemokine receptors. Treatment of human cell lines with soluble monomeric gp120 at 37 degrees C induced an association between the surface CD4-gp120 complex and a 45-kilodalton protein, which can be down-modulated by the phorbol ester phorbol 12-myristate 13-acetate. The three proteins were coprecipitated from the cell membranes with antibodies to CD4 or to gp120. The 45-kilodalton protein comigrated with fusin on sodium dodecyl sulfate gels and reacted with rabbit antisera to fusin in protein immunoblots. No 45-kilodalton protein could be coprecipitated from similarly treated nonhuman cells. However, infection of 3T3.CD4.401 cells with vaccinia-fusin recombinant virus (vCBYF1), followed by gp120 treatment, resulted in coprecipitation of fusin and CD4.401 molecules from their membranes. Together these data provide evidence for physical association between fusin and the CD4-gp120 complex on cell membranes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lapham, C K -- Ouyang, J -- Chandrasekhar, B -- Nguyen, N Y -- Dimitrov, D S -- Golding, H -- New York, N.Y. -- Science. 1996 Oct 25;274(5287):602-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Viral Products, Center for Biologics Evaluation and Research (CBER), Food and Drug Administration, 8800 Rockville Pike, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8849450" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Antigens, CD4/immunology/*metabolism ; Cell Line ; Cell Membrane/*metabolism ; Giant Cells ; HIV Envelope Protein gp120/immunology/*metabolism/pharmacology ; Humans ; Immunoblotting ; Membrane Fusion ; Membrane Proteins/chemistry/immunology/*metabolism ; Mice ; Molecular Sequence Data ; Molecular Weight ; Precipitin Tests ; Receptors, CXCR4 ; Receptors, HIV/chemistry/immunology/*metabolism ; T-Lymphocytes ; Tetradecanoylphorbol Acetate/pharmacology ; Vaccinia virus/genetics/physiology
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  • 163
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    Suppression of TNF-alpha-induced apoptosis by NF-kappaB (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-11-01
    Description: Tumor necrosis factor alpha (TNF-alpha) signaling gives rise to a number of events, including activation of transcription factor NF-kappaB and programmed cell death (apoptosis). Previous studies of TNF-alpha signaling have suggested that these two events occur independently. The sensitivity and kinetics of TNF-alpha-induced apoptosis are shown to be enhanced in a number of cell types expressing a dominant-negative IkappaBalpha (IkappaBalphaM). These findings suggest that a negative feedback mechanism results from TNF-alpha signaling in which NF-kappaB activation suppresses the signals for cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van Antwerp, D J -- Martin, S J -- Kafri, T -- Green, D R -- Verma, I M -- GM52735/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Nov 1;274(5288):787-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, Salk Institute, La Jolla, CA 92037, USA. Jolla Institute for Allergy and Immu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8864120" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Annexin A5/metabolism ; *Apoptosis ; Cells, Cultured ; DNA-Binding Proteins/genetics/physiology ; Feedback ; Humans ; *I-kappa B Proteins ; Jurkat Cells ; Mice ; NF-kappa B/*antagonists & inhibitors/*physiology ; Phosphatidylserines/metabolism ; *Signal Transduction ; Transcription Factor RelA ; Tumor Necrosis Factor-alpha/*pharmacology
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  • 164
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    Neoteny in lymphocytes: Rag1 and Rag2 expression in germinal center B cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: The products of the Rag1 and Rag2 genes drive genomic V(D)J rearrangements that assemble functional immunoglobulin and T cell antigen receptor genes. Expression of the Rag genes has been thought to be limited to developmentally immature lymphocyte populations that in normal adult animals are primarily restricted to the bone marrow and thymus. Abundant RAG1 and RAG2 protein and messenger RNA was detected in the activated B cells that populate murine splenic and Peyer's patch germinal centers. Germinal center B cells thus share fundamental characteristics of immature lymphocytes, raising the possibility that antigen-dependent secondary V(D)J rearrangements modify the peripheral antibody repertoire.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, S -- Zheng, B -- Schatz, D G -- Spanopoulou, E -- Kelsoe, G -- AG10207/AG/NIA NIH HHS/ -- AI24335/AI/NIAID NIH HHS/ -- AI32524/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2094-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of Maryland School of Medicine, 655 West Baltimore Street, Baltimore, MD 21201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953043" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology/*metabolism ; DNA Nucleotidyltransferases/metabolism ; *DNA-Binding Proteins ; Female ; *Gene Expression ; Gene Rearrangement ; Genes, Immunoglobulin ; *Genes, RAG-1 ; Germinal Center/*cytology/immunology ; *Homeodomain Proteins ; Immunization ; Immunoglobulin Class Switching ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Polymerase Chain Reaction ; Protein Biosynthesis ; Proteins/*genetics ; VDJ Recombinases
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  • 165
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    C3d of complement as a molecular adjuvant: bridging innate and acquired immunity (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-19
    Description: An optimal immune response should differentiate between harmful and innocuous antigens. Primitive systems of innate immunity, such as the complement system, may play a role in this distinction. When activated, the C3 component of complement attaches to potential antigens on microorganisms. To determine whether this alters acquired immune recognition, mice were immunized with a recombinant model antigen, hen egg lysozyme (HEL), fused to murine C3d. HEL bearing two and three copies of C3d was 1000- and 10,000-fold more immunogenic, respectively, than HEL alone. Thus, C3d is a molecular adjuvant of innate immunity that profoundly influences an acquired immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dempsey, P W -- Allison, M E -- Akkaraju, S -- Goodnow, C C -- Fearon, D T -- AI07247/AI/NIAID NIH HHS/ -- AI19512/AI/NIAID NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1996 Jan 19;271(5247):348-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Immunology Unit, Department of Medicine, University of Cambridge School of Medicine, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8553069" target="_blank"〉PubMed〈/a〉
    Keywords: *Adjuvants, Immunologic ; Animals ; *Antibody Formation ; Antigens, CD19/immunology/metabolism ; B-Lymphocytes/immunology ; Complement C3d/*immunology/metabolism ; Freund's Adjuvant/immunology ; Hemocyanin/immunology ; Humans ; *Immunity, Innate ; Immunoglobulin G/biosynthesis ; Male ; Mice ; Mice, Inbred CBA ; Mice, Transgenic ; Muramidase/immunology ; Receptors, Complement 3d/immunology/metabolism ; Recombinant Fusion Proteins/immunology/metabolism ; Tumor Cells, Cultured
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  • 166
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    PTH/PTHrP receptor in early development and Indian hedgehog-regulated bone growth (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-02
    Description: The PTH/PTHrP receptor binds to two ligands with distinct functions: the calcium-regulating hormone, parathyroid hormone (PTH), and the paracrine factor, PTH-related protein (PTHrP). Each ligand, in turn, is likely to activate more than one receptor. The functions of the PTH/PTHrP receptor were investigated by deletion of the murine gene by homologous recombination. Most PTH/PTHrP receptor (-/-) mutant mice died in mid-gestation, a phenotype not observed in PTHrP (-/-) mice, perhaps because of the effects of maternal PTHrP. Mice that survived exhibited accelerated differentiation of chondrocytes in bone, and their bones, grown in explant culture, were resistant to the effects of PTHrP and Sonic hedgehog. These results suggest that the PTH/PTHrP receptor mediates the effects of Indian Hedgehog and PTHrP on chondrocyte differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lanske, B -- Karaplis, A C -- Lee, K -- Luz, A -- Vortkamp, A -- Pirro, A -- Karperien, M -- Defize, L H -- Ho, C -- Mulligan, R C -- Abou-Samra, A B -- Juppner, H -- Segre, G V -- Kronenberg, H M -- DK 47038/DK/NIDDK NIH HHS/ -- DK 47237/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 2;273(5275):663-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662561" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Development ; Cartilage/*cytology/metabolism ; Cell Differentiation ; Cell Division ; Cloning, Molecular ; Culture Techniques ; Feedback ; Gene Deletion ; Gene Targeting ; Growth Plate/*cytology/metabolism ; Hedgehog Proteins ; Mice ; Mice, Inbred C57BL ; Osteoblasts/cytology ; *Osteogenesis ; Parathyroid Hormone ; Parathyroid Hormone-Related Protein ; Protein Biosynthesis ; Proteins/pharmacology/physiology ; Receptor, Parathyroid Hormone, Type 1 ; Receptors, Parathyroid Hormone/genetics/*physiology ; Stem Cells ; *Trans-Activators
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    Resistance to Leishmania major in mice (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Demant, P -- Lipoldova, M -- Svobodova, M -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1392-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966604" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytokines/pharmacology ; Genetic Predisposition to Disease ; Immunity, Innate/genetics ; Interleukin-12/immunology ; Leishmania major/*immunology ; Leishmaniasis, Cutaneous/genetics/*immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; T-Lymphocytes/*immunology ; Th1 Cells/immunology
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  • 168
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    Requirement for invariant chain in B cell maturation and function (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-04
    Description: Previously the role of invariant chain (Ii) had been described only as a chaperone that facilitates folding and transport of major histocompatability complex class II molecules; here it is shown that Ii is required for B cell development. B cells from mice lacking Ii were found to have a low response to T-independent type II antigen and could not proliferate after the mice were injected with antigen. Study of cell surface markers revealed a developmental arrest that prevented immature virgin B cells from becoming mature B cells in the periphery. This block was independent of major histocompatability complex class II expression and was an intrinsic feature of B cells that correlated with the amount of Ii. Thus, Ii participates by an unknown mechanism in B cell maturation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shachar, I -- Flavell, R A -- New York, N.Y. -- Science. 1996 Oct 4;274(5284):106-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8810244" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; Antigens, Differentiation, B-Lymphocyte/*physiology ; B-Lymphocytes/*immunology/physiology ; Bone Marrow Cells ; Cells, Cultured ; Histocompatibility Antigens Class II/*physiology ; Immunization ; Immunoglobulin D/analysis ; Immunoglobulin M/analysis ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Mice, Transgenic ; Receptors, IgE/analysis
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  • 169
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    Muscling transplants into mice (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1996 Jul 5;273(5271):33.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658188" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Transplantation ; Diabetes Mellitus, Experimental/*surgery ; Fas Ligand Protein ; Genetic Engineering ; Graft Rejection/*prevention & control ; Graft Survival ; *Islets of Langerhans Transplantation ; Membrane Glycoproteins/*biosynthesis ; Mice ; Muscle Fibers, Skeletal/*cytology/*metabolism/transplantation ; Recombinant Proteins/biosynthesis ; T-Lymphocytes/cytology ; Transfection ; Transplantation, Heterotopic
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  • 170
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    Rearrangement-enhancing element upstream of the mouse immunoglobulin kappa chain J cluster (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-08
    Description: Transcriptional regulatory elements have been shown to be necessary but not sufficient for the developmental regulation of immunoglobulin gene rearrangement in mouse precursor B cells. In the chicken lambda light chain locus, additional elements in the V-J intervening sequence are involved in negative and positive regulation of rearrangement. Here, mutation of the mouse homolog of a chicken element, located in the V(K)-J(K) intervening sequence upstream of the J(K) cluster, was shown to significantly decrease rearrangement. This cis-acting recombination-enhancing element affects the rearrangement process without being involved in regulating transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferradini, L -- Gu, H -- De Smet, A -- Rajewsky, K -- Reynaud, C A -- Weill, J C -- New York, N.Y. -- Science. 1996 Mar 8;271(5254):1416-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U373, Institut Necker, Faculte de Medecine, Universite Paris V, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596914" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; B-Lymphocytes/cytology/immunology ; Base Sequence ; Chimera ; Enhancer Elements, Genetic ; *Gene Rearrangement, B-Lymphocyte ; Gene Rearrangement, T-Lymphocyte ; Gene Targeting ; *Genes, Immunoglobulin ; Immunoglobulin J-Chains/*genetics ; Immunoglobulin Variable Region/genetics ; Immunoglobulin kappa-Chains/*genetics ; Introns ; Mice ; Mice, Inbred C57BL ; Mice, SCID ; Molecular Sequence Data ; Mutation ; Recombination, Genetic ; *Regulatory Sequences, Nucleic Acid ; Stem Cells
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  • 171
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    The immunological evolution of catalysis (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-23
    Description: The germline genes used by the mouse to generate the esterolytic antibody 48G7 were cloned and expressed in an effort to increase our understanding of the detailed molecular mechanisms by which the immune system evolves catalytic function. The nine replacement mutations that were fixed during affinity maturation increased affinity for the transition state analogue by a factor of 10(4), primarily the result of a decrease in the dissociation rate of the hapten-antibody complex. There was a corresponding increase in the rate of reaction of antibody with substrate, k(cat)/k(m), from 1.7 x 10(2)M(-1) min(-1) to 1.4 x 10(4)M(-1) min(-1). The three-dimensional crystal structure of the 48G7-transition state analogue complex at 2.0 angstroms resolution indicates that one of the nine residues in which somatic mutations have been fixed directly contact the hapten. Thus, in the case of 48G7, affinity maturation appears to play a conformational role, either in reorganizing the active site geometry of limiting side-chain and backbone flexibility of the germline antibody. The crystal structure and analysis of somatic and directed active site mutants underscore the role of transition state stabilization in the evolution of this catalytic antibody.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patten, P A -- Gray, N S -- Yang, P L -- Marks, C B -- Wedemayer, G J -- Boniface, J J -- Stevens, R C -- Schultz, P G -- R01 AL24695/PHS HHS/ -- New York, N.Y. -- Science. 1996 Feb 23;271(5252):1086-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Chemistry, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8599084" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Catalytic/chemistry/genetics/*immunology/metabolism ; Antibody Affinity ; Antigen-Antibody Complex ; Antigen-Antibody Reactions ; Base Sequence ; Binding Sites ; Catalysis ; Cloning, Molecular ; Crystallization ; Crystallography, X-Ray ; *Evolution, Molecular ; Genes, Immunoglobulin ; Haptens/immunology ; Immunoglobulin Fab Fragments/genetics/immunology ; Immunoglobulin Heavy Chains/genetics/immunology ; Immunoglobulin Light Chains/genetics/immunology ; Mice ; Molecular Sequence Data ; Mutation ; Protein Conformation
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    Blocked Ras activation in anergic CD4+ T cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: T cell anergy is a state of functional unresponsiveness characterized by the inability to produce interleukin-2 (IL-2) upon T cell receptor stimulation. The mitogen-activated protein kinases ERK-1 and ERK-2 and the guanosine triphosphate-binding protein p21ras were found to remain unactivated upon stimulation of anergic murine T helper cell 1 clones. The inability to activate the Ras pathway did not result from a defect in association among Shc, Grb-2, and murine Son of Sevenless, nor from a defect in their tyrosine phosphorylation. This block in Ras activation may lead to defective transactivation at activator protein 1 sites in anergic cells and may enable T cells to shut down IL-2 production selectively during anergy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fields, P E -- Gajewski, T F -- Fitch, F W -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1276-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ben May Institute, Department of Pathology, University of Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638108" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD4/immunology ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; *Clonal Anergy ; Clone Cells ; GRB2 Adaptor Protein ; Guanine Nucleotide Exchange Factors ; Guanosine Triphosphate/metabolism ; Interleukin-2/biosynthesis ; Ionomycin/pharmacology ; Lymphocyte Activation ; Mice ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Protein-Tyrosine Kinases/metabolism ; Proteins/metabolism ; Proto-Oncogene Proteins p21(ras)/*metabolism ; Receptors, Antigen, T-Cell/immunology ; *Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; Th1 Cells/*immunology/metabolism ; ras Guanine Nucleotide Exchange Factors
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  • 173
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    Mouse models of atherosclerosis (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-03
    Description: As a species the mouse is highly resistant to atherosclerosis. However, through induced mutations it has been possible to develop lines of mice that are susceptible to this disease. For example, mice that are deficient in apolipoprotein E, a ligand important in lipoprotein clearance, develop atherosclerotic lesions resembling those observed in humans. These lesions are exacerbated when the mice are fed a high-cholesterol, high-fat, Western-type diet. Other promising models are mice that are deficient in the low density lipoprotein receptor and transgenic mice that express human apolipoprotein B and transdominant mutant forms of apolipoprotein E. These models are now being used to study the pathogenesis of atherosclerotic lesions, as well as the influence of genetics, environment, hormones, and drugs on lesion development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Breslow, J L -- New York, N.Y. -- Science. 1996 May 3;272(5262):685-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York, 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614828" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoproteins B/deficiency/genetics ; Apolipoproteins E/deficiency/genetics ; *Arteriosclerosis/etiology/genetics/metabolism ; Cholesterol, Dietary/administration & dosage ; Dietary Fats/administration & dosage ; *Disease Models, Animal ; Genetic Predisposition to Disease ; Humans ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Mice, Transgenic ; Mutation ; Receptors, LDL/deficiency/genetics
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  • 174
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    Reduction of morphine abstinence in mice with a mutation in the gene encoding CREB (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-02
    Description: Chronic morphine administration induces an up-regulation of several components of the cyclic adenosine 5'-monophosphate (cAMP) signal transduction cascade. The behavioral and biochemical consequences of opiate withdrawal were investigated in mice with a genetic disruption of the alpha and Delta isoforms of the cAMP-responsive element-binding protein (CREB). In CREBalphadelta mutant mice the main symptoms of morphine withdrawal were strongly attenuated. No change in opioid binding sites or in morphine-induced analgesia was observed in these mutant mice, and the increase of adenylyl cyclase activity and immediate early gene expression after morphine withdrawal was normal. Thus, CREB-dependent gene transcription is a factor in the onset of behavioral manifestations of opiate dependence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maldonado, R -- Blendy, J A -- Tzavara, E -- Gass, P -- Roques, B P -- Hanoune, J -- Schutz, G -- New York, N.Y. -- Science. 1996 Aug 2;273(5275):657-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departement de Pharmacochimie Moleculaire et Structurale, Unite de Recherche Associee D1500 CNRS, Universite Rene Descartes, Faculte de Pharmacie, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662559" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Analgesia ; Animals ; Behavior, Animal ; Cerebral Cortex/enzymology ; Cyclic AMP Response Element-Binding Protein/*genetics/*physiology ; Drug Tolerance ; Gene Expression Regulation ; Gene Targeting ; Genes, Immediate-Early ; Locus Coeruleus/metabolism ; Mice ; Morphine/*administration & dosage/adverse effects/pharmacology ; Morphine Dependence/*etiology/metabolism ; Mutation ; Naloxone/pharmacology ; Receptors, Opioid/metabolism ; Signal Transduction ; Substance Withdrawal Syndrome/*physiopathology
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  • 175
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    Control of MHC restriction by TCR Valpha CDR1 and CDR2 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-16
    Description: Individual T cell receptor (TCR) Valpha elements are expressed preferentially in CD4 or CD8 peripheral T cell subsets. The closely related Valpha3.1 and Valpha3.2 elements show reciprocal selection into CD4 and CD8 subsets, respectively. Transgenic mice expressing site-directed mutants of a Valpha3.1 gene were used to show that individual residues in either the complementarity-determining region 1 (CDR1) or CDR2 were sufficient to change selection from the CD4 subset to the CD8 subset. Thus, the germline-encoded Valpha elements are a major influence on major histocompatibility class complex (MHC) restriction, most likely by a preferential interaction with one or the other class of MHC molecule.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sim, B C -- Zerva, L -- Greene, M I -- Gascoigne, N R -- R01 GM48002/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 16;273(5277):963-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. University of Pennsylvania, Philadelphia, PA 1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8688082" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Histocompatibility Antigens Class I/*immunology ; Histocompatibility Antigens Class II/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Mutagenesis, Site-Directed ; Receptors, Antigen, T-Cell, alpha-beta/chemistry/genetics/*immunology ; Transgenes
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    The POU factor Oct-6 and Schwann cell differentiation (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-26
    Description: The POU transcription factor Oct-6, also known as SCIP or Tst-1, has been implicated as a major transcriptional regulator in Schwann cell differentiation. Microscopic and immunochemical analysis of sciatic nerves of Oct-6(-/-) mice at different stages of postnatal development reveals a delay in Schwann cell differentiation, with a transient arrest at the promyelination stage. Thus, Oct-6 appears to be required for the transition of promyelin cells to myelinating cells. Once these cells progress past this point, Oct-6 is no longer required, and myelination occurs normally.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaegle, M -- Mandemakers, W -- Broos, L -- Zwart, R -- Karis, A -- Visser, P -- Grosveld, F -- Meijer, D -- New York, N.Y. -- Science. 1996 Jul 26;273(5274):507-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Genetics Center, Department of Cell Biology and Genetics, Erasmus University, Post Office Box 1738, 3000 DR Rotterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662541" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Axons/ultrastructure ; Base Sequence ; Cell Differentiation ; Gene Expression ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Myelin P0 Protein/genetics/metabolism ; Myelin Proteins/genetics/metabolism ; Myelin Sheath/physiology ; Octamer Transcription Factor-6 ; Recombination, Genetic ; Schwann Cells/*cytology/physiology ; Sciatic Nerve/cytology/growth & development ; Stem Cells ; Transcription Factors/*genetics/*physiology
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    Regulation of T cell receptor signaling by tyrosine phosphatase SYP association with CTLA-4 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-24
    Description: The absence of CTLA-4 results in uncontrolled T cell proliferation. The T cell receptor-specific kinases FYN, LCK, and ZAP-70 as well as the RAS pathway were found to be activated in T cells of Ctla-4-/- mutant mice. In addition, CTLA-4 specifically associated with the tyrosine phosphatase SYP, an interaction mediated by the SRC homology 2 (SH2) domains of SYP and the phosphotyrosine sequence Tyr-Val-Lys-Met within the CTLA-4 cytoplasmic tail. The CTLA-4-associated SYP had phosphatase activity toward the RAS regulator p52SHC. Thus, the RAS pathway and T cell activation through the T cell receptor are regulated by CTLA-4-associated SYP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marengere, L E -- Waterhouse, P -- Duncan, G S -- Mittrucker, H W -- Feng, G S -- Mak, T W -- New York, N.Y. -- Science. 1996 May 24;272(5265):1170-3.〈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/8638161" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; *Adaptor Proteins, Signal Transducing ; *Adaptor Proteins, Vesicular Transport ; Amino Acid Sequence ; Animals ; Antigens, CD ; Antigens, CD3/metabolism ; Antigens, Differentiation/chemistry/*metabolism ; CTLA-4 Antigen ; GRB2 Adaptor Protein ; *Immunoconjugates ; Intracellular Signaling Peptides and Proteins ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 ; Protein Tyrosine Phosphatases/*metabolism ; Protein-Tyrosine Kinases/metabolism ; Proteins/metabolism ; Receptors, Antigen, B-Cell/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Recombinant Fusion Proteins/metabolism ; SH2 Domain-Containing Protein Tyrosine Phosphatases ; Shc Signaling Adaptor Proteins ; *Signal Transduction ; T-Lymphocytes/immunology/*metabolism ; ras Proteins/metabolism ; src Homology Domains
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  • 178
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    Regulation of the inositol 1,4,5-trisphosphate receptor by tyrosine phosphorylation (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-07
    Description: Tyrosine kinases indirectly raise intracellular calcium concentration ([Ca2+]i) by activating phospholipases that generate inositol 1,4,5-trisphosphate (IP3). IP3 activates the IP3 receptor (IP3R), an intracellular calcium release channel on the endoplasmic reticulum. T cell receptor stimulation triggered a physical association between the nonreceptor protein tyrosine kinase Fyn and the IP3R, which induced tyrosine phosphorylation of the IP3R. Fyn activated an IP3-gated calcium channel in vitro, and tyrosine phosphorylation of the IP3R during T cell activation was reduced in thymocytes from fyn-/- mice. Thus, activation of the IP3R by tyrosine phosphorylation may play a role in regulating [Ca2+]i.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jayaraman, T -- Ondrias, K -- Ondriasova, E -- Marks, A R -- N529814/PHS HHS/ -- New York, N.Y. -- Science. 1996 Jun 7;272(5267):1492-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Molecular Cardiology, Department of Medicine, Mount Sinai School of Medicine, New York 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8633244" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Calcium/metabolism ; Calcium Channels/*metabolism ; Humans ; Inositol 1,4,5-Trisphosphate/*metabolism/pharmacology ; Inositol 1,4,5-Trisphosphate Receptors ; Lipid Bilayers ; Lymphocyte Activation ; Mice ; Phosphorylation ; Phosphotyrosine/*metabolism ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism/pharmacology ; Proto-Oncogene Proteins c-fyn ; Receptors, Cytoplasmic and Nuclear/*metabolism ; T-Lymphocytes/immunology/metabolism ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 179
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    A model of host-microbial interactions in an open mammalian ecosystem (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-09-06
    Description: The maintenance and significance of the complex populations of microbes present in the mammalian intestine are poorly understood. Comparison of conventionally housed and germ-free NMRI mice revealed that production of fucosylated glycoconjugates and an alpha1, 2-fucosyltransferase messenger RNA in the small-intestinal epithelium requires the normal microflora. Colonization of germ-free mice with Bacteroides thetaiotaomicron, a component of this flora, restored the fucosylation program, whereas an isogenic strain carrying a transposon insertion that disrupts its ability to use L-fucose as a carbon source did not. Simplified models such as this should aid the study of open microbial ecosystems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bry, L -- Falk, P G -- Midtvedt, T -- Gordon, J I -- DK30292/DK/NIDDK NIH HHS/ -- DK37960/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Sep 6;273(5280):1380-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8703071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteroides/growth & development/metabolism/*physiology ; Base Sequence ; Cell Differentiation ; Cell Lineage ; Colony Count, Microbial ; Ecosystem ; Fucose/*metabolism ; Fucosyltransferases/genetics/metabolism ; Germ-Free Life ; Glycoconjugates/*metabolism ; Intestinal Mucosa/cytology/*microbiology ; Intestine, Small/cytology/metabolism/*microbiology ; Male ; Mice ; Mice, Inbred Strains ; Molecular Sequence Data ; Polymerase Chain Reaction ; RNA, Messenger/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 180
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    Adaptive evolution of human immunodeficiency virus-type 1 during the natural course of infection (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-26
    Description: The rate of progression to disease varies considerably among individuals infected with human immunodeficiency virus-type 1 (HIV-1). Analyses of semiannual blood samples obtained from six infected men showed that a rapid rate of CD4 T cell loss was associated with relative evolutionary stasis of the HIV-1 quasispecies virus population. More moderate rates of CD4 T cell loss correlated with genetic evolution within three of four subjects. Consistent with selection by the immune constraints of these subjects, amino acid changes were apparent within the appropriate epitopes of human leukocyte antigen class I-restricted cytotoxic T lymphocytes. Thus, the evolutionary dynamics exhibited by the HIV-1 quasispecies virus populations under natural selection are compatible with adaptive evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolinsky, S M -- Korber, B T -- Neumann, A U -- Daniels, M -- Kunstman, K J -- Whetsell, A J -- Furtado, M R -- Cao, Y -- Ho, D D -- Safrit, J T -- AI32535/AI/NIAID NIH HHS/ -- AI35522/AI/NIAID NIH HHS/ -- AI45218/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Apr 26;272(5261):537-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Northwestern University Medical School, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614801" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology/virology ; Amino Acid Sequence ; Animals ; *Antigenic Variation ; Base Sequence ; Biological Evolution ; CD4 Lymphocyte Count ; Cohort Studies ; Disease Progression ; HIV Antibodies/immunology ; HIV Antigens/immunology ; HIV Infections/*immunology/*virology ; HIV-1/*genetics/immunology/pathogenicity/physiology ; Histocompatibility Antigens Class I/immunology ; Humans ; Male ; Mice ; Mice, SCID ; Molecular Sequence Data ; Mutation ; Phenotype ; RNA, Viral/blood ; T-Lymphocytes, Cytotoxic/*immunology ; Virulence ; Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 181
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    Is the new variant of Creutzfeldt-Jakob disease from mad cows? (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, P G -- Cousens, S N -- New York, N.Y. -- Science. 1996 Aug 9;273(5276):748.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Epidemiology and Population Sciences, London School of Hygiene and Tropical Medicine, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8701324" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Feed ; Animals ; Cattle ; Creutzfeldt-Jakob Syndrome/epidemiology/*transmission ; Encephalopathy, Bovine Spongiform/epidemiology/*transmission ; Food Contamination ; Great Britain/epidemiology ; Humans ; Meat ; Mice
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 182
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    Structures of an MHC class II molecule with covalently bound single peptides (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-17
    Description: The high-resolution x-ray crystal structures of the murine major histocompatibility complex (MHC) class II molecule, I-E(k), occupied by either of two antigenic peptides were determined. They reveal the structural basis for the I-E(k) peptide binding motif and suggest general principles for additional alleles. A buried cluster of acidic amino acids in the binding groove predicted to be conserved among all murine I-E and human DR MHC class II molecules suggests how pH may influence MHC binding or exchange of peptides. These structures also complement mutational studies on the importance of individual peptide residues to T cell receptor recognition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fremont, D H -- Hendrickson, W A -- Marrack, P -- Kappler, J -- New York, N.Y. -- Science. 1996 May 17;272(5264):1001-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry and Molecular Biophysics, Columbia University, New York, 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638119" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/chemistry ; Animals ; Antigen Presentation ; Antigens/*chemistry/immunology/metabolism ; Crystallography, X-Ray ; HLA-DR Antigens/chemistry/immunology/metabolism ; HSP70 Heat-Shock Proteins/chemistry ; Hemoglobins/chemistry ; Histocompatibility Antigens Class II/*chemistry/immunology/metabolism ; Humans ; Hydrogen Bonding ; Hydrogen-Ion Concentration ; Mice ; Models, Molecular ; Molecular Sequence Data ; Peptide Fragments/*chemistry/immunology/metabolism ; Protein Binding ; Protein Conformation ; Protein Structure, Secondary ; Receptors, Antigen, T-Cell/metabolism
    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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  • 183
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    Teetering on the brink of danger (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1665-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596923" target="_blank"〉PubMed〈/a〉
    Keywords: Adjuvants, Immunologic ; Animals ; Animals, Newborn/immunology ; Antigen-Presenting Cells/immunology ; Female ; Immune System/*immunology ; *Immune Tolerance ; Immunization ; Lymphocyte Activation ; Male ; Mice ; *Self Tolerance ; T-Lymphocytes/*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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  • 184
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    Small peptides as potent mimetics of the protein hormone erythropoietin (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-26
    Description: Random phage display peptide libraries and affinity selective methods were used to isolate small peptides that bind to and activate the receptor for the cytokine erythropoietin (EPO). In a panel of in vitro biological assays, the peptides act as full agonists and they can also stimulate erythropoiesis in mice. These agonists are represented by a 14- amino acid disulfide-bonded, cyclic peptide with the minimum consensus sequence YXCXXGPXTWXCXP, where X represents positions allowing occupation by several amino acids. The amino acid sequences of these peptides are not found in the primary sequence of EPO. The signaling pathways activated by these peptides appear to be identical to those induced by the natural ligand. This discovery may form the basis for the design of small molecule mimetics of EPO.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wrighton, N C -- Farrell, F X -- Chang, R -- Kashyap, A K -- Barbone, F P -- Mulcahy, L S -- Johnson, D L -- Barrett, R W -- Jolliffe, L K -- Dower, W J -- New York, N.Y. -- Science. 1996 Jul 26;273(5274):458-64.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Affymax Research Institute, 4001 Miranda Avenue, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662529" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bacteriophages ; Cell Division/drug effects ; Cell Line ; Cloning, Molecular ; Erythropoiesis/drug effects ; Erythropoietin/chemistry/*metabolism/*pharmacology ; Humans ; Ligands ; Mice ; *Molecular Mimicry ; Molecular Sequence Data ; Mutagenesis ; Peptides, Cyclic/chemistry/*metabolism/*pharmacology ; Phosphorylation ; Protein Structure, Secondary ; Receptors, Erythropoietin/*agonists/chemistry/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Signal Transduction ; Solubility ; Tyrosine/metabolism
    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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