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  • Mice  (184)
  • American Association for the Advancement of Science (AAAS)  (184)
  • Annual Reviews
  • 2005-2009
  • 1995-1999  (184)
  • 1990-1994
  • 1980-1984
  • 1945-1949
  • 1996  (184)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (184)
  • Annual Reviews
  • Springer  (1)
Years
  • 2005-2009
  • 1995-1999  (184)
  • 1990-1994
  • 1980-1984
  • 1945-1949
Year
  • 1
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    IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-02
    Description: Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. An inhibitory form of IRS-1 was observed in muscle and fat tissues from obese rats. These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hotamisligil, G S -- Peraldi, P -- Budavari, A -- Ellis, R -- White, M F -- Spiegelman, B M -- DK 42539/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):665-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Biology, Dana-Farber Cancer Institute, Boston, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571133" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/*metabolism ; Adipose Tissue/metabolism ; Animals ; Cells, Cultured ; Insulin/pharmacology ; Insulin Receptor Substrate Proteins ; Insulin Resistance/*physiology ; Male ; Mice ; Muscle, Skeletal/metabolism ; Obesity/*metabolism ; Phosphoproteins/metabolism/*physiology ; Phosphorylation ; Rats ; Rats, Zucker ; Receptor, Insulin/*antagonists & inhibitors/metabolism ; Serine/metabolism ; Signal Transduction ; Tumor Necrosis Factor-alpha/*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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  • 2
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    Disputed results now just a footnote (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1996 Jul 12;273(5272):174-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8668989" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Anti-Idiotypic/*immunology ; Hybridomas ; Immune System/*immunology ; Immunoglobulin Idiotypes/biosynthesis/*immunology ; Mice ; Mice, Transgenic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Abnormal centrosome amplification in the absence of p53 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-22
    Description: The centrosome plays a vital role in mitotic fidelity, ensuring establishment of bipolar spindles and balanced chromosome segregation. Centrosome duplication occurs only once during the cell cycle and is therefore highly regulated. Here, it is shown that in mouse embryonic fibroblasts (MEFs) lacking the p53 tumor suppressor protein, multiple copies of functionally competent centrosomes are generated during a single cell cycle. In contrast, MEFs prepared from normal mice or mice deficient in the retinoblastoma tumor suppressor gene product do not display these abnormalities. The abnormally amplified centrosomes profoundly affect mitotic fidelity, resulting in unequal segregation of chromosomes. These observations implicate p53 in the regulation of centrosome duplication and suggest one possible mechanism by which the loss of p53 may cause genetic instability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukasawa, K -- Choi, T -- Kuriyama, R -- Rulong, S -- Vande Woude, G F -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1744-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, MD 21702-1201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596939" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood ; Cells, Cultured ; Centrosome/*metabolism ; Culture Media ; Fibroblasts ; Genes, Retinoblastoma ; Genes, p53 ; *Interphase ; Mice ; *Mitosis ; Spindle Apparatus/metabolism/ultrastructure ; Tumor Suppressor Protein p53/*physiology
    Print ISSN: 0036-8075
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  • 4
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    RAC regulation of actin polymerization and proliferation by a pathway distinct from Jun kinase (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-22
    Description: The RAC guanine nucleotide binding proteins regulate multiple biological activities, including actin polymerization, activation of the Jun kinase (JNK) cascade, and cell proliferation. RAC effector loop mutants were identified that separate the ability of RAC to interact with different downstream effectors. One mutant of activated human RAC protein, RACV12H40 (with valine and histidine substituted at position 12 and 40, respectively), was defective in binding to PAK3, a Ste20-related p21-activated kinase (PAK), but bound to POR1, a RAC-binding protein. This mutant failed to stimulate PAK and JNK activity but still induced membrane ruffling and mediated transformation. A second mutant, RACV12L37 (with leucine substituted at position 37), which bound PAK but not POR1, induced JNK activation but was defective in inducing membrane ruffling and transformation. These results indicate that the effects of RAC on the JNK cascade and on actin polymerization and cell proliferation are mediated by distinct effector pathways that diverge at the level of RAC itself.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joneson, T -- McDonough, M -- Bar-Sagi, D -- Van Aelst, L -- CA55360/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1374-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, State University of New York, Stony Brook, NY 11794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8910277" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Actins/*metabolism ; *Adaptor Proteins, Signal Transducing ; Animals ; COS Cells ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Carrier Proteins/metabolism ; *Cell Division ; Cell Line ; Cell Line, Transformed ; Cell Membrane/ultrastructure ; Enzyme Activation ; GTP-Binding Proteins/genetics/metabolism/*physiology ; Humans ; JNK Mitogen-Activated Protein Kinases ; Mice ; *Mitogen-Activated Protein Kinases ; Mutagenesis ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Transfection ; p21-Activated Kinases ; rac GTP-Binding Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Inhibition of myogenic bHLH and MEF2 transcription factors by the bHLH protein Twist (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-07
    Description: The myogenic basic helix-loop-helix (bHLH) and MEF2 transcription factors are expressed in the myotome of developing somites and cooperatively activate skeletal muscle gene expression. The bHLH protein Twist is expressed throughout the epithelial somite and is subsequently excluded from the myotome. Ectopically expressed mouse Twist (Mtwist) was shown to inhibit myogenesis by blocking DNA binding by MyoD, by titrating E proteins, and by inhibiting trans-activation by MEF2. For inhibition of MEF2, Mtwist required heterodimerization with E proteins and an intact basic domain and carboxyl-terminus. Thus, Mtwist inhibits both families of myogenic regulators and may regulate myotome formation temporally or spatially.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spicer, D B -- Rhee, J -- Cheung, W L -- Lassar, A B -- 5-F32-AR08214-02/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jun 7;272(5267):1476-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8633239" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors ; Cell Differentiation ; Cell Line ; Creatine Kinase/genetics ; DNA/metabolism ; DNA-Binding Proteins/*antagonists & inhibitors/chemistry/genetics/metabolism ; Drosophila ; Drosophila Proteins ; Helix-Loop-Helix Motifs/*physiology ; Inhibitor of Differentiation Protein 1 ; MEF2 Transcription Factors ; Mice ; Muscle, Skeletal/*cytology/metabolism ; MyoD Protein/metabolism/physiology ; Myogenic Regulatory Factors ; Nuclear Proteins/chemistry/metabolism/*physiology ; *Repressor Proteins ; TCF Transcription Factors ; Transcription Factor 7-Like 1 Protein ; Transcription Factors/*antagonists & ; inhibitors/chemistry/genetics/metabolism/physiology ; Transcriptional Activation ; Transfection ; Twist Transcription Factor
    Print ISSN: 0036-8075
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  • 6
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    An enhanced immune response in mice lacking the transcription factor NFAT1 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-10
    Description: Transcription factors of the NFAT family are thought to play a major role in regulating the expression of cytokine genes and other inducible genes during the immune response. The role of NFAT1 was investigated by targeted disruption of the NFAT1 gene. Unexpectedly, cells from NFAT1 -/- mice showed increased primary responses to Leishmania major and mounted increased secondary responses to ovalbumin in vitro. In an in vivo model of allergic inflammation, the accumulation of eosinophils and levels of serum immunoglobulin E were increased in NFAT1 -/- mice. These results suggest that NFAT1 exerts a negative regulatory influence on the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xanthoudakis, S -- Viola, J P -- Shaw, K T -- Luo, C -- Wallace, J D -- Bozza, P T -- Luk, D C -- Curran, T -- Rao, A -- CA42471/CA/NCI NIH HHS/ -- GM46227/GM/NIGMS NIH HHS/ -- P30 CA21765/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 May 10;272(5263):892-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurogenetics Program, Department of CNS Research, Hoffmann-LaRoche, Nutley, NJ 07110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8629027" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, Protozoan/immunology ; Cell Line ; Cytokines/biosynthesis ; DNA-Binding Proteins/genetics/*physiology ; Eosinophils/immunology ; Gene Targeting ; Hypersensitivity/*immunology ; *Immunity ; Immunoglobulin E/biosynthesis ; Immunologic Memory ; Leishmania major/immunology ; *Lymphocyte Activation ; Mice ; Molecular Sequence Data ; NFATC Transcription Factors ; *Nuclear Proteins ; Ovalbumin/immunology ; T-Lymphocytes/immunology ; Transcription Factors/genetics/*physiology
    Print ISSN: 0036-8075
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  • 7
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    Antigen presentation and T cell development in H2-M-deficient mice (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: HLA-DM (DM) facilitates peptide loading of major histocompatibility complex class II molecules in human cell lines. Mice lacking functional H2-M, the mouse equivalent of DM, have normal amounts of class II molecules at the cell surface, but most of these are associated with invariant chain-derived CLIP peptides. These mice contain large numbers of CD4+ T cells, which is indicative of positive selection in the thymus. Their CD4+ cells were unresponsive to self H2-M-deficient antigen-presenting cells (APCs) but were hyperreactive to wild-type APCs. H2-M-deficient APCs failed to elicit proliferative responses from wild-type T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fung-Leung, W P -- Surh, C D -- Liljedahl, M -- Pang, J -- Leturcq, D -- Peterson, P A -- Webb, S R -- Karlsson, L -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1278-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638109" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigen-Presenting Cells/*immunology ; Antigens, Differentiation, B-Lymphocyte/immunology/metabolism ; Base Sequence ; CD4-Positive T-Lymphocytes/*immunology ; Cells, Cultured ; Gene Targeting ; Histocompatibility Antigens Class II/genetics/*immunology/metabolism ; Isoantigens/immunology ; Lymphocyte Activation ; Mice ; Molecular Sequence Data ; Mutation
    Print ISSN: 0036-8075
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  • 8
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    Resistance to Leishmania major induced by tolerance to a single antigen (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-18
    Description: In mice, susceptibility to Leishmania major is associated with the early expansion of T helper 2 cells (TH2) cells, but nothing is known of the specificity of these cells. A previously identified antigen, Leishmania homolog of receptors for activated C kinase (LACK), was found to be the focus of this initial response. Mice made tolerant to LACK by the transgenic expression of the antigen in the thymus exhibited both a diminished TH2 response and a healing phenotype. Thus, T cells that are activated early and are reactive to a single antigen play a pivotal role in directing the immune response to the entire parasite.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Julia, V -- Rassoulzadegan, M -- Glaichenhaus, N -- New York, N.Y. -- Science. 1996 Oct 18;274(5286):421-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS, Institut de Pharmacologie Moleculaire et Cellulaire, 660 Route des Lucioles, 06560 Valbonne, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8832890" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, Protozoan/*immunology ; Crosses, Genetic ; Female ; Immune Tolerance ; Immunity, Innate ; Immunization ; Interleukin-4/secretion ; Interleukin-5/secretion ; Leishmania major/*immunology ; Leishmaniasis, Cutaneous/*immunology ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Molecular Sequence Data ; Phenotype ; Protozoan Proteins/*immunology ; Th1 Cells/immunology ; Th2 Cells/*immunology
    Print ISSN: 0036-8075
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  • 9
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    Intestinal secretory defects and dwarfism in mice lacking cGMP-dependent protein kinase II (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: Cyclic guanosine 3',5'-monophosphate (cGMP)-dependent protein kinases (cGKs) mediate cellular signaling induced by nitric oxide and cGMP. Mice deficient in the type II cGK were resistant to Escherichia coli STa, an enterotoxin that stimulates cGMP accumulation and intestinal fluid secretion. The cGKII-deficient mice also developed dwarfism that was caused by a severe defect in endochondral ossification at the growth plates. These results indicate that cGKII plays a central role in diverse physiological processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfeifer, A -- Aszodi, A -- Seidler, U -- Ruth, P -- Hofmann, F -- Fassler, R -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2082-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut f-ur Pharmakologie und Toxikologie, Technische Universitat Munchen, Biedersteiner Strasse 29, D-80802 M-unchen, Germany. pfeifer@ipt.med.tu-muenchen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953039" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Animals ; Bacterial Toxins/toxicity ; Body Water/secretion ; *Bone Development ; Crosses, Genetic ; Cyclic GMP/analogs & derivatives/metabolism/pharmacology ; Cyclic GMP-Dependent Protein Kinases/deficiency/genetics/*metabolism ; Diarrhea/physiopathology ; Dwarfism/*enzymology/genetics/pathology ; Enterotoxins/toxicity ; Escherichia coli Proteins ; Female ; Gene Deletion ; Growth Plate/enzymology/pathology ; Intestinal Mucosa/*secretion ; Male ; Mice ; Mice, Inbred C57BL ; Osteogenesis ; Signal Transduction
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  • 10
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    G protein-mediated neuronal DNA fragmentation induced by familial Alzheimer's disease-associated mutants of APP (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-31
    Description: Missense mutations in the 695-amino acid form of the amyloid precursor protein (APP695) cosegregate with disease phenotype in families with dominantly inherited Alzheimer's disease. These mutations convert valine at position 642 to isoleucine, phenylalanine, or glycine. Expression of these mutant proteins, but not of normal APP695, was shown to induce nucleosomal DNA fragmentation in neuronal cells. Induction of DNA fragmentation required the cytoplasmic domain of the mutants and appeared to be mediated by heterotrimeric guanosine triphosphate-binding proteins (G proteins).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamatsuji, T -- Matsui, T -- Okamoto, T -- Komatsuzaki, K -- Takeda, S -- Fukumoto, H -- Iwatsubo, T -- Suzuki, N -- Asami-Odaka, A -- Ireland, S -- Kinane, T B -- Giambarella, U -- Nishimoto, I -- New York, N.Y. -- Science. 1996 May 31;272(5266):1349-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Center, Massachusetts General Hospital, Department of Medicine, Harvard Medical School, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650548" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/chemistry/genetics/*physiology ; Animals ; Apoptosis ; Base Sequence ; Culture Media, Conditioned ; DNA/*metabolism ; GTP-Binding Proteins/*physiology ; Humans ; Hybrid Cells ; Mice ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Mutation ; Neurons/cytology/*metabolism ; Nucleosomes/*metabolism ; Peptide Fragments/metabolism ; Rats ; Transfection
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  • 11
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    Binding of zinc finger protein ZPR1 to the epidermal growth factor receptor (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-21
    Description: ZPR1 is a zinc finger protein that binds to the cytoplasmic tyrosine kinase domain of the epidermal growth factor receptor (EGFR). Deletion analysis demonstrated that this binding interaction is mediated by the zinc fingers of ZPR1 and subdomains X and XI of the EGFR tyrosine kinase. Treatment of mammalian cells with EGF caused decreased binding of ZPR1 to the EGFR and the accumulation of ZPR1 in the nucleus. The effect of EGF to regulate ZPR1 binding is dependent on tyrosine phosphorylation of the EGFR. ZPR1 therefore represents a prototype for a class of molecule that binds to the EGFR and is released from the receptor after activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galcheva-Gargova, Z -- Konstantinov, K N -- Wu, I H -- Klier, F G -- Barrett, T -- Davis, R J -- R01-CA58396/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Jun 21;272(5269):1797-802.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, Worcester, 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650580" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Carrier Proteins/chemistry/*metabolism/secretion ; Cell Line ; Cell Nucleus/metabolism ; Cloning, Molecular ; Cytoplasm/metabolism ; Epidermal Growth Factor/pharmacology ; Humans ; Immunoblotting ; Male ; Mice ; Molecular Sequence Data ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Structure, Secondary ; RNA, Messenger/genetics/metabolism ; Receptor, Epidermal Growth Factor/chemistry/*metabolism ; Testis/metabolism ; Type C Phospholipases/metabolism ; Vanadates/pharmacology ; *Zinc Fingers ; src Homology Domains
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  • 12
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    A docking receptor for HDL cholesterol esters (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steinberg, D -- New York, N.Y. -- Science. 1996 Jan 26;271(5248):460-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California at San Diego, La Jolla 92093-0613, USA. dsteinberg@UCSD.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8560256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD36/genetics/*metabolism ; Biological Transport ; *Carrier Proteins ; Cholesterol/metabolism ; Cholesterol Esters/*metabolism ; Gene Targeting ; Lipoproteins, HDL/genetics/*metabolism ; Liver/metabolism ; *Membrane Proteins ; Mice ; *RNA-Binding Proteins ; *Receptors, Immunologic ; Receptors, Lipoprotein/*metabolism ; Receptors, Scavenger ; Scavenger Receptors, Class B
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  • 13
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    Role of mutant CFTR in hypersusceptibility of cystic fibrosis patients to lung infections (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-05
    Description: Cystic fibrosis (CF) patients are hypersusceptible to chronic Pseudomonas aeruginosa lung infections. Cultured human airway epithelial cells expressing the delta F508 allele of the cystic fibrosis transmembrane conductance regulator (CFTR) were defective in uptake of P. aeruginosa compared with cells expressing the wild-type allele. Pseudomonas aeruginosa lipopolysaccharide (LPS)-core oligosaccharide was identified as the bacterial ligand for epithelial cell ingestion; exogenous oligosaccharide inhibited bacterial ingestion in a neonatal mouse model, resulting in increased amounts of bacteria in the lungs. CFTR may contribute to a host-defense mechanism that is important for clearance of P. aeruginosa from the respiratory tract.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3677515/" 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/PMC3677515/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pier, G B -- Grout, M -- Zaidi, T S -- Olsen, J C -- Johnson, L G -- Yankaskas, J R -- Goldberg, J B -- AI22806/AI/NIAID NIH HHS/ -- AI35674/AI/NIAID NIH HHS/ -- HL42384/HL/NHLBI NIH HHS/ -- R01 HL058398/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 5;271(5245):64-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115-5899, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8539601" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cell Line, Transformed ; Cystic Fibrosis/*complications/genetics/microbiology ; Cystic Fibrosis Transmembrane Conductance Regulator/genetics/*physiology ; Disease Susceptibility ; Epithelium/microbiology ; Humans ; Lipopolysaccharides/pharmacology ; Lung/microbiology ; Mice ; Mice, Inbred BALB C ; Pseudomonas Infections/*etiology/microbiology ; Pseudomonas aeruginosa/*physiology ; Respiratory System/*microbiology ; Respiratory Tract Infections/*etiology/microbiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    CD40 ligand-dependent T cell activation: requirement of B7-CD28 signaling through CD40 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-09-27
    Description: The role of CD40 ligand (CD40L) in the primary activation of T cells is not clear. The cellular and humoral immune responses to adenoviral vectors in a murine model of liver-directed gene transfer were studied to define the mechanisms responsible for CD40L-dependent T cell priming. CD40L-deficient mice did not develop effective cytotoxic T cells to transduced hepatocytes, and T cell-dependent B cell responses were absent. Full reconstitution of cellular and humoral immunity was achieved in CD40L-deficient mice by administration of an activating antibody to CD40 that increased expression of B7.2 on spleen cells. Wild-type mice could be made nonresponsive to vector by administration of antibodies to B7. Thus, CD40L-dependent activation of T cells occurs through signaling of CD40 in the antigen-presenting cell to enhance requisite costimulatory pathways that include B7.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Y -- Wilson, J M -- New York, N.Y. -- Science. 1996 Sep 27;273(5283):1862-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Human Gene Therapy, University of Pennsylvania Medical Center, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8791591" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Animals ; Antigen-Presenting Cells/immunology ; Antigens, CD/*metabolism ; Antigens, CD28/*metabolism ; Antigens, CD86 ; CD4-Positive T-Lymphocytes/immunology ; CD40 Ligand ; Female ; Gene Transfer Techniques ; Genetic Vectors ; Liver/immunology/metabolism ; *Lymphocyte Activation ; Membrane Glycoproteins/*metabolism ; Mice ; Mice, Inbred C57BL ; *Signal Transduction ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/immunology ; Transgenes
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Selective activation of NF-kappa B by nerve growth factor through the neurotrophin receptor p75 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-26
    Description: Nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) selectively bind to distinct members of the Trk family of tyrosine kinase receptors, but all three bind with similar affinities to the neurotrophin receptor p75 (p75NTR). The biological significance of neurotrophin binding to p75NTR in cells that also express Trk receptors has been difficult to ascertain. In the absence of TrkA, NGF binding to p75NGR activated the transcription factor nuclear factor kappa B (NF-kappa B) in rat Schwann cells. This activation was not observed in Schwann cells isolated from mice that lacked p75NTR. The effect was selective for NGF; NF-kappa B was not activated by BDNF or NT-3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carter, B D -- Kaltschmidt, C -- Kaltschmidt, B -- Offenhauser, N -- Bohm-Matthaei, R -- Baeuerle, P A -- Barde, Y A -- New York, N.Y. -- Science. 1996 Apr 26;272(5261):542-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiochemistry, Max-Planck Institute for Psychiatry, Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614802" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Brain-Derived Neurotrophic Factor ; Cell Nucleus/metabolism ; Cells, Cultured ; DNA/metabolism ; L Cells (Cell Line) ; Mice ; Molecular Sequence Data ; NF-kappa B/*metabolism ; Nerve Growth Factors/*metabolism/pharmacology ; Nerve Tissue Proteins/metabolism/pharmacology ; Neurotrophin 3 ; Proto-Oncogene Proteins/metabolism ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Nerve Growth Factor ; Receptor, trkA ; Receptors, Nerve Growth Factor/*metabolism ; Schwann Cells/*metabolism ; Signal Transduction/*physiology
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  • 16
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    Requirement of p27Kip1 for restriction point control of the fibroblast cell cycle (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-10
    Description: Cells deprived of serum mitogens will either undergo immediate cell cycle arrest or complete mitosis and arrest in the next cell cycle. The transition from mitogen dependence to mitogen independence occurs in the mid-to late G1 phase of the cell cycle and is called the restriction point. Murine Balb/c-3T3 fibroblasts deprived of serum mitogens accumulated the cyclin-dependent kinase (CDK) inhibitor p27Kip1. This was correlated with inactivation of essential G1 cyclin-CDK complexes and with cell cycle arrest in G1. The ability of specific mitogens to allow transit through the restriction point paralleled their ability to down-regulate p27, and antisense inhibition of p27 expression prevented cell cycle arrest in response to mitogen depletion. Therefore, p27 is an essential component of the pathway that connects mitogenic signals to the cell cycle at the restriction point.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coats, S -- Flanagan, W M -- Nourse, J -- Roberts, J M -- New York, N.Y. -- Science. 1996 May 10;272(5263):877-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8629023" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Base Sequence ; *Cell Cycle Proteins ; Culture Media ; Cyclin-Dependent Kinase Inhibitor p27 ; Cyclin-Dependent Kinases/*antagonists & inhibitors/metabolism ; Cyclins/metabolism ; Down-Regulation ; Enzyme Inhibitors/*metabolism ; Epidermal Growth Factor/pharmacology ; *G1 Phase ; Gene Expression/drug effects ; Insulin-Like Growth Factor I/pharmacology ; Mice ; Microtubule-Associated Proteins/biosynthesis/genetics/*metabolism ; Mitogens/pharmacology ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacology ; Platelet-Derived Growth Factor/pharmacology ; Proto-Oncogene Proteins c-sis ; *Tumor Suppressor Proteins
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    Complexities in the treatment of autoimmune disease (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McFarland, H F -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2037-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroimmunology Branch, National Institutes of Health, Bethesda, MD 20892, USA. henrymcf@helix.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8984662" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; Autoimmune Diseases/immunology/*therapy ; CD8-Positive T-Lymphocytes/*immunology ; Callithrix ; Cytokines/*immunology ; Diabetes Mellitus, Type 1/immunology/therapy ; Encephalomyelitis, Autoimmune, Experimental/immunology/therapy ; Humans ; Immune Tolerance ; Immunotherapy/*adverse effects ; Mice ; Myelin Proteins ; Myelin-Associated Glycoprotein/immunology ; Myelin-Oligodendrocyte Glycoprotein ; Ovalbumin/immunology ; Th1 Cells/*immunology ; Th2 Cells/*immunology
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  • 18
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    Does leptin contribute to diabetes caused by obesity? (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taylor, S I -- Barr, V -- Reitman, M -- New York, N.Y. -- Science. 1996 Nov 15;274(5290):1151-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-1829, USA. simeon_taylor@nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966588" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/physiology ; Animals ; Carrier Proteins/metabolism ; Diabetes Mellitus/*etiology ; Diabetes Mellitus, Type 2/*etiology ; Gene Expression Regulation, Enzymologic ; Humans ; Insulin/*metabolism ; Insulin Antagonists ; Insulin Receptor Substrate Proteins ; Insulin Resistance ; Leptin ; Liver/metabolism ; Mice ; Mice, Obese ; Obesity/physiopathology ; Phosphoenolpyruvate Carboxykinase (GTP)/genetics ; Phosphoproteins/metabolism ; Phosphorylation ; Proteins/pharmacology/*secretion ; Receptor, Insulin/metabolism ; *Receptors, Cell Surface ; Receptors, Leptin ; Signal Transduction
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  • 19
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    Identification of a putative target for Rho as the serine-threonine kinase protein kinase N (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-02
    Description: Rho, a Ras-like small guanosine triphosphatase, has been implicated in cytoskeletal responses to extracellular signals such as lysophosphatidic acid (LPA) to form stress fibers and focal contacts. The form of RhoA bound to guanosine triphosphate directly bound to and activated a serine-threonine kinase, protein kinase N (PKN). Activated RhoA formed a complex with PKN and activated it in COS-7 cells. PKN was phosphorylated in Swiss 3T3 cells stimulated with LPA, and this phosphorylation was blocked by treatment of cells with botulinum C3 exoenzyme. Activation of Rho may be linked directly to a serine-threonine kinase pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amano, M -- Mukai, H -- Ono, Y -- Chihara, K -- Matsui, T -- Hamajima, Y -- Okawa, K -- Iwamatsu, A -- Kaibuchi, K -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):648-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Signal Transduction, Nara Institute of Science and Technology, Ikoma, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571127" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; ADP Ribose Transferases/pharmacology ; Amino Acid Sequence ; Animals ; *Botulinum Toxins ; Cell Line ; Chromatography, Affinity ; Enzyme Activation ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; Guanosine Triphosphate/metabolism ; Lysophospholipids/pharmacology ; Mice ; Molecular Sequence Data ; Phosphorylation ; Protein Kinase C/*metabolism ; Recombinant Fusion Proteins/metabolism ; rhoA GTP-Binding Protein
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  • 20
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    A new turn (or two) for twist (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michelson, A M -- New York, N.Y. -- Science. 1996 Jun 7;272(5267):1449-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Brigham and Women's Hospital, Boston, MA 02115, USA. michelson@rascal.med.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8633234" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Drosophila/*embryology/genetics ; Drosophila Proteins ; Gene Expression Regulation, Developmental ; Genes, Insect ; Helix-Loop-Helix Motifs ; Mesoderm/*cytology ; Mice ; Muscles/*cytology ; Nuclear Proteins/genetics/*physiology ; Transcription Factors/genetics/*physiology ; Twist Transcription Factor
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  • 21
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    New data help toxicologists home in on assessing risks (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, J -- New York, N.Y. -- Science. 1996 Apr 12;272(5259):200.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8602503" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asthma/*etiology ; Carcinogens/*toxicity ; Glutathione/metabolism ; Humans ; Immune System/drug effects ; Methylene Chloride/metabolism/*toxicity ; Mice ; Nitrogen Dioxide/*toxicity ; Rats
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  • 22
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    New 'Alzheimer's mouse' produced (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1996 Oct 11;274(5285):177-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8927978" target="_blank"〉PubMed〈/a〉
    Keywords: *Alzheimer Disease/genetics/metabolism/pathology ; Amyloid beta-Peptides/blood/metabolism ; Amyloid beta-Protein Precursor/*genetics ; Animals ; Brain/pathology ; Brain Chemistry ; *Disease Models, Animal ; Learning Disorders/etiology ; Memory Disorders/etiology ; Mice ; Mice, Inbred C57BL ; *Mice, Transgenic ; Mutation ; Peptide Fragments/blood/metabolism ; Transgenes
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  • 23
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    Binding of APC to the human homolog of the Drosophila discs large tumor suppressor protein (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-05-17
    Description: The adenomatous polyposis coli gene (APC) is mutated in familial adenomatous polyposis and in sporadic colorectal tumors, and its product binds to the adherens junction protein beta-catenin. Overexpression of APC blocks cell cycle progression. The APC-beta-catenin complex was shown to bind to DLG, the human homolog of the Drosophila discs large tumor suppressor protein. This interaction required the carboxyl-terminal region of APC and the DLG homology repeat region of DLG. APC colocalized with DLG at the lateral cytoplasm in rat colon epithelial cells and at the synapse in cultured hippocampal neurons. These results suggest that the APC-DLG complex may participate in regulation of both cell cycle progression and neuronal function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsumine, A -- Ogai, A -- Senda, T -- Okumura, N -- Satoh, K -- Baeg, G H -- Kawahara, T -- Kobayashi, S -- Okada, M -- Toyoshima, K -- Akiyama, T -- New York, N.Y. -- Science. 1996 May 17;272(5264):1020-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncogene Research, Institute for Microbial Diseases, Osaka University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638125" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Amino Acid Sequence ; Animals ; Cell Cycle ; Cells, Cultured ; Colon/chemistry/cytology ; Cytoskeletal Proteins/analysis/chemistry/*metabolism ; Drosophila ; *Drosophila Proteins ; Epithelial Cells ; Epithelium/chemistry ; Fluorescent Antibody Technique ; Hippocampus/chemistry/cytology ; Humans ; Insect Hormones/analysis/chemistry/*metabolism ; Mice ; Molecular Sequence Data ; Neurons/chemistry/cytology ; Protein Binding ; Recombinant Fusion Proteins/metabolism ; Synapses/chemistry ; *Trans-Activators ; *Tumor Suppressor Proteins ; beta Catenin
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  • 24
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    Age-dependent diarrhea induced by a rotaviral nonstructural glycoprotein (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-05
    Description: The rotavirus nonstructural glycoprotein NSP4 is an intracellular receptor that mediates the acquisition of a transient membrane envelope as subviral particles bud into the endoplasmic reticulum. NSP4 also causes an increase in intracellular calcium in insect cells. Purified NSP4 or a peptide corresponding to NSP4 residues 114 to 135 induced diarrhea in young (6 to 10 days old) CD1 mice. This disease response was age-dependent, dose-dependent, and specific. Electrophysiologic data from intestinal mucosa showed that the NSP4 114-135 peptide potentiates chloride secretion by a calcium-dependent signaling pathway. Diarrhea is induced when NSP4, acting as a viral enterotoxin, triggers a signal transduction pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ball, J M -- Tian, P -- Zeng, C Q -- Morris, A P -- Estes, M K -- DK 30144/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Apr 5;272(5258):101-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Virology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8600515" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Amino Acid Sequence ; Animals ; Calcium/metabolism ; Carbachol/pharmacology ; Chlorides/metabolism ; Colforsin/pharmacology ; Diarrhea/*etiology/prevention & control/virology ; Enterotoxins/*toxicity ; Glycoproteins/immunology/*toxicity ; Immune Sera/administration & dosage ; Immunization ; In Vitro Techniques ; Intestinal Mucosa/drug effects/secretion ; Mice ; Molecular Sequence Data ; Peptide Fragments/toxicity ; Receptors, Virus ; Rotavirus/*pathogenicity ; Rotavirus Infections/prevention & control/*virology ; Signal Transduction ; Toxins, Biological ; Viral Nonstructural Proteins/immunology/*toxicity
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  • 25
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    Homocysteine antagonism of nitric oxide-related cytostasis in Salmonella typhimurium (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-19
    Description: Nitric oxide (NO) is associated with broad-spectrum antimicrobial activity of particular importance in infections caused by intracellular pathogens. An insertion mutation in the metL gene of Salmonella typhimurium conferred specific hypersusceptibility to S-nitrosothiol NO-donor compounds and attenuated virulence of the organism in mice. The metL gene product catalyzes two proximal metabolic steps required for homocysteine biosynthesis. S-Nitrosothiol resistance was restored by exogenous homocysteine or introduction of the metL gene on a plasmid. Measurement of expression of the homocysteine-sensitive metH gene indicated that S-nitrosothiols may directly deplete intracellular homocysteine. Homocysteine may act as an endogenous NO antagonist in diverse processes including infection, atherosclerosis, and neurologic disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Groote, M A -- Testerman, T -- Xu, Y -- Stauffer, G -- Fang, F C -- AI32463/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Apr 19;272(5260):414-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8602531" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspartokinase Homoserine Dehydrogenase/genetics/*metabolism ; Base Sequence ; Drug Resistance, Microbial ; Female ; Glutathione/analogs & derivatives/pharmacology ; Homocysteine/metabolism/pharmacology/*physiology ; *Mercaptoethanol ; Mice ; Mice, Inbred C3H ; Microbial Sensitivity Tests ; Molecular Sequence Data ; Mutagenesis, Insertional ; Nitric Oxide/*antagonists & inhibitors/metabolism ; Nitroso Compounds/pharmacology ; S-Nitrosoglutathione ; *S-Nitrosothiols ; Salmonella Infections, Animal/microbiology ; Salmonella typhimurium/cytology/drug effects/pathogenicity/*physiology ; Virulence
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  • 26
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    Fertile results: bringing up baby (eggs) (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roush, W -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):594-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571119" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Culture Techniques ; Cells, Cultured ; Female ; Fertilization in Vitro ; Granulosa Cells/cytology/*physiology ; Mice ; Oocytes/cytology/*physiology ; *Oogenesis ; Organ Culture Techniques ; Ovary/physiology
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    Modified microbe may boost TB vaccine (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roush, W -- New York, N.Y. -- Science. 1996 Jan 26;271(5248):447.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8560254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BCG Vaccine/genetics/*immunology/therapeutic use ; Bacterial Proteins/immunology ; Cytokines/*biosynthesis/genetics/immunology ; Genetic Engineering ; Humans ; Mice ; Mycobacterium tuberculosis/immunology ; Neoplasms/therapy ; T-Lymphocytes/immunology ; Tuberculosis/immunology/prevention & control ; Vaccines, Synthetic/genetics/*immunology/therapeutic use
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Protein matchmaker may lead new gene therapy to the altar (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, M -- New York, N.Y. -- Science. 1996 Jul 12;273(5272):183.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8668994" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/chemistry/*metabolism ; Crystallography, X-Ray ; DNA-Binding Proteins/chemistry/*metabolism ; *Gene Expression Regulation ; Genetic Therapy ; Growth Hormone/*genetics ; Heat-Shock Proteins/chemistry/*metabolism ; Humans ; *Immunophilins ; Mice ; *Phosphotransferases (Alcohol Group Acceptor) ; Polyenes/chemistry/*metabolism ; Sirolimus ; TOR Serine-Threonine Kinases ; Tacrolimus Binding Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The new genomics: global views of biology (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lander, E S -- New York, N.Y. -- Science. 1996 Oct 25;274(5287):536-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA. lander@genome.wi.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8928008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioethics ; DNA/genetics ; Gene Expression ; Genetic Techniques ; Genetic Variation ; *Human Genome Project ; Humans ; Mice ; *Molecular Biology/education ; Proteins/chemistry/metabolism ; RNA/genetics ; Sequence Analysis, DNA
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  • 30
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    Protein kinase N (PKN) and PKN-related protein rhophilin as targets of small GTPase Rho (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-02
    Description: The Rho guanosine 5'-triphosphatase (GTPase) cycles between the active guanosine triphosphate (GTP)-bound form and the inactive guanosine diphosphate-bound form and regulates cell adhesion and cytokinesis, but how it exerts these actions is unknown. The yeast two-hybrid system was used to clone a complementary DNA for a protein (designated Rhophilin) that specifically bound to GTP-Rho. The Rho-binding domain of this protein has 40 percent identity with a putative regulatory domain of a protein kinase, PKN. PKN itself bound to GTP-Rho and was activated by this binding both in vitro and in vivo. This study indicates that a serine-threonine protein kinase is a Rho effector and presents an amino acid sequence motif for binding to GTP-Rho that may be shared by a family of Rho target proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Watanabe, G -- Saito, Y -- Madaule, P -- Ishizaki, T -- Fujisawa, K -- Morii, N -- Mukai, H -- Ono, Y -- Kakizuka, A -- Narumiya, S -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):645-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Kyoto University Faculty of Medicine, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571126" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Cell Line ; Cloning, Molecular ; Enzyme Activation ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/chemistry/*metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Membrane Proteins/*metabolism ; Mice ; Molecular Sequence Data ; Phosphorylation ; Protein Kinase C/chemistry/*metabolism ; *Protein-Serine-Threonine Kinases ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/genetics ; Signal Transduction ; ras Proteins ; *rho GTP-Binding Proteins ; rhoA GTP-Binding Protein ; rhoB GTP-Binding Protein
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    Central hypotensive effects of the alpha2a-adrenergic receptor subtype (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-09
    Description: alpha2-Adrenergic receptors (alpha2ARs) present in the brainstem decrease blood pressure and are targets for clinically effective antihypertensive drugs. The existence of three alpha2AR subtypes, the lack of subtype-specific ligands, and the cross-reactivity of alpha2AR agonists with imidazoline receptors has precluded an understanding of the role of individual alpha2AR subtypes in the hypotensive response. Gene targeting was used to introduce a point mutation into the alpha2aAR subtype in the mouse genome. The hypotensive response to alpha2AR agonists was lost in the mutant mice, demonstrating that the alpha2aAR subtype plays a principal role in this response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacMillan, L B -- Hein, L -- Smith, M S -- Piascik, M T -- Limbird, L E -- HL38120/HL/NHLBI NIH HHS/ -- HL43671/HL/NHLBI NIH HHS/ -- HL48638/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 9;273(5276):801-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Vanderbilt University, Nashville, TN 37232, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8670421" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic alpha-2 Receptor Agonists ; Adrenergic alpha-Agonists/pharmacology ; Animals ; Antihypertensive Agents/pharmacology ; Base Sequence ; Blood Pressure/drug effects/*physiology ; Brain Stem/physiology ; Brimonidine Tartrate ; Gene Targeting ; Heart Rate/drug effects/physiology ; Imidazoles/pharmacology ; Medetomidine ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Point Mutation ; Quinoxalines/pharmacology ; Receptors, Adrenergic, alpha-2/genetics/metabolism/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Tumor cells fight back to beat immune system (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, N -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1302.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966600" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/*physiology ; *Apoptosis ; Fas Ligand Protein ; Humans ; Melanoma/chemistry/*immunology ; Membrane Glycoproteins/analysis/*physiology ; Mice ; T-Lymphocytes, Cytotoxic/*cytology/immunology ; Tumor Cells, Cultured ; *Tumor Escape
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 33
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    Locus control region function and heterochromatin-induced position effect variegation (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-23
    Description: Human CD2 locus control region (LCR) sequences are shown here to be essential for establishing an open chromatin configuration. Transgenic mice carrying an hCD2 mini-gene attached only to the 3' CD2 transcriptional enhancer exhibited variegated expression when the transgene integrated in the centromere. In contrast, mice carrying a transgene with additional 3' sequences showed no variegation even when the latter integrated in centromeric positions. This result suggests that LCRs operate by ensuring an open chromatin configuration and that a short region, with no enhancer activity, functions in the establishment, maintenance, or both of an open chromatin domain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Festenstein, R -- Tolaini, M -- Corbella, P -- Mamalaki, C -- Parrington, J -- Fox, M -- Miliou, A -- Jones, M -- Kioussis, D -- TGT06S01/Telethon/Italy -- TGT95000/Telethon/Italy -- New York, N.Y. -- Science. 1996 Feb 23;271(5252):1123-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Immunology, National Institute for Medical Research, The Ridgeway, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8599090" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD2/analysis/*genetics ; Centromere/genetics ; Enhancer Elements, Genetic ; *Gene Expression Regulation ; Heterochromatin/*genetics ; Humans ; In Situ Hybridization, Fluorescence ; Mice ; Mice, Transgenic ; *Regulatory Sequences, Nucleic Acid ; T-Lymphocytes/*immunology ; *Transgenes
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 34
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    T cell inactivation linked to Ras block (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, N -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1234.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638102" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD28/metabolism ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; *Clonal Anergy ; Interleukin-2/biosynthesis ; Mice ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Proto-Oncogene Proteins p21(ras)/*metabolism ; Receptors, Antigen, T-Cell/immunology ; *Signal Transduction ; T-Lymphocytes/*immunology/metabolism
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    Another twist to MHC-peptide recognition (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, I A -- New York, N.Y. -- Science. 1996 May 17;272(5264):973-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, 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/8638141" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigens/chemistry/*metabolism ; Antigens, Differentiation, B-Lymphocyte/chemistry/*metabolism ; HLA-DR1 Antigen/chemistry/metabolism ; Histocompatibility Antigens Class II/chemistry/immunology/*metabolism ; Humans ; Hydrogen Bonding ; Hydrogen-Ion Concentration ; Mice ; Models, Molecular ; Protein Conformation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 36
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    Will a twist of viral fate lead to a new cancer treatment? (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1996 Oct 18;274(5286):342-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8927990" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus E1B Proteins/*genetics/metabolism ; Adenoviruses, Human/genetics/*physiology ; Animals ; Clinical Trials, Phase I as Topic ; Cytopathogenic Effect, Viral ; Genes, Viral ; *Genes, p53 ; Head and Neck Neoplasms/*therapy/virology ; Humans ; Mice ; Mutation ; Neoplasm Transplantation ; Neoplasms, Experimental/*therapy/virology ; Tumor Suppressor Protein p53/metabolism ; Virus Replication
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  • 37
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    Identification of MAP kinase domains by redirecting stress signals into growth factor responses (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-14
    Description: Mitogen-activated protein kinase (MAPK) cascades, termed MAPK modules, channel extracellular signals into specific cellular responses. Chimeric molecules were constructed between p38 and p44 MAPKs, which transduce stress and growth factor signals, respectively. A discrete region of 40 residues located in the amono-terminal p38MAPK lobe directed the specificity of response to extracellular signals, whereas the p44MAPK chimera, expressed in vivo, redirected stress signals into early mitogenic responses, demonstrating the functional independence of these domains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunet, A -- Pouyssegur, J -- New York, N.Y. -- Science. 1996 Jun 14;272(5268):1652-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre de Biochemie-CNRS, UMR134, Parc Valrose, Faculte des Sciences, Nice, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658140" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Anisomycin/pharmacology ; Binding Sites ; Calcium-Calmodulin-Dependent Protein Kinases/genetics/*metabolism ; Cell Division ; Cell Line ; Cricetinae ; Cricetulus ; Enzyme Activation ; Gene Expression Regulation ; Genes, fos ; Growth Substances/metabolism ; Mice ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Phosphorylation/drug effects ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Recombinant Fusion Proteins/genetics/metabolism ; Ribosomal Protein S6 Kinases ; Signal Transduction ; Sorbitol/pharmacology ; Substrate Specificity ; p38 Mitogen-Activated Protein Kinases
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  • 38
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    Attenuation of the obesity syndrome of ob/ob mice by the loss of neuropeptide Y (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-06
    Description: The obesity syndrome of ob/ob mice results from lack of leptin, a hormone released by fat cells that acts in the brain to suppress feeding and stimulate metabolism. Neuropeptide Y (NPY) is a neuromodulator implicated in the control of energy balance and is overproduced in the hypothalamus of ob/ob mice. To determine the role of NPY in the response to leptin deficiency, ob/ob mice deficient for NPY were generated. In the absence of NPY, ob/ob mice are less obese because of reduced food intake and increased energy expenditure, and are less severely affected by diabetes, sterility, and somatotropic defects. These results suggest that NPY is a central effector of leptin deficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Erickson, J C -- Hollopeter, G -- Palmiter, R D -- New York, N.Y. -- Science. 1996 Dec 6;274(5293):1704-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Box 357370, Seattle, WA 98195-7370, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8939859" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/pathology ; Animals ; Blood Glucose/analysis ; Body Composition ; Body Height ; Body Weight ; Diabetes Mellitus/etiology ; Diabetes Mellitus, Type 2/etiology ; Eating ; Energy Metabolism ; Female ; Fertility ; Insulin-Like Growth Factor I/metabolism ; Leptin ; Male ; Mice ; Mice, Mutant Strains ; Mice, Obese ; Neuropeptide Y/deficiency/genetics/*physiology ; Obesity/pathology/*physiopathology ; Oxygen Consumption ; Proteins/genetics/*physiology ; RNA, Messenger/metabolism
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    Fraud strikes top genome lab (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1996 Nov 8;274(5289):908-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966566" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Inversion ; *Chromosomes, Human, Pair 16 ; Genetic Research ; History, 20th Century ; Human Genome Project ; Humans ; Leukemia, Myelomonocytic, Acute/*genetics ; Mice ; National Institutes of Health (U.S.) ; *Scientific Misconduct ; United States
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  • 40
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    Activation of BTK by a phosphorylation mechanism initiated by SRC family kinases (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-09
    Description: Bruton's tyrosine kinase (BTK) is pivotal in B cell activation and development through its participation in the signaling pathways of multiple hematopoietic receptors. The mechanisms controlling BTK activation were studied here by examination of the biochemical consequences of an interaction between BTK and SRC family kinases. This interaction of BTK with SRC kinases transphosphorylated BTK on tyrosine at residue 551, which led to BTK activation. BTK then autophosphorylated at a second site. The same two sites were phosphorylated upon B cell antigen receptor cross-linking. The activated BTK was predominantly membrane-associated, which suggests that BTK integrates distinct receptor signals resulting in SRC kinase activation and BTK membrane targeting.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rawlings, D J -- Scharenberg, A M -- Park, H -- Wahl, M I -- Lin, S -- Kato, R M -- Fluckiger, A C -- Witte, O N -- Kinet, J P -- AR01912/AR/NIAMS NIH HHS/ -- AR36834/AR/NIAMS NIH HHS/ -- CA09120-20/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Feb 9;271(5250):822-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, University of California, Los Angeles 90095-1662, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8629002" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; B-Lymphocytes/*enzymology ; Cell Line, Transformed ; Cell Membrane/enzymology ; Enzyme Activation ; Immunoglobulin M/immunology ; Lymphocyte Activation ; Mice ; Mutation ; Phosphopeptides/analysis ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/chemistry/genetics/*metabolism ; Receptors, Antigen, B-Cell/metabolism ; Signal Transduction ; src-Family Kinases/*metabolism
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  • 41
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    A quasi-monoclonal mouse (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-14
    Description: As a model for studying the generation of antibody diversity, a gene-targeted mouse was produced that is hemizygous for a rearranged V(D)J segment at the immunoglobulin (Ig) heavy chain locus, the other allele being nonfunctional. The mouse also has no functional kappa light chain allele. The heavy chain, when paired with any lambda light chain, is specific for the hapten (4-hydroxy-3-nitrophenyl) acetyl (NP). The primary repertoire of this quasi-monoclonal mouse is monospecific, but somatic hypermutation and secondary rearrangements change the specificity of 20 percent of the antigen receptors on B cells. The serum concentrations of the Ig isotypes are similar to those in nontransgenic littermates, but less than half of the serum IgM binds to NP, and none of the other isotypes do. Thus, neither network interactions nor random activation of a small fraction of the B cell population can account for serum Ig concentrations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cascalho, M -- Ma, A -- Lee, S -- Masat, L -- Wabl, M -- 1R01 GM37699/GM/NIGMS NIH HHS/ -- P60 AR20684/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jun 14;272(5268):1649-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California, San Francisco 94143-0670, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658139" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*genetics/immunology ; *Antigens, CD ; Antigens, CD43 ; Antigens, CD45/immunology ; B-Lymphocytes/cytology/immunology ; Base Sequence ; Cell Line ; Cloning, Molecular ; Dna ; Flow Cytometry ; Gene Rearrangement, B-Lymphocyte, Heavy Chain ; Haptens/immunology ; Immunoglobulin Heavy Chains/*genetics/immunology ; Immunoglobulin Isotypes/genetics ; Immunoglobulin J-Chains/genetics ; Immunoglobulin Light Chains/genetics/immunology ; Immunoglobulin Variable Region/genetics ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout/genetics/*immunology ; Molecular Sequence Data ; Nitrophenols/immunology ; Phenylacetates ; Recombinant Proteins/genetics/immunology ; Sialoglycoproteins/immunology
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  • 42
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    Requirement for BMP signaling in interdigital apoptosis and scale formation (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-03
    Description: Interdigital cell death leads to regression of soft tissue between embryonic digits in many vertebrates. Although the signals that regulate interdigital apoptosis are not known, BMPs--signaling molecules of the transforming growth factor-beta superfamily--are expressed interdigitally. A dominant negative type I BMP receptor (dnBMPR-IB) was used here to block BMP signaling. Expression of dnBMPR in chicken embryonic hind limbs greatly reduced interdigital apoptosis and resulted in webbed feet. In addition, scales were transformed into feathers. The similarity of the webbing to webbed duck feet led to studies that indicate that BMPs are not expressed in the duck interdigit. These results indicate BMP signaling actively mediates cell death in the embryonic limb.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zou, H -- Niswander, L -- New York, N.Y. -- Science. 1996 May 3;272(5262):738-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614838" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Bone Morphogenetic Protein Receptors, Type I ; Bone Morphogenetic Proteins ; Chick Embryo ; Ducks ; Feathers/cytology/*embryology ; Foot/embryology ; Gene Expression ; Hindlimb/cytology/*embryology ; In Situ Hybridization ; Mesoderm/metabolism ; Mice ; Mutagenesis, Site-Directed ; Phenotype ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Proteins/genetics/*physiology ; RNA/genetics/metabolism ; Receptors, Growth Factor/genetics/*metabolism ; *Signal Transduction ; Transfection
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    Does nature drive nurture? (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1996 Aug 2;273(5275):577-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8701307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Genetics, Behavioral ; Maternal Behavior/*physiology ; Mice ; Mice, Knockout/genetics/*physiology ; Neurons/metabolism ; Preoptic Area/metabolism/physiology ; Proto-Oncogene Proteins c-fos/*genetics/physiology
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  • 44
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    Identification of scavenger receptor SR-BI as a high density lipoprotein receptor (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-26
    Description: High density lipoprotein (HDL) and low density lipoprotein (LDL) are cholesterol transport particles whose plasma concentrations are directly (LDL) and inversely (HDL) correlated with risk for atherosclerosis. LDL catabolism involves cellular uptake and degradation of the entire particle by a well-characterized receptor. HDL, in contrast, selectively delivers its cholesterol, but not protein, to cells by unknown receptors. Here it is shown that the class B scavenger receptor SR-BI is an HDL receptor. SR-BI binds HDL with high affinity, is expressed primarily in liver and nonplacental steroidogenic tissues, and mediates selective cholesterol uptake by a mechanism distinct from the classic LDL receptor pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Acton, S -- Rigotti, A -- Landschulz, K T -- Xu, S -- Hobbs, H H -- Krieger, M -- HL09047/HL/NHLBI NIH HHS/ -- HL41484/HL/NHLBI NIH HHS/ -- HL52212/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Jan 26;271(5248):518-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8560269" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/metabolism ; Animals ; Antigens, CD36/genetics/*metabolism ; CHO Cells ; *Carrier Proteins ; Cholesterol/metabolism ; Cholesterol Esters/*metabolism ; Cricetinae ; Female ; Fluorescent Dyes/metabolism ; Lipoproteins, HDL/*metabolism ; Liver/metabolism ; *Membrane Proteins ; Mice ; Molecular Sequence Data ; Ovary/metabolism ; *RNA-Binding Proteins ; *Receptors, Immunologic ; Receptors, LDL/metabolism ; Receptors, Lipoprotein/*metabolism ; Receptors, Scavenger ; Scavenger Receptors, Class B ; Thiazines/metabolism ; Transfection
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  • 45
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    Regulation of myosin phosphatase by Rho and Rho-associated kinase (Rho-kinase) (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-12
    Description: The small guanosine triphosphatase Rho is implicated in myosin light chain (MLC) phosphorylation, which results in contraction of smooth muscle and interaction of actin and myosin in nonmuscle cells. The guanosine triphosphate (GTP)-bound, active form of RhoA (GTP.RhoA) specifically interacted with the myosin-binding subunit (MBS) of myosin phosphatase, which regulates the extent of phosphorylation of MLC. Rho-associated kinase (Rho-kinase), which is activated by GTP.RhoA, phosphorylated MBS and consequently inactivated myosin phosphatase. Overexpression of RhoA or activated RhoA in NIH 3T3 cells increased phosphorylation of MBS and MLC. Thus, Rho appears to inhibit myosin phosphatase through the action of Rho-kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimura, K -- Ito, M -- Amano, M -- Chihara, K -- Fukata, Y -- Nakafuku, M -- Yamamori, B -- Feng, J -- Nakano, T -- Okawa, K -- Iwamatsu, A -- Kaibuchi, K -- New York, N.Y. -- Science. 1996 Jul 12;273(5272):245-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Signal Transduction, Nara Institute of Science and Technology, Ikoma 630-01, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662509" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Actins/metabolism ; Amino Acid Sequence ; Animals ; Cattle ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; Intracellular Signaling Peptides and Proteins ; Isopropyl Thiogalactoside/pharmacology ; Mice ; Molecular Sequence Data ; Muscle Contraction ; Muscle, Smooth/physiology ; Myosin Light Chains/metabolism ; Myosin-Light-Chain Phosphatase ; Oxazoles/pharmacology ; Phosphoprotein Phosphatases/*antagonists & inhibitors/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/*metabolism ; rho-Associated Kinases ; rhoA GTP-Binding Protein
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  • 46
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    Identification of a committed precursor for the mast cell lineage (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-09
    Description: Mast cells originate from hematopoietic stem cells, but the mast cell-committed precursor has not been identified. In the study presented here, a cell population in murine fetal blood that fulfills the criteria of progenitor mastocytes was identified. It is defined by the phenotype Thy-1loc-Kithi, contains cytoplasmic granules, and expresses RNAs encoding mast cell-associated proteases but lacks expression of the high-affinity immunoglobulin E receptor. Thy-1loc-Kithi cells generated functionally competent mast cells at high frequencies in vitro but lacked developmental potential for other hematopoietic lineages. When transferred intraperitoneally, this population reconstituted the peritoneal mast cell compartment of genetically mast cell-deficient W/Wv mice to wild-type levels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodewald, H R -- Dessing, M -- Dvorak, A M -- Galli, S J -- AI-33372/AI/NIAID NIH HHS/ -- AI/CA-23990/AI/NIAID NIH HHS/ -- CA/AI-72074/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 9;271(5250):818-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8629001" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Thy-1/analysis ; Base Sequence ; Cell Lineage ; Cell Transplantation ; Cells, Cultured ; Cytoplasmic Granules/ultrastructure ; Endopeptidases/genetics/metabolism ; Fetal Blood ; Hematopoietic Stem Cells/*cytology/physiology/ultrastructure ; Immunophenotyping ; Interleukin-3/pharmacology ; Mast Cells/*cytology/physiology/ultrastructure ; Mice ; Molecular Sequence Data ; Peritoneal Cavity/cytology ; Proto-Oncogene Proteins c-kit/analysis ; RNA, Messenger/genetics/metabolism ; Receptors, IgE/analysis/genetics ; Stem Cell Factor/pharmacology
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  • 47
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    Visualization of slow axonal transport in vivo (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-09
    Description: In axons, cytoskeletal constituents move by slow transport. However, it remains controversial whether axonal neurofilaments are dynamic structures in which only subunits are transported or whether filaments assemble in the proximal axon and are transported intact as polymers to the axon terminus. To investigate the form neurofilament proteins take during transport, neurons of transgenic mice lacking axonal neurofilaments were infected with a recombinant adenoviral vector encoding epitope-tagged neurofilament M. Confocal and electron microscopy revealed that the virally encoded neurofilament M was transported in unpolymerized form along axonal microtubules. Thus, neurofilament proteins are probably transported as subunits or small oligomers along microtubules, which are major routes for slow axonal transport.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Terada, S -- Nakata, T -- Peterson, A C -- Hirokawa, N -- New York, N.Y. -- Science. 1996 Aug 9;273(5276):784-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉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/8670416" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Animals ; *Axonal Transport ; Axons/chemistry/*metabolism/ultrastructure ; Ganglia, Spinal/virology ; Genetic Vectors ; Mice ; Mice, Transgenic ; Microscopy, Confocal ; Microscopy, Immunoelectron ; Microtubules/*metabolism ; Neurofilament Proteins/analysis/*metabolism ; Proto-Oncogene Proteins c-myc/genetics/metabolism ; Recombinant Proteins/metabolism ; Sciatic Nerve/chemistry/ultrastructure
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  • 48
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    Regulation of an early developmental checkpoint in the B cell pathway by Ig beta (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-19
    Description: Many of the cell fate decisions in precursor B cells and more mature B cells are controlled by membrane immunoglobulin (Ig)M heavy chain (mu) and the Ig alpha-Ig beta signal transducers. The role of Ig beta in regulating early B cell development was examined in mice that lack Ig beta (Ig beta-/-). These mice had a complete block in B cell development at the immature CD43+B220+ stage. Immunoglobulin heavy chain diversity (DH) and joining (JH) segments rearranged, but variable (VH) to DJH recombination and immunoglobulin messenger RNA expression were compromised. These experiments define an unexpected, early requirement for Ig(beta) to produce B cells that can complete VDJH recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gong, S -- Nussenzweig, M C -- New York, N.Y. -- Science. 1996 Apr 19;272(5260):411-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8602530" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/genetics/*physiology ; Antigens, CD79 ; B-Lymphocytes/cytology/*immunology ; Gene Expression ; *Gene Rearrangement, B-Lymphocyte, Heavy Chain ; Gene Targeting ; Genes, Immunoglobulin ; Immunoglobulin Heavy Chains/*genetics ; Immunoglobulin Joining Region/genetics ; Immunoglobulin Light Chains/*genetics ; Immunoglobulin Variable Region/genetics ; Immunoglobulin mu-Chains/biosynthesis/genetics/physiology ; Lymph Nodes ; Mice ; Mice, Inbred C57BL ; Mutation ; RNA, Messenger/genetics ; Receptors, Antigen, B-Cell/physiology ; *Recombination, Genetic ; Signal Transduction
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  • 49
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    Selective activation of calcium permeability by aspartate in Purkinje cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-23
    Description: Glutamate and aspartate are endogenous excitatory amino acid neurotransmitters widely distributed in the mammalian central nervous system. Aspartate was shown to induce a large membrane current sensitive to N-methyl-D-aspartate (NMDA) and non-NMDA receptor antagonists in Purkinje cells from mice lacking functional NMDA receptors (NR1(-/-)). This response was accompanied by high permeability to calcium. In contrast, no current was induced by aspartate in hippocampal neurons and cerebellar granule cells from NR1(-/-) mice. Several other glutamate receptor agonists failed to evoke this response. Thus, in Purkinje cells, aspartate activates a distinct response capable of contributing to synaptic plasticity through calcium permeability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yuzaki, M -- Forrest, D -- Curran, T -- Connor, J A -- P30CA21765/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 23;273(5278):1112-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Neurobiology, St. Jude Children's Research Hospital, 332 North Lauderdale, Memphis, TN 38105-2794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8688099" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspartic Acid/*pharmacology ; Calcium/*metabolism ; Cerebellum/cytology/metabolism ; Excitatory Amino Acid Agonists/pharmacology ; Excitatory Amino Acid Antagonists/pharmacology ; Glutamic Acid/pharmacology ; Hippocampus/cytology/metabolism ; Homocysteine/analogs & derivatives/pharmacology ; Magnesium/pharmacology ; Mice ; Mice, Knockout ; N-Methylaspartate/pharmacology ; Neuronal Plasticity ; Neurons/drug effects/metabolism ; Patch-Clamp Techniques ; Permeability ; Purkinje Cells/drug effects/*metabolism ; Receptors, Amino Acid/drug effects/*metabolism ; Receptors, N-Methyl-D-Aspartate/agonists/antagonists & inhibitors/physiology
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  • 50
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    Lymphocyte apoptosis: mediation by increased type 3 inositol 1,4,5-trisphosphate receptor (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-07-26
    Description: B and T lymphocytes undergoing apoptosis in response to anti-immunoglobulin M antibodies and dexamethasone, respectively, were found to have increased amounts of messenger RNA for the inositol 1,4,5-trisphosphate receptor (IP3R) and increased amounts of IP3R protein. Immunohistochemical analysis revealed that the augmented receptor population was localized to the plasma membrane. Type 3 IP3R (IP3R3) was selectively increased during apoptosis, with no enhancement of type 1 IP3R (IP3R1). Expression of IP3R3 antisense constructs in S49 T cells blocked dexamethasone-induced apoptosis, whereas IP3R3 sense, IP3R1 sense, or IP3R1 antisense control constructs did not block cell death. Thus, the increases in IP3R3 may be causally related to apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Khan, A A -- Soloski, M J -- Sharp, A H -- Schilling, G -- Sabatini, D M -- Li, S H -- Ross, C A -- Snyder, S H -- AI-20922/AI/NIAID NIH HHS/ -- AI-37934/AI/NIAID NIH HHS/ -- MH43040/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Jul 26;273(5274):503-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662540" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Apoptosis ; B-Lymphocytes/*cytology/metabolism ; Base Sequence ; Calcium/metabolism ; Calcium Channels/genetics/immunology/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; DNA, Antisense ; Dexamethasone/pharmacology ; Immunoblotting ; Inositol 1,4,5-Trisphosphate/*metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; Mice ; Molecular Sequence Data ; Receptors, Cytoplasmic and Nuclear/genetics/immunology/*metabolism ; T-Lymphocytes/*cytology/metabolism ; Transfection ; Tumor Cells, Cultured
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    A mouse model of familial hypertrophic cardiomyopathy (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-05-03
    Description: A mouse model of familial hypertrophic cardiomyopathy (FHC) was generated by the introduction of an Arg 403 --〉 Gln mutation into the alpha cardiac myosin heavy chain (MHC) gene. Homozygous alpha MHC 403/403 mice died 7 days after birth, and sedentary heterozygous alpha MHC 403/+ mice survived for 1 year. Cardiac histopathology and dysfunction in the alpha MHC 403/+ mice resembled human FHC. Cardiac dysfunction preceded histopathologic changes, and myocyte disarray, hypertrophy, and fibrosis increased with age. Young male alpha MHC 403/+ mice showed more evidence of disease than did their female counterparts. Preliminary results suggested that exercise capacity may have been compromised in the alpha MHC 403/+ mice. This mouse model may help to define the natural history of FHC.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geisterfer-Lowrance, A A -- Christe, M -- Conner, D A -- Ingwall, J S -- Schoen, F J -- Seidman, C E -- Seidman, J G -- New York, N.Y. -- Science. 1996 May 3;272(5262):731-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614836" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cardiac Output ; Cardiomyopathy, Hypertrophic/*genetics/pathology/physiopathology ; *Disease Models, Animal ; Female ; Gene Transfer Techniques ; Heart/*physiopathology ; Heterozygote ; Homozygote ; Humans ; Male ; Mice ; Mice, Mutant Strains ; Molecular Sequence Data ; Mutation ; Myocardium/chemistry/*pathology ; Myosin Heavy Chains/*genetics ; Physical Exertion ; Sex Characteristics ; Ventricular Function, Left
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    Liver failure and defective hepatocyte regeneration in interleukin-6-deficient mice (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-11-22
    Description: Liver regeneration stimulated by a loss of liver mass leads to hepatocyte and nonparenchymal cell proliferation and rapid restoration of liver parenchyma. Mice with targeted disruption of the interleukin-6 (IL-6) gene had impaired liver regeneration characterized by liver necrosis and failure. There was a blunted DNA synthetic response in hepatocytes of these mice but not in nonparenchymal liver cells. Furthermore, there were discrete G1 phase (prereplicative stage in the cell cycle) abnormalities including absence of STAT3 (signal transducer and activator of transcription protein 3) activation and depressed AP-1, Myc, and cyclin D1 expression. Treatment of IL-6-deficient mice with a single preoperative dose of IL-6 returned STAT3 binding, gene expression, and hepatocyte proliferation to near normal and prevented liver damage, establishing that IL-6 is a critical component of the regenerative response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cressman, D E -- Greenbaum, L E -- DeAngelis, R A -- Ciliberto, G -- Furth, E E -- Poli, V -- Taub, R -- DK44237/DK/NIDDK NIH HHS/ -- DK49210/DK/NIDDK NIH HHS/ -- DK49629/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1379-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Medicine, University of Pennsylvania School of Medicine, 705a Stellar-Chance, 422 Curie Boulevard, Philadelphia, PA 19104-6145, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8910279" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclin D1 ; Cyclins/biosynthesis ; DNA/biosynthesis/metabolism ; DNA-Binding Proteins/metabolism ; G1 Phase ; Gene Expression Regulation ; Gene Targeting ; Genes, Immediate-Early ; Hepatectomy ; Interleukin-6/deficiency/genetics/pharmacology/*physiology ; Liver/*cytology/metabolism/pathology ; Liver Failure/*etiology/pathology ; *Liver Regeneration ; Mice ; Mice, Inbred C57BL ; Mitosis ; Mutation ; Necrosis ; Oncogene Proteins/biosynthesis ; Proto-Oncogene Proteins c-myc/biosynthesis ; STAT3 Transcription Factor ; Trans-Activators/metabolism ; Transcription Factor AP-1/biosynthesis
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  • 53
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    Role of lymphotoxin and the type I TNF receptor in the formation of germinal centers (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: In mice deficient in either lymphotoxin-alpha (LT-alpha) or the type I tumor necrosis factor (TNF) receptor, but not the type II TNF receptor, germinal centers failed to develop in peripheral lymphoid organs. Germinal center formation was restored in LT-alpha-deficient mice by transplantation of normal bone marrow, indicating that the LT-alpha-expressing cells required to establish this lymphoid structure are derived from bone marrow.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsumoto, M -- Mariathasan, S -- Nahm, M H -- Baranyay, F -- Peschon, J J -- Chaplin, D D -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1289-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology and Howard Hughes Medical Institute, 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/8638112" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells ; Bone Marrow Transplantation ; Gene Targeting ; Germinal Center/cytology/immunology/*physiology ; Immunization ; Lymphotoxin-alpha/genetics/*physiology ; Mice ; Receptors, Tumor Necrosis Factor/genetics/*physiology ; Spleen/anatomy & histology/*immunology
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  • 54
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    Guiding neurons to the cortex (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1996 Nov 15;274(5290):1100-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966585" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/abnormalities/embryology ; Brain Diseases/genetics ; Cell Adhesion Molecules, Neuronal/*genetics/physiology ; Cell Movement ; Cerebral Cortex/cytology/*embryology ; Cloning, Molecular ; Cyclin-Dependent Kinase 5 ; *Cyclin-Dependent Kinases ; Extracellular Matrix Proteins/*genetics/physiology ; Female ; Humans ; Intellectual Disability/genetics ; Male ; Mice ; Mice, Neurologic Mutants ; Nerve Tissue Proteins/genetics/physiology ; Neurons/*physiology ; Protein-Serine-Threonine Kinases/physiology ; Serine Endopeptidases
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-19
    Description: About 90 percent of human pancreatic carcinomas show allelic loss at chromosome 18q. To identify candidate tumor suppressor genes on 18q, a panel of pancreatic carcinomas were analyzed for convergent sites of homozygous deletion. Twenty-five of 84 tumors had homozygous deletions at 18q21.1, a site that excludes DCC (a candidate suppressor gene for colorectal cancer) and includes DPC4, a gene similar in sequence to a Drosophila melanogaster gene (Mad) implicated in a transforming growth factor-beta (TGF-beta)-like signaling pathway. Potentially inactivating mutations in DPC4 were identified in six of 27 pancreatic carcinomas that did not have homozygous deletions at 18q21.1. These results identify DPC4 as a candidate tumor suppressor gene whose inactivation may play a role in pancreatic and possibly other human cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hahn, S A -- Schutte, M -- Hoque, A T -- Moskaluk, C A -- da Costa, L T -- Rozenblum, E -- Weinstein, C L -- Fischer, A -- Yeo, C J -- Hruban, R H -- Kern, S E -- CA62924/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 19;271(5247):350-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8553070" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Division ; Chromosome Mapping ; *Chromosomes, Human, Pair 18 ; *DNA-Binding Proteins ; Gene Deletion ; Gene Expression ; *Genes, Tumor Suppressor ; Genetic Markers ; Humans ; Mice ; Molecular Sequence Data ; Mutation ; Neoplasm Transplantation ; Pancreatic Neoplasms/*genetics/pathology ; Proteins/chemistry/*genetics/physiology ; Signal Transduction ; Smad4 Protein ; *Trans-Activators ; Transforming Growth Factor beta/physiology ; Transplantation, Heterologous ; Tumor Cells, Cultured
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    Lipid A: target for antibacterial drugs (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vaara, M -- New York, N.Y. -- Science. 1996 Nov 8;274(5289):939-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bacteriology, University of Helsinki, Finland. martti.vaara@helsinki.fi〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966574" target="_blank"〉PubMed〈/a〉
    Keywords: Amidohydrolases/*antagonists & inhibitors/genetics ; Animals ; Anti-Bacterial Agents/*pharmacology ; Escherichia coli/drug effects/genetics ; Escherichia coli Infections/drug therapy/microbiology ; Gram-Negative Bacteria/*drug effects ; Hydroxamic Acids/*pharmacology ; Lipid A/*biosynthesis ; Mice ; Microbial Sensitivity Tests
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Mutant mice and worms help solve mysteries of olfaction (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1996 Oct 25;274(5287):500-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8928002" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/genetics/physiology ; Cyclic AMP/*physiology ; Inositol Phosphates/physiology ; Ion Channels/genetics/*physiology ; Mice ; Mice, Knockout ; Mutation ; Neurons, Afferent/physiology ; Odors ; Olfactory Receptor Neurons/*physiology ; Sensation/*physiology ; Sexual Behavior, Animal ; Signal Transduction ; Smell/*physiology
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    Fetal immune response (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sarfati, M -- Delespesse, G -- New York, N.Y. -- Science. 1996 Aug 9;273(5276):722-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8701318" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn/immunology ; Female ; Fetal Blood/immunology ; Fetus/*immunology ; Humans ; Immunoglobulins/blood ; Infant, Newborn/*immunology ; Mice ; Pregnancy ; Tetanus Toxoid/*immunology ; Th2 Cells/*immunology ; Vaccination
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Nonselective and G betagamma-insensitive weaver K+ channels (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-28
    Description: Homozygous weaver mice are profoundly ataxic because of the loss of granule cell neurons during cerebellar development. This granule cell loss appears to be caused by a genetic defect in the pore region (Gly156--〉Ser) of the heterotrimeric guanine nucleotide-binding protein (G protein)-gated inwardly rectifying potassium (K+) channel subunit (GIRK2). A related subunit, GIRK1, associates with GIRK2 to constitute a neuronal G protein-gated inward rectifier K+ channel. The weaver allele of the GIRK2 subunit (wvGIRK2) caused loss of K+ selectivity when expressed either as wvGIRK2 homomultimers or as GIRK1-wvGIRK2 heteromultimers. The mutation also let to loss of sensitivity to G protein betagamma dimers. Expression of wvGIRK2 subunits let to increased cell death, presumably as a result of basal nonselective channel opening.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Navarro, B -- Kennedy, M E -- Velimirovic, B -- Bhat, D -- Peterson, A S -- Clapham, D E -- New York, N.Y. -- Science. 1996 Jun 28;272(5270):1950-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Mayo Foundation, Rochester, Minnesota 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658170" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antisense Elements (Genetics) ; CHO Cells ; Cell Death ; Cell Line ; Cerebellum/cytology/*metabolism ; Cricetinae ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; GTP-Binding Proteins/*physiology ; Membrane Potentials ; Mice ; Mice, Neurologic Mutants ; Molecular Sequence Data ; Neurons/cytology/metabolism ; Oocytes/cytology ; Patch-Clamp Techniques ; Point Mutation ; Potassium Channels/genetics/*metabolism ; *Potassium Channels, Inwardly Rectifying ; Transfection
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    Obesity: leptin receptor weighs in (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1996 Jan 5;271(5245):29.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8539591" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood-Brain Barrier ; *Brain Chemistry ; Carrier Proteins/*genetics/isolation & purification/metabolism ; Choroid Plexus/metabolism ; Humans ; Leptin ; Mice ; Obesity/drug therapy/genetics/metabolism ; Proteins/*metabolism ; *Receptors, Cell Surface ; Receptors, Leptin
    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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    Two genetically separable steps in the differentiation of thymic epithelium (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-10
    Description: The development of the thymus depends initially on epithelial-mesenchymal and subsequently on reciprocal lympho-stromal interactions. The genetic steps governing development and differentiation of the thymic microenvironment are unknown. With the use of a targeted disruption of the whn gene, which recapitulates the phenotype of the athymic nude mouse, the WHN transcription factor was shown to be the product of the nude locus. Formation of the thymic epithelial primordium before the entry of lymphocyte progenitors did not require the activity of WHN. However, subsequent differentiation of primitive precursor cells into subcapsular, cortical, and medullary epithelial cells of the postnatal thymus did depend on activity of the whn gene. These results define the first genetically separable steps during thymic epithelial differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nehls, M -- Kyewski, B -- Messerle, M -- Waldschutz, R -- Schuddekopf, K -- Smith, A J -- Boehm, T -- New York, N.Y. -- Science. 1996 May 10;272(5263):886-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Deutsches Krebsforschungszentrum, Im Neuenheimer Feld, Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8629026" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Animals, Newborn ; Base Sequence ; Cell Differentiation/*genetics ; Crosses, Genetic ; DNA-Binding Proteins/*genetics/physiology ; Epithelial Cells ; Female ; Forkhead Transcription Factors ; Gene Expression Regulation, Developmental ; Gene Targeting ; Genetic Complementation Test ; Male ; Mice ; Mice, Nude ; Molecular Sequence Data ; T-Lymphocytes/*cytology ; Thymus Gland/*cytology/embryology/metabolism ; Transcription Factors/*genetics/physiology
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    Researchers nail down leptin receptor (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1996 Feb 16;271(5251):913.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8584929" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/biosynthesis/chemistry/*genetics ; Chromosome Mapping ; Cloning, Molecular ; Diabetes Mellitus/*genetics ; Humans ; Leptin ; Mice ; Mutation ; Obesity/*genetics ; Proteins/genetics ; RNA, Messenger/genetics ; Rats ; *Receptors, Cell Surface ; Receptors, Cytokine/biosynthesis/chemistry/*genetics ; Receptors, Leptin
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    In vitro development of primitive and definitive erythrocytes from different precursors (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-03
    Description: During mouse embryogenesis the production of "primitive" erythrocytes (EryP) precedes the production of "definitive" erythrocytes (EryD) in parallel with the transition of the hematopoietic site from the yolk sac to the fetal liver. On a macrophage colony-stimulating factor-deficient stromal cell line OP9, mouse embryonic stem cells were shown to give rise to EryP and EryD sequentially with a time course similar to that seen in murine ontogeny. Studies of the different growth factor requirements and limiting dilution analysis of precursor frequencies indicate that most EryP and EryD probably developed from different precursors by way of distinct differentiation pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakano, T -- Kodama, H -- Honjo, T -- New York, N.Y. -- Science. 1996 May 3;272(5262):722-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Faculty of Medicine, Kyoto University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614833" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Line ; Cell Lineage ; Cell Separation ; Cells, Cultured ; Coculture Techniques ; Erythroid Precursor Cells/*cytology ; *Erythropoiesis ; Erythropoietin/pharmacology ; Kinetics ; Mice ; Signal Transduction ; Stem Cell Factor/physiology
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    Interfering with apoptosis: Ca(2+)-binding protein ALG-2 and Alzheimer's disease gene ALG-3 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-26
    Description: Two apoptosis-linked genes, named ALG-2 and ALG-3, were identified by means of a functional selection strategy. ALG-2 codes for a Ca(2+)-binding protein required for T cell receptor-, Fas-, and glucocorticoid-induced cell death. ALG-3, a partial complementary DNA that is homologous to the familial Alzheimer's disease gene STM2, rescues a T cell hybridoma from T cell receptor- and Fas-induced apoptosis. These findings suggest that ALG-2 may mediate Ca(2+)-regulated signals along the death pathway and that cell death may play a role in Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vito, P -- Lacana, E -- D'Adamio, L -- New York, N.Y. -- Science. 1996 Jan 26;271(5248):521-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉T Cell Molecular Biology Unit, National Institute of Allergy and Infectious 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/8560270" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaloids/pharmacology ; Alzheimer Disease/*genetics ; Amino Acid Sequence ; Animals ; Antigens, CD95/metabolism ; *Apoptosis/drug effects ; Apoptosis Regulatory Proteins ; Calcium/metabolism ; Calcium-Binding Proteins/chemistry/genetics/*physiology ; Cell Line ; Cloning, Molecular ; DNA, Complementary ; Dactinomycin/pharmacology ; Dexamethasone/pharmacology ; Fas Ligand Protein ; Hybridomas ; Interleukin-2/metabolism ; Membrane Glycoproteins/metabolism ; Membrane Proteins/chemistry/genetics/*physiology ; Mice ; Molecular Sequence Data ; Presenilin-2 ; Receptors, Antigen, T-Cell/physiology ; Signal Transduction ; Staurosporine ; T-Lymphocytes ; Transfection ; Up-Regulation
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    Induction of protective CTL responses in newborn mice by a murine retrovirus (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-22
    Description: The susceptibility of neonates to virus-induced disease is thought to reflect, in part, the immaturity of their immune systems. However, inoculation of newborn mice with low doses of Cas-Br-M murine leukemia virus induced a protective cytotoxic T lymphocyte (CTL) response. The inability of neonates to develop a CTL response to high doses of virus was not the result of immunological immaturity but correlated with the induction of a nonprotective type 2 cytokine response. Thus, the initial viral dose is critical in the development of protective immunity in newborns.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sarzotti, M -- Robbins, D S -- Hoffman, P M -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1726-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rsearch Service, Veterans Affairs Medical Center, Baltimore, MD 21201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596933" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn/*immunology ; Cells, Cultured ; Cytotoxicity, Immunologic ; Dose-Response Relationship, Immunologic ; Immunotherapy, Adoptive ; Interferon-gamma/biosynthesis ; Interleukin-4/biosynthesis ; Leukemia Virus, Murine/*immunology ; Mice ; Retroviridae Infections/*immunology ; T-Lymphocytes, Cytotoxic/*immunology ; Tumor Virus Infections/*immunology
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    Immunostimulatory DNA sequences necessary for effective intradermal gene immunization (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-19
    Description: Vaccination with naked DNA elicits cellular and humoral immune responses that have a T helper cell type 1 bias. However, plasmid vectors expressing large amounts of gene product do not necessarily induce immune responses to the encoded antigens. Instead, the immunogenicity of plasmid DNA (pDNA) requires short immunostimulatory DNA sequences (ISS) that contain a CpG dinucleotide in a particular base context. Human monocytes transfected with pDNA or double-stranded oligonucleotides containing the ISS, but not those transfected with ISS-deficient pDNA or oligonucleotides, transcribed large amounts of interferon-alpha, interferon-beta, and interleukin-12. Although ISS are necessary for gene vaccination, they down-regulate gene expression and thus may interfere with gene replacement therapy by inducing proinflammatory cytokines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sato, Y -- Roman, M -- Tighe, H -- Lee, D -- Corr, M -- Nguyen, M D -- Silverman, G J -- Lotz, M -- Carson, D A -- Raz, E -- AI36214/AI/NIAID NIH HHS/ -- AI37305/AI/NIAID NIH HHS/ -- AR41897/AR/NIAMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Jul 19;273(5273):352-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine and The Sam and Rose Stein Institute for Research on Aging, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0663, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662521" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Ampicillin Resistance/*genetics ; Animals ; *Antibody Formation ; Base Sequence ; CpG Islands ; Cytokines/*biosynthesis ; DNA/chemistry/genetics/*immunology ; Female ; Gene Expression Regulation ; Genetic Vectors ; Humans ; Injections, Intradermal ; Interferons/biosynthesis ; Interleukin-12/biosynthesis ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Monocytes/immunology ; Plasmids/genetics/*immunology ; Th1 Cells/immunology ; Transfection ; *Vaccination ; beta-Galactosidase/*immunology
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    Enhancement of antitumor immunity by CTLA-4 blockade (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-22
    Description: One reason for the poor immunogenicity of many tumors may be that they cannot provide signals for CD28-mediated costimulation necessary to fully activate T cells. It has recently become apparent that CTLA-4, a second counterreceptor for the B7 family of costimulatory molecules, is a negative regulator of T cell activation. Here, in vivo administration of antibodies to CTLA-4 resulted in the rejection of tumors, including preestablished tumors. Furthermore, this rejection resulted in immunity to a secondary exposure to tumor cells. These results suggest that blockade of the inhibitory effects of CTLA-4 can allow for, and potentiate, effective immune responses against tumor cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leach, D R -- Krummel, M F -- Allison, J P -- CA09179/CA/NCI NIH HHS/ -- CA40041/CA/NCI NIH HHS/ -- CA57986/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1734-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Laboratory, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596936" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antibodies/immunology ; Antigens, CD ; Antigens, CD28/immunology ; Antigens, CD80/immunology ; Antigens, Differentiation/*immunology ; CTLA-4 Antigen ; Female ; Graft Rejection ; *Immunoconjugates ; Immunologic Memory ; *Lymphocyte Activation ; Mice ; Mice, Inbred A ; Mice, Inbred BALB C ; Neoplasm Transplantation ; Neoplasms, Experimental/*immunology ; T-Lymphocytes/*immunology ; Transfection ; Tumor Cells, Cultured
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    Susceptibility to Leishmania major infection in interleukin-4-deficient mice (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-16
    Description: Interleukin-4 (IL-4), a pleiotropic cytokine, is a major regulator of the immune system and is considered crucial for the development of T helper cell type 2 (TH2) responses. The susceptibility of BALB/c mice to infection with Leishmania major has been associated with a polarized TH2 response and an inability to down-modulate IL-4 production. The role of IL-4 in vivo was examined directly by disrupting the IL-4 gene in BALB/c embryonic stem cells. Despite the absence of IL-4, the genetically pure BALB/c mutant mice remained susceptible to L. major infection, showed no signs of lesion healing or parasite clearance, and did not switch to a TH1 phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noben-Trauth, N -- Kropf, P -- Muller, I -- 1R29 AI37636-01/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 16;271(5251):987-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jackson Laboratory, Bar Harbor, ME 04609, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8584936" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cytokines/analysis ; Disease Susceptibility ; Immunity, Innate ; Immunoglobulin E/blood ; Immunoglobulin G/blood ; Interferon-gamma/biosynthesis ; Interleukin-4/biosynthesis/deficiency/genetics/*immunology ; Leishmania major/*immunology ; Leishmaniasis, Cutaneous/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Molecular Sequence Data ; Th1 Cells/immunology ; Th2 Cells/*immunology
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    An essential role for NF-kappaB in preventing TNF-alpha-induced cell death (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-01
    Description: Studies on mice deficient in nuclear factor kappa B (NF-kappaB) subunits have shown that this transcription factor is important for lymphocyte responses to antigens and cytokine-inducible gene expression. In particular, the RelA (p65) subunit is required for induction of tumor necrosis factor-alpha (TNF-alpha)-dependent genes. Treatment of RelA-deficient (RelA-/-) mouse fibroblasts and macrophages with TNF-alpha resulted in a significant reduction in viability, whereas RelA+/+ cells were unaffected. Cytotoxicity to both cell types was mediated by TNF receptor 1. Reintroduction of RelA into RelA-/- fibroblasts resulted in enhanced survival, demonstrating that the presence of RelA is required for protection from TNF-alpha. These results have implications for the treatment of inflammatory and proliferative diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beg, A A -- Baltimore, D -- New York, N.Y. -- Science. 1996 Nov 1;274(5288):782-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8864118" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Antigens, CD/metabolism ; *Cell Death ; Cell Survival ; Cells, Cultured ; Gene Expression Regulation ; Humans ; Macrophages/cytology ; Mice ; NF-kappa B/genetics/*physiology ; Receptors, Tumor Necrosis Factor/metabolism ; Receptors, Tumor Necrosis Factor, Type I ; Signal Transduction ; Transcription Factor RelA ; Transfection ; 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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    Exposure to methylene chloride (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Norman, W C 3rd -- New York, N.Y. -- Science. 1996 Oct 18;274(5286):327.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8927983" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests ; Carcinogens/*toxicity ; Humans ; Methylene Chloride/*toxicity ; Mice ; Neoplasms/*chemically induced ; Rats
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    Luteinizing hormone deficiency and female infertility in mice lacking the transcription factor NGFI-A (Egr-1) (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-30
    Description: The immediate-early transcription factor NGFI-A (also called Egr-1, zif/268, or Krox-24) is thought to couple extracellular signals to changes in gene expression. Although activins and inhibins regulate follicle-stimulating hormone (FSH) synthesis, no factor has been identified that exclusively regulates luteinizing hormone (LH) synthesis. An analysis of NGFI-A-deficient mice derived from embryonic stem cells demonstrated female infertility that was secondary to LH-beta deficiency. Ovariectomy led to increased amounts of FSH-beta but not LH-beta messenger RNA, which suggested a pituitary defect. A conserved, canonical NGFI-A site in the LH-beta promoter was required for synergistic activation by NGFI-A and steroidogenic factor-1 (SF-1). NGFI-A apparently influences female reproductive capacity through its regulation of LH-beta transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, S L -- Sadovsky, Y -- Swirnoff, A H -- Polish, J A -- Goda, P -- Gavrilina, G -- Milbrandt, J -- CA53524/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 30;273(5279):1219-21.〈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/8703054" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; DNA-Binding Proteins/*genetics ; Early Growth Response Protein 1 ; Female ; Follicle Stimulating Hormone/genetics ; Follicle Stimulating Hormone, beta Subunit ; Fushi Tarazu Transcription Factors ; *Gene Expression Regulation ; Gene Targeting ; Gonadotropins/pharmacology ; Homeodomain Proteins ; *Immediate-Early Proteins ; Infertility, Female/*genetics ; Luteinizing Hormone/analysis/*deficiency/*genetics ; Male ; Mice ; Molecular Sequence Data ; Ovary/drug effects/physiology ; Pituitary Gland/metabolism ; Promoter Regions, Genetic ; Receptors, Cytoplasmic and Nuclear ; Steroidogenic Factor 1 ; Transcription Factors/*genetics ; Transfection ; Uterus/drug effects ; Zinc Fingers
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    Ocular dominance plasticity under metabotropic glutamate receptor blockade (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-26
    Description: Occluding vision through one eye during a critical period in early life nearly abolishes responses to that eye in visual cortex. This phenomenon is mimicked by long-term depression of synaptic transmission in vitro, which may require metabotropic glutamate receptors (mGluRs) and is age-dependent. Peaks in mGluR expression and glutamate-stimulated phosphoinositide turnover during visual cortical development have been proposed as biochemical bases for the critical period. Pharmacological blockade of mGluRs specifically prevented synapse weakening in mouse visual cortical slices but did not alter kitten ocular dominance plasticity in vivo. Thus, a heightened mGluR response does not account for the critical period in development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hensch, T K -- Stryker, M P -- EY02874/EY/NEI NIH HHS/ -- R01 EY002874/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1996 Apr 26;272(5261):554-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Graduate Program, W. M. Keck Foundation Center for Integrative Neuroscience, Department of Physiology, University of California, San Francisco, 94143-0444, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614806" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzoates/*pharmacology ; Cats ; Excitatory Amino Acid Agonists/pharmacology ; Excitatory Amino Acid Antagonists/*pharmacology ; Glycine/*analogs & derivatives/pharmacology ; In Vitro Techniques ; Membrane Potentials ; Mice ; Mice, Inbred C57BL ; Neuronal Plasticity/drug effects/*physiology ; Photic Stimulation ; Receptors, Metabotropic Glutamate/antagonists & inhibitors/*physiology ; Sensory Deprivation ; Vision, Monocular ; Visual Cortex/drug effects/*physiology ; Visual Pathways
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Immunodeficiency in protein kinase cbeta-deficient mice (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-09
    Description: Cross-linking of the antigen receptor on lymphocytes by antigens or antibodies to the receptor results in activation of enzymes of the protein kinase C (PKC) family. Mice homozygous for a targeted disruption of the gene encoding the PKC-betaI and PKC-betaII isoforms develop an immunodeficiency characterized by impaired humoral immune responses and reduced cellular responses of B cells, which is similar to X-linked immunodeficiency in mice. Thus PKC-betaI and PKC-betaII play an important role in B cell activation and may be functionally linked to Bruton's tyrosine kinase in antigen receptor-mediated signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leitges, M -- Schmedt, C -- Guinamard, R -- Davoust, J -- Schaal, S -- Stabel, S -- Tarakhovsky, A -- New York, N.Y. -- Science. 1996 Aug 9;273(5276):788-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Delbruck-Laboratorium in der Max-Planck-Gesellschaft, Carl-von-Linne-Weg 10, D-50829 Koln, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8670417" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Gene Targeting ; Genetic Linkage ; Immunoglobulin G/blood ; Immunoglobulin M/blood/immunology ; Immunoglobulins/*blood ; Immunologic Deficiency Syndromes/enzymology/*immunology ; Lymphocyte Activation ; Lymphocyte Count ; Mice ; Protein Kinase C/deficiency/genetics/*physiology ; Protein Kinase C beta ; Protein-Tyrosine Kinases/genetics/metabolism ; Receptors, Antigen, B-Cell/immunology ; Signal Transduction ; T-Lymphocytes/immunology ; X Chromosome
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    Regulation of rate of cartilage differentiation by Indian hedgehog and PTH-related protein (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-02
    Description: Proper regulation of chondrocyte differentiation is necessary for the morphogenesis of skeletal elements, yet little is known about the molecular regulation of this process. A chicken homolog of Indian hedgehog (Ihh), a member of the conserved Hedgehog family of secreted proteins that is expressed during bone formation, has now been isolated. Ihh has biological properties similar to those of Sonic hedgehog (Shh), including the ability to regulate the conserved targets Patched (Ptc) and Gli. Ihh is expressed in the prehypertrophic chondrocytes of cartilage elements, where it regulates the rate of hypertrophic differentiation. Misexpression of Ihh prevents proliferating chondrocytes from initiating the hypertrophic differentiation process. The direct target of Ihh signaling is the perichondrium, where Gli and Ptc flank the expression domain of Ihh. Ihh induces the expression of a second signal, parathyroid hormone-related protein (PTHrP), in the periarticular perichondrium. Analysis of PTHrP (-/-) mutant mice indicated that the PTHrP protein signals to its receptor in the prehypertrophic chondrocytes, thereby blocking hypertrophic differentiation. In vitro application of Hedgehog or PTHrP protein to normal or PTHrP (-/-) limb explants demonstrated that PTHrP mediates the effects of Ihh through the formation of a negative feedback loop that modulates the rate of chondrocyte differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vortkamp, A -- Lee, K -- Lanske, B -- Segre, G V -- Kronenberg, H M -- Tabin, C J -- DK47038/DK/NIDDK NIH HHS/ -- DK4723/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 2;273(5275):613-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Bone Development ; Cartilage/*cytology/metabolism ; Cell Differentiation ; Cell Division ; Chick Embryo ; Cloning, Molecular ; Culture Techniques ; Extremities/embryology ; Feedback ; Gene Expression Regulation ; Growth Plate/*cytology/metabolism ; Hedgehog Proteins ; Mice ; Molecular Sequence Data ; Morphogenesis ; *Osteogenesis ; Parathyroid Hormone ; Parathyroid Hormone-Related Protein ; Phenotype ; Proteins/pharmacology/*physiology ; Receptor, Parathyroid Hormone, Type 1 ; Receptors, Parathyroid Hormone/physiology ; Signal Transduction ; *Trans-Activators
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    Gastric mucosa abnormalities and tumorigenesis in mice lacking the pS2 trefoil protein (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-10-11
    Description: To determine the function of the pS2 trefoil protein, which is normally expressed in the gastric mucosa, the mouse pS2 (mpS2) gene was inactivated. The antral and pyloric gastric mucosa of mpS2-null mice was dysfunctional and exhibited severe hyperplasia and dysplasia. All homozygous mutant mice developed antropyloric adenoma, and 30 percent developed multifocal intraepithelial or intramucosal carcinomas. The small intestine was characterized by enlarged villi and an abnormal infiltrate of lymphoid cells. These results indicate that mpS2 is essential for normal differentiation of the antral and pyloric gastric mucosa and may function as a gastric-specific tumor suppressor gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lefebvre, O -- Chenard, M P -- Masson, R -- Linares, J -- Dierich, A -- LeMeur, M -- Wendling, C -- Tomasetto, C -- Chambon, P -- Rio, M C -- New York, N.Y. -- Science. 1996 Oct 11;274(5285):259-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS/INSERM/Universite Louis Pasteur/College de France, Communaute Urbaine de Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8824193" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/etiology/pathology ; Animals ; Base Sequence ; Cell Differentiation ; Cloning, Molecular ; Female ; Gastric Mucosa/cytology/*pathology ; Gene Targeting ; Genes, Tumor Suppressor ; Intestinal Mucosa/cytology/*pathology ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Neoplasm Proteins/genetics/*physiology ; Phenotype ; *Proteins ; Pyloric Antrum ; Stomach Neoplasms/*etiology/pathology ; Tumor Suppressor Proteins
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    Lysogenic conversion by a filamentous phage encoding cholera toxin (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-28
    Description: Vibrio cholerae, the causative agent of cholera, requires two coordinately regulated factors for full virulence: cholera toxin (CT), a potent enterotoxin, and toxin-coregulated pili (TCP), surface organelles required for intestinal colonization. The structural genes for CT are shown here to be encoded by a filamentous bacteriophage (designated CTXphi), which is related to coliphage M13. The CTXphi genome chromosomally integrated or replicated as a plasmid. CTXphi used TCP as its receptor and infected V. cholerae cells within the gastrointestinal tracts of mice more efficiently than under laboratory conditions. Thus, the emergence of toxigenic V. cholerae involves horizontal gene transfer that may depend on in vivo gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waldor, M K -- Mekalanos, J J -- AI01321/AI/NIAID NIH HHS/ -- AI18045/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Jun 28;272(5270):1910-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Shipley Institute of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658163" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bacteriophages/*genetics/physiology ; Base Sequence ; Cholera/*microbiology ; Cholera Toxin/*genetics ; DNA Primers ; Digestive System/microbiology ; Fimbriae, Bacterial/physiology/virology ; Gene Expression ; Genes, Bacterial ; *Lysogeny ; Mice ; Molecular Sequence Data ; Morphogenesis ; Mutation ; Transduction, Genetic ; Vibrio cholerae/genetics/*pathogenicity/*virology ; Virulence/genetics
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    Reexpression of RAG-1 and RAG-2 genes in activated mature mouse B cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: Recombination activating genes (RAG-1 and RAG-2), involved in V(D)J rearrangement of immunoglobulin genes, have been thought to be expressed only in immature stages of B-cell development. However, RAG-1 and RAG-2 transcripts were found to be reexpressed in mature mouse B cells after culture with interleukin-4 in association with several different co-stimuli. Reexpression was also detected in draining lymph nodes from immunized mice. RAG-1 and RAG-2 proteins could be detected by immunofluorescence microscopy in the nuclei of B cells cultured in vitro and in the germinal centers of draining lymph nodes. These findings suggest that RAG gene products play a heretofore unsuspected role in mature B cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hikida, M -- Mori, M -- Takai, T -- Tomochika, K -- Hamatani, K -- Ohmori, H -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2092-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biotechnology, Faculty of Engineering, Okayama University, Tsushima-Naka, Okayama 700, Japan. hit2224@cc.okayama-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953042" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology/*metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; *DNA-Binding Proteins ; *Gene Expression ; *Genes, RAG-1 ; Germinal Center/metabolism ; *Homeodomain Proteins ; Immunoglobulin Class Switching ; Interleukin-4/pharmacology ; Interleukins/pharmacology ; Lipopolysaccharides/pharmacology ; Lymph Nodes/metabolism ; *Lymphocyte Activation ; Mice ; Mice, Inbred C3H ; Microscopy, Fluorescence ; Protein Biosynthesis ; Proteins/*genetics
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    Protection against atherogenesis in mice mediated by human apolipoprotein A-IV (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-16
    Description: Apolipoproteins are protein constituents of plasma lipid transport particles. Human apolipoprotein A-IV (apoA-IV) was expressed in the liver of C57BL/6 mice and mice deficient in apoE, both of which are prone to atherosclerosis, to investigate whether apoA-IV protects against this disease. In transgenic C57BL/6 mice on an atherogenic diet, the serum concentration of high density lipoprotein (HDL) cholesterol increased by 35 percent, whereas the concentration of endogenous apoA-I decreased by 29 percent, relative to those in transgenic mice on a normal diet. Expression of human apoA-IV in apoE-deficient mice on a normal diet resulted in an even more severe atherogenic lipoprotein profile, without affecting the concentration of HDL cholesterol, than that in nontransgenic apoE-deficient mice. However, transgenic mice of both backgrounds showed a substantial reduction in the size of atherosclerotic lesions. Thus, apoA-IV appears to protect against atherosclerosis by a mechanism that does not involve an increase in HDL cholesterol concentration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duverger, N -- Tremp, G -- Caillaud, J M -- Emmanuel, F -- Castro, G -- Fruchart, J C -- Steinmetz, A -- Denefle, P -- New York, N.Y. -- Science. 1996 Aug 16;273(5277):966-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rhone-Poulenc Rorer, Gencell Division, Atherosclerosis Department, Centre de Recherches de Vitry-Alfortville, 94403 Vitry sur Seine Cedex, France. G. C.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8688083" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoprotein A-I/blood ; Apolipoproteins A/blood/*physiology ; Apolipoproteins E/blood/deficiency ; Arteriosclerosis/*prevention & control ; Cholesterol/blood ; Cholesterol, HDL/blood ; Diet, Atherogenic ; Female ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic
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    Resistance to apoptosis conferred by Cdk inhibitors during myocyte differentiation (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-07-19
    Description: Proliferating murine C2C12 myoblasts can undergo either terminal differentiation or programmed cell death under conditions of mitogen deprivation. Unlike myoblasts, differentiated myotubes were resistant to apoptosis. During myogenesis the appearance of the apoptosis-resistant phenotype was correlated with the induction of the cyclin-dependent kinase (Cdk) inhibitor p21(CIP1) but not with the appearance of myogenin, a marker expressed earlier in differentiation. Forced expression of the Cdk inhibitors p21(CIP1) or p16(INK4A) blocked apoptosis during myocyte differentiation. These data indicate that induction of Cdk inhibitors may serve to protect differentiating myocytes from programmed cell death as well as play a role in establishing the postmitotic state.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3641673/" 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/PMC3641673/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, J -- Walsh, K -- AR40197/AR/NIAMS NIH HHS/ -- HL50692/HL/NHLBI NIH HHS/ -- R01 AG015052/AG/NIA NIH HHS/ -- R01 AR040197/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jul 19;273(5273):359-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cardiovascular Research, St. Elizabeth's Medical Center and Tufts University School of Medicine, Boston, MA 02135, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662523" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Carrier Proteins/biosynthesis/genetics/*physiology ; *Cell Differentiation ; Cell Line ; Culture Media ; Cyclin-Dependent Kinase Inhibitor p16 ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinases/*antagonists & inhibitors ; Cyclins/biosynthesis/genetics/*physiology ; Enzyme Inhibitors/metabolism ; Mice ; Muscles/*cytology/metabolism ; Myogenin/biosynthesis ; Phenotype ; Transfection
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    Blocked signal transduction to the ERK and JNK protein kinases in anergic CD4+ T cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: T cells activated by antigen receptor stimulation in the absence of accessory cell-derived costimulatory signals lose the capacity to synthesize the growth factor interleukin-2 (IL-2), a state called clonal anergy. An analysis of CD3- and CD28-induced signal transduction revealed reduced ERK and JNK enzyme activities in murine anergic T cells. The amounts of ERK and JNK proteins were unchanged, and the kinases could be fully activated in the presence of phorbol 12-myristate 13-acetate. Dephosphorylation of the calcineurin substrate NFATp (preexisting nuclear factor of activated T cells) also remained inducible. These results suggest that a specific block in the activation of ERK and JNK contributes to defective IL-2 production in clonal anergy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, W -- Whaley, C D -- Mondino, A -- Mueller, D L -- R29 AI 31669/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1272-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Minnesota Medical School, Minneapolis 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638107" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD28/immunology ; Antigens, CD3/immunology ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; *Clonal Anergy ; Clone Cells ; Cyclosporine/pharmacology ; DNA-Binding Proteins/metabolism ; Enhancer Elements, Genetic ; Enzyme Activation ; Interleukin-2/biosynthesis ; Ionomycin/pharmacology ; JNK Mitogen-Activated Protein Kinases ; Lymphocyte Activation ; Mice ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; NFATC Transcription Factors ; *Nuclear Proteins ; Protein-Tyrosine Kinases/metabolism ; *Signal Transduction ; T-Lymphocytes, Helper-Inducer/enzymology/*immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription Factor AP-1/metabolism ; Transcription Factors/metabolism
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    Stress-induced phosphorylation and activation of the transcription factor CHOP (GADD153) by p38 MAP Kinase (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-31
    Description: CHOP, a member of the C/EBP family of transcription factors, mediates effects of cellular stress on growth and differentiation. It accumulates under conditions of stress and undergoes inducible phosphorylation on two adjacent serine residues (78 and 81). In vitro, CHOP is phosphorylated on these residues by p38 mitogen-activated protein kinase (MAP kinase). A specific inhibitor of p38 MAP kinase, SB203580, abolished the stress-inducible in vivo phosphorylation of CHOP. Phosphorylation of CHOP on these residues enhanced its ability to function as a transcriptional activator and was also required for the full inhibitory effect of CHOP on adipose cell differentiation. CHOP thus serves as a link between a specific stress-activated protein kinase, p38, and cellular growth and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, X Z -- Ron, D -- New York, N.Y. -- Science. 1996 May 31;272(5266):1347-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Skirball Institute of Biomolecular Medicine, New York University Medical Center, 10016, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650547" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adipocytes/cytology ; Amino Acid Sequence ; Animals ; *CCAAT-Enhancer-Binding Proteins ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Differentiation ; Cell Division ; Culture Media ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Enzyme Inhibitors/pharmacology ; Imidazoles/pharmacology ; Methyl Methanesulfonate/pharmacology ; Mice ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Phosphorylation ; Pyridines/pharmacology ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription Factor CHOP ; Transcription Factors/chemistry/genetics/*metabolism ; Transcriptional Activation ; p38 Mitogen-Activated Protein Kinases
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    CD5-mediated negative regulation of antigen receptor-induced growth signals in B-1 B cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-13
    Description: A subset of B lymphocytes present primarily in the peritoneal and pleural cavities is defined by the expression of CD5 and is elevated in autoimmune diseases. Upon signaling through membrane immunoglobulin M (mIgM), splenic B lymphocytes (B-2) proliferate, whereas peritoneal B cells (B-1) undergo apoptosis. However, in CD5-deficient mice, B-1 cells responded to mIgM crosslinking by developing a resistance to apoptosis and entering the cell cycle. In wild-type B-1 cells, prevention of association between CD5 and mIgM rescued their growth response to mIgM crosslinking. Thus the B cell receptor-mediated signaling is negatively regulated by CD5 in normal B-1 cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bikah, G -- Carey, J -- Ciallella, J R -- Tarakhovsky, A -- Bondada, S -- AG05731/AG/NIA NIH HHS/ -- AI21490/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 13;274(5294):1906-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology and Center on Aging, University of Kentucky, Lexington, KY 40536, USA. sbonda@pop.uky.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8943203" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD5/*physiology ; Apoptosis ; B-Lymphocyte Subsets/*cytology/*immunology/metabolism ; Calcium/metabolism ; Cell Division ; Cell Nucleus/metabolism ; Cross-Linking Reagents ; Female ; Immunoglobulin M/immunology/metabolism ; *Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; NF-kappa B/metabolism ; Peritoneal Cavity/cytology ; Receptors, Antigen, B-Cell/immunology/metabolism/*physiology ; *Signal Transduction
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  • 83
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    Chain migration of neuronal precursors (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-16
    Description: In the brain of adult mice, cells that divide in the subventricular zone of the lateral ventricle migrate up to 5 millimeters to the olfactory bulb where they differentiate into neurons. These migrating cells were found to move as chains through a well-defined pathway, the rostral migratory stream. Electron microscopic analysis of serial sections showed that these chains contained only closely apposed, elongated neuroblasts connected by membrane specializations. A second cell type, which contained glial fibrillary acidic protein, ensheathed the chains of migrating neuroblasts. Thus, during chain migration, neural precursors moved associated with each other and were not guided by radial glial or axonal fibers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lois, C -- Garcia-Verdugo, J M -- Alvarez-Buylla, A -- HD32116/HD/NICHD NIH HHS/ -- NS28478/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 16;271(5251):978-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rockefeller University, New York 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8584933" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Membrane/ultrastructure ; Cell Movement ; Cerebral Ventricles/*cytology ; Glial Fibrillary Acidic Protein/analysis ; Male ; Mice ; Microscopy, Electron ; Mitosis ; Neural Cell Adhesion Molecules/analysis ; Neuroglia/chemistry/*cytology/physiology ; Neurons/*cytology/ultrastructure ; Olfactory Bulb/cytology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 84
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    Releasing the brakes on antitumor immune response (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pardoll, D -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1691.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncology, Johns Hopkins University Medical School, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596929" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antibodies/therapeutic use ; Antigens, CD ; Antigens, Differentiation/*immunology ; CTLA-4 Antigen ; Humans ; *Immunoconjugates ; *Immunotherapy ; *Lymphocyte Activation ; Mice ; Neoplasms/*immunology/therapy ; T-Lymphocytes/*immunology ; Vaccines/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 85
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    Synapse-making molecules revealed (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1996 May 24;272(5265):1100.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638153" target="_blank"〉PubMed〈/a〉
    Keywords: Agrin/genetics/*metabolism ; Animals ; Brain/metabolism ; Mice ; Mice, Knockout ; Muscle, Skeletal/enzymology ; Neuromuscular Junction/enzymology/*metabolism ; Receptor Protein-Tyrosine Kinases/*metabolism ; *Receptors, Cholinergic ; Receptors, Growth Factor/*metabolism ; Synapses/*metabolism
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  • 86
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    Inhibition of adipogenesis through MAP kinase-mediated phosphorylation of PPARgamma (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: Adipocyte differentiation is an important component of obesity and other metabolic diseases. This process is strongly inhibited by many mitogens and oncogenes. Several growth factors that inhibit fat cell differentiation caused mitogen-activated protein (MAP) kinase-mediated phosphorylation of the dominant adipogenic transcription factor peroxisome proliferator-activated receptor gamma (PPARgamma) and reduction of its transcriptional activity. Expression of PPARgamma with a nonphosphorylatable mutation at this site (serine-112) yielded cells with increased sensitivity to ligand-induced adipogenesis and resistance to inhibition of differentiation by mitogens. These results indicate that covalent modification of PPARgamma by serum and growth factors is a major regulator of the balance between cell growth and differentiation in the adipose cell lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, E -- Kim, J B -- Sarraf, P -- Spiegelman, B M -- R37DK31405/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2100-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953045" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adipocytes/*cytology/metabolism ; Animals ; Blood ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/*metabolism ; Cell Differentiation ; Cell Line ; Enzyme Inhibitors/pharmacology ; Epidermal Growth Factor/pharmacology ; Flavonoids/pharmacology ; Insulin/pharmacology ; Ligands ; Mice ; Mitogens/pharmacology ; Mutation ; Phosphorylation ; Rats ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription Factors/chemistry/genetics/*metabolism ; Transcription, Genetic/drug effects ; Transfection
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  • 87
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    Methylene chloride (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huff, J -- Bucher, J -- Barrett, J C -- New York, N.Y. -- Science. 1996 May 24;272(5265):1083-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638144" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests ; Carcinogens/*toxicity ; Female ; Humans ; Liver Neoplasms, Experimental/chemically induced ; Lung Neoplasms/chemically induced ; Male ; Methylene Chloride/*toxicity ; Mice ; Mutagens/*toxicity ; Neoplasms/*chemically induced ; Rats
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  • 88
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    HIV-1 entry cofactor: functional cDNA cloning of a seven-transmembrane, G protein-coupled receptor (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-10
    Description: A cofactor for HIV-1 (human immunodeficiency virus-type 1) fusion and entry was identified with the use of a novel functional complementary DNA (cDNA) cloning strategy. This protein, designated "fusin," is a putative G protein-coupled receptor with seven transmembrane segments. Recombinant fusin enabled CD4-expressing nonhuman cell types to support HIV-1 Env-mediated cell fusion and HIV-1 infection. Antibodies to fusin blocked cell fusion and infection with normal CD4-positive human target cells. Fusin messenger RNA levels correlated with HIV-1 permissiveness in diverse human cell types. Fusin acted preferentially for T cell line-tropic isolates, in comparison to its activity with macrophagetropic HIV-1 isolates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng, Y -- Broder, C C -- Kennedy, P E -- Berger, E A -- New York, N.Y. -- Science. 1996 May 10;272(5263):872-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8629022" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Antigens, CD4/*physiology ; CD4-Positive T-Lymphocytes/virology ; Cell Line ; Cell Membrane/virology ; Chemokines/physiology ; *Cloning, Molecular ; DNA, Complementary/genetics ; Disease Models, Animal ; GTP-Binding Proteins/metabolism ; Giant Cells ; HIV Envelope Protein gp120/physiology ; HIV-1/*pathogenicity/physiology ; HeLa Cells ; Humans ; Leukocytes, Mononuclear/virology ; Macrophages/virology ; *Membrane Fusion ; Membrane Proteins/genetics/*physiology ; Mice ; Molecular Sequence Data ; RNA, Messenger/metabolism ; Receptors, CXCR4 ; Recombinant Proteins ; Transfection
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  • 89
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    Shaking out the cause of addiction (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hyman, S E -- New York, N.Y. -- Science. 1996 Aug 2;273(5275):611-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Mental Health, Rockville, MD 20857, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8701316" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclic AMP/metabolism ; Cyclic AMP Response Element-Binding Protein/genetics/*physiology ; Drug Tolerance ; Locus Coeruleus/metabolism/physiology ; Mice ; Mice, Knockout ; Narcotics/*administration & dosage/adverse effects/pharmacology ; Neuronal Plasticity ; Neurons/physiology ; Opioid-Related Disorders/*etiology/metabolism ; Receptors, Opioid, mu/metabolism ; Signal Transduction ; Substance Withdrawal Syndrome/etiology/metabolism ; Up-Regulation
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  • 90
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    Phage transfer: a new player turns up in cholera infection (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, N -- New York, N.Y. -- Science. 1996 Jun 28;272(5270):1869-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658152" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bacterial Proteins ; Bacteriophages/*genetics/physiology ; Cholera/*microbiology ; Cholera Toxin/genetics ; Cholera Vaccines ; DNA-Binding Proteins/genetics ; Fimbriae, Bacterial/physiology ; Genes, Bacterial ; Humans ; *Lysogeny ; Mice ; Transcription Factors/genetics ; Transduction, Genetic ; Vibrio cholerae/genetics/*pathogenicity/*virology ; Virulence/genetics
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  • 91
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    Hyperresponsive B cells in CD22-deficient mice (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-01
    Description: CD22 is a surface glycoprotein of B lymphocytes that is rapidly phosphorylated on cytoplasmic tyrosines after antigen receptor cross-linking. Splenic B cells from mice with a disrupted CD22 gene were found to be hyperresponsive to receptor signaling: Heightened calcium fluxes and cell proliferation were obtained at lower ligand concentrations. The mice gave an augmented immune response, had an expanded peritoneal B-1 cell population, and contained increased serum titers of autoantibody. Thus, CD22 is a negative regulator of antigen receptor signaling whose onset of expression at the mature B cell stage may serve to raise the antigen concentration threshold required for B cell triggering.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Keefe, T L -- Williams, G T -- Davies, S L -- Neuberger, M S -- New York, N.Y. -- Science. 1996 Nov 1;274(5288):798-801.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8864124" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Antinuclear/blood ; Antibody Formation ; Antigens, CD/genetics/*immunology/metabolism ; Antigens, Differentiation, B-Lymphocyte/genetics/*immunology/metabolism ; B-Lymphocytes/*immunology/metabolism ; Calcium/metabolism ; *Cell Adhesion Molecules ; Female ; Gene Targeting ; Immunization ; Immunoglobulin M/blood ; Immunophenotyping ; *Lectins ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Phosphorylation ; Receptors, Antigen, B-Cell/immunology/physiology ; Sialic Acid Binding Ig-like Lectin 2 ; Signal Transduction ; Transfection
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  • 92
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    Immunological tolerance (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Silverstein, A M -- New York, N.Y. -- Science. 1996 Jun 7;272(5267):1405-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8633222" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn/*immunology ; *Immune Tolerance ; Immunity, Active ; Mice ; Self Tolerance
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  • 93
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    Protective effect of rotavirus VP6-specific IgA monoclonal antibodies that lack neutralizing activity (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-05
    Description: Rotaviruses are the leading cause of severe gastroenteritis and dehydrating diarrhea in young children and animals worldwide. A murine model and "backpack tumor" transplantation were used to determine the protective effect of antibodies against VP4(an outer capsid viral protein) and VP6(a major inner capsid viral protein). Only two non-neutralizing immunoglobulin A (IgA) antibodies to VP6 were capable of preventing primary and resolving chronic murine rotavirus infections. These antibodies were not active, however, when presented directly to the luminal side of the intestinal tract. These findings support the hypothesis that in vivo intracellular viral inactivation by secretory IgA during transcytosis is a mechanism of host defense against rotavirus infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burns, J W -- Siadat-Pajouh, M -- Krishnaney, A A -- Greenberg, H B -- DK38707/DK/NIDDK NIH HHS/ -- R37AI21362/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Apr 5;272(5258):104-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Stanford University School of Medicine, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8600516" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/administration & dosage/*immunology/metabolism ; Antibodies, Viral/administration & dosage/*immunology/metabolism ; *Antigens, Viral ; Capsid/*immunology ; *Capsid Proteins ; Feces/chemistry/virology ; Hybridomas ; Ileum/immunology/virology ; Immunization, Passive ; Immunoglobulin A, Secretory/administration & dosage/*immunology/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, SCID ; Neutralization Tests ; Rotavirus/*immunology/physiology ; Rotavirus Infections/*immunology/prevention & control/virology ; Virus Replication ; Virus Shedding
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  • 94
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    Induction of autoimmune diabetes by oral administration of autoantigen (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-06
    Description: An antigen administered orally can induce immunological tolerance to a subsequent challenge with the same antigen. Evidence has been provided for the efficacy of this approach in the treatment of human autoimmune diseases such as rheumatoid arthritis and multiple sclerosis. However, oral administration of autoantigen in mice was found to induce a cytotoxic T lymphocyte response that could lead to the onset of autoimmune diabetes. Thus, feeding autoantigen can cause autoimmunity, which suggests that caution should be used when applying this approach to the treatment of human autoimmune diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blanas, E -- Carbone, F R -- Allison, J -- Miller, J F -- Heath, W R -- AI-29385/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 6;274(5293):1707-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8939860" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Animals ; Autoantigens/administration & dosage/*immunology ; Autoimmune Diseases/*immunology ; CD4-Positive T-Lymphocytes/immunology ; Chimera ; Diabetes Mellitus/*immunology ; Dose-Response Relationship, Immunologic ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Ovalbumin/administration & dosage/*immunology ; T-Lymphocytes, Cytotoxic/*immunology
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  • 95
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    Cardiovascular regulation in mice lacking alpha2-adrenergic receptor subtypes b and c (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-09
    Description: alpha2-Adrenergic receptors (alpha2ARs) are essential components of the neural circuitry regulating cardiovascular function. The role of specific alpha2AR subtypes (alpha2a, alpha2b, and alpha2c) was characterized with hemodynamic measurements obtained from strains of genetically engineered mice deficient in either alpha2b or alpha2c receptors. Stimulation of alpha2b receptors in vascular smooth muscle produced hypertension and counteracted the clinically beneficial hypotensive effect of stimulating alpha2a receptors in the central nervous system. There were no hemodynamic effects produced by disruption of the alpha2c subtype. These results provide evidence for the clinical efficacy of more subtype-selective alpha2AR drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Link, R E -- Desai, K -- Hein, L -- Stevens, M E -- Chruscinski, A -- Bernstein, D -- Barsh, G S -- Kobilka, B K -- GM07365/GM/NIGMS NIH HHS/ -- HL48638/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 9;273(5276):803-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8670422" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic alpha-Agonists/pharmacology ; Adrenergic alpha-Antagonists/metabolism/pharmacology ; Animals ; Blood Pressure/drug effects/*physiology ; Gene Targeting ; Heart Rate/drug effects/*physiology ; Imidazoles/pharmacology ; Kidney/metabolism ; Medetomidine ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Mice, Knockout ; Muscle, Smooth, Vascular/metabolism ; Phenylephrine/pharmacology ; Prazosin/pharmacology ; Receptors, Adrenergic, alpha-2/genetics/*physiology ; Yohimbine/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
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    Antibacterial agents that inhibit lipid A biosynthesis (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-08
    Description: Lipid A constitutes the outer monolayer of the outer membrane of Gram-negative bacteria and is essential for bacterial growth. Synthetic antibacterials were identified that inhibit the second enzyme (a unique deacetylase) of lipid A biosynthesis. The inhibitors are chiral hydroxamic acids bearing certain hydrophobic aromatic moieties. They may bind to a metal in the active site of the deacetylase. The most potent analog (with an inhibition constant of about 50 nM) displayed a minimal inhibitory concentration of about 1 microgram per milliliter against Escherichia coli, caused three logs of bacterial killing in 4 hours, and cured mice infected with a lethal intraperitoneal dose of E. coli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Onishi, H R -- Pelak, B A -- Gerckens, L S -- Silver, L L -- Kahan, F M -- Chen, M H -- Patchett, A A -- Galloway, S M -- Hyland, S A -- Anderson, M S -- Raetz, C R -- New York, N.Y. -- Science. 1996 Nov 8;274(5289):980-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Merck Research Laboratories, Rahway, NJ 07065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8875939" target="_blank"〉PubMed〈/a〉
    Keywords: Amidohydrolases/*antagonists & inhibitors/metabolism ; Animals ; Anti-Bacterial Agents/chemistry/*pharmacology ; Binding Sites ; Escherichia coli/drug effects ; Escherichia coli Infections/drug therapy ; Gram-Negative Bacteria/*drug effects ; Hydroxamic Acids/chemistry/*pharmacology ; Lipid A/*biosynthesis ; Mice ; Microbial Sensitivity Tests ; Oxazoles/chemistry/pharmacology ; Pseudomonas/drug effects ; Serratia/drug effects ; Stereoisomerism ; Structure-Activity Relationship
    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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  • 97
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    Control of memory formation through regulated expression of a CaMKII transgene (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-06
    Description: One of the major limitations in the use of genetically modified mice for studying cognitive functions is the lack of regional and temporal control of gene function. To overcome these limitations, a forebrain-specific promoter was combined with the tetracycline transactivator system to achieve both regional and temporal control of transgene expression. Expression of an activated calcium-independent form of calcium-calmodulin-dependent kinase II (CaMKII) resulted in a loss of hippocampal long-term potentiation in response to 10-hertz stimulation and a deficit in spatial memory, a form of explicit memory. Suppression of transgene expression reversed both the physiological and the memory deficit. When the transgene was expressed at high levels in the lateral amygdala and the striatum but not other forebrain structures, there was a deficit in fear conditioning, an implicit memory task, that also was reversible. Thus, the CaMKII signaling pathway is critical for both explicit and implicit memory storage, in a manner that is independent of its potential role in development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mayford, M -- Bach, M E -- Huang, Y Y -- Wang, L -- Hawkins, R D -- Kandel, E R -- New York, N.Y. -- Science. 1996 Dec 6;274(5293):1678-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, College of Physicians and Surgeons of Columbia University, and Howard Hughes Medical Institute, 722 West 168 Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8939850" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/physiology ; Animals ; Brain/*physiology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/genetics/*metabolism ; Conditioning (Psychology) ; Corpus Striatum/physiology ; Doxycycline/pharmacology ; Fear ; *Gene Expression Regulation, Enzymologic ; Genes, Reporter ; Hippocampus/physiology ; Long-Term Potentiation ; Maze Learning ; Memory/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neuronal Plasticity ; Promoter Regions, Genetic ; Prosencephalon/physiology ; Signal Transduction ; Transgenes
    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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  • 98
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    Hypertension induced in pregnant mice by placental renin and maternal angiotensinogen (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-08
    Description: Maternal hypertension is a common complication of pregnancy and its pathophysiology is poorly understood. This phenomenon was studied in an animal model by mating transgenic mice expressing components of the human renin-angiotensin system. When transgenic females expressing angiotensinogen were mated with transgenic males expressing renin, the pregnant females displayed a transient elevation of blood pressure in late pregnancy, due to secretion of placental human renin into the maternal circulation. Blood pressure returned to normal levels after delivery of the pups. Histopathologic examination revealed uniform enlargement of glomeruli associated with an increase in urinary protein excretion, myocardial hypertrophy, and necrosis and edema in the placenta. These mice may provide molecular insights into pregnancy-associated hypertension in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takimoto, E -- Ishida, J -- Sugiyama, F -- Horiguchi, H -- Murakami, K -- Fukamizu, A -- New York, N.Y. -- Science. 1996 Nov 8;274(5289):995-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Applied Biochemistry and Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, Ibaraki 305, Japan. akif@sakura.cc.tsukuba.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8875944" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/blood ; Angiotensinogen/genetics/*metabolism ; Animals ; Blood Pressure ; Cardiomegaly ; Crosses, Genetic ; Disease Models, Animal ; Female ; Humans ; Hypertension/pathology/*physiopathology ; Kidney Glomerulus/pathology ; Male ; Mice ; Mice, Transgenic ; Placenta/metabolism/pathology ; Pregnancy ; Pregnancy Complications, Cardiovascular/pathology/*physiopathology ; Renin/blood/genetics/*secretion
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    Tickling memory T cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ahmed, R -- New York, N.Y. -- Science. 1996 Jun 28;272(5270):1904.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emory Vaccine Center, Emory University School of Medicine, Atlanta, Georgia 30322, USA. holcombe@microbio.emory.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658161" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD44/analysis ; CD8-Positive T-Lymphocytes/*immunology ; *Immunologic Memory ; Interferon Inducers/pharmacology ; Interferon Type I/*immunology/pharmacology ; Lymphocyte Activation ; Mice ; Poly I-C/pharmacology ; T-Lymphocyte Subsets/*immunology ; Virus Diseases/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    Neonatal tolerance revisited: turning on newborn T cells with dendritic cells (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-03-22
    Description: For some time it has been thought that antigenic challenge in neonatal life is a tolerogenic rather than immunogenic event. Reexamination of the classic neonatal tolerance experiments of Billingham, Brent, and Medawar showed that tolerance is not an intrinsic property of the newborn immune system, but that the nature of the antigen-presenting cell determines whether the outcome is neonatal tolerance or immunization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ridge, J P -- Fuchs, E J -- Matzinger, P -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1723-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious 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/8596932" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn/*immunology ; B-Lymphocytes/immunology ; Cytotoxicity Tests, Immunologic ; Cytotoxicity, Immunologic ; Dendritic Cells/*immunology ; Female ; H-Y Antigen/immunology ; *Immune Tolerance ; *Immunization ; Male ; Mice ; Mice, Inbred C57BL ; Self Tolerance ; T-Lymphocytes/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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