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  • Mice  (184)
  • Mutation  (141)
  • American Association for the Advancement of Science (AAAS)  (296)
  • American Institute of Physics (AIP)
  • MDPI Publishing
  • 1995-1999  (296)
  • 1996  (296)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (296)
  • American Institute of Physics (AIP)
  • MDPI Publishing
  • Springer  (5)
  • Wiley-Blackwell  (1)
Years
  • 1995-1999  (296)
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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    Estimating the age of the common ancestor of men from the ZFY intron (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fu, Y X -- Li, W H -- New York, N.Y. -- Science. 1996 May 31;272(5266):1356-7; author reply 1361-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650550" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bayes Theorem ; Biological Evolution ; Confidence Intervals ; DNA-Binding Proteins/*genetics ; *Genetics, Population ; Hominidae/*genetics ; Humans ; Introns/*genetics ; Kruppel-Like Transcription Factors ; Male ; Mutation ; Population Density ; Probability ; Time Factors ; Transcription Factors/*genetics ; Y Chromosome/*genetics
    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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  • 3
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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
    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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  • 4
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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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
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  • 6
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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
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  • 7
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    Identification of BIME as a subunit of the anaphase-promoting complex (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-15
    Description: The initiation of anaphase and exit from mitosis require the activation of a proteolytic system that ubiquitinates and degrades cyclin B. The regulated component of this system is a large ubiquitin ligase complex, termed the anaphase-promoting complex (APC) or cyclosome. Purified Xenopus laevis APC was found to be composed of eight major subunits, at least four of which became phosphorylated in mitosis. In addition to CDC27, CDC16, and CDC23, APC contained a homolog of Aspergillus nidulans BIME, a protein essential for anaphase. Because mutation of bimE can bypass the interphase arrest induced by either nimA mutation or unreplicated DNA, it appears that ubiquitination catalyzed by APC may also negatively regulate entry into mitosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peters, J M -- King, R W -- Hoog, C -- Kirschner, M W -- New York, N.Y. -- Science. 1996 Nov 15;274(5290):1199-201.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8895470" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Anaphase ; Animals ; Aspergillus/chemistry/cytology/metabolism ; Cell Cycle Proteins/*chemistry/metabolism ; Cyclins/metabolism ; Electrophoresis, Polyacrylamide Gel ; Fungal Proteins/analysis/*chemistry/genetics/metabolism ; Ligases/*chemistry/metabolism ; *Mitosis ; Molecular Sequence Data ; Mutation ; Ovum ; Phosphorylation ; Ubiquitin-Protein Ligases ; Xenopus laevis
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Stimulation of membrane ruffling and MAP kinase activation by distinct effectors of RAS (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-09
    Description: The RAS guanine nucleotide binding proteins activate multiple signaling events that regulate cell growth and differentiation. In quiescent fibroblasts, ectopic expression of activated H-RAS (H-RASV12, where V12 indicates valine-12) induces membrane ruffling, mitogen-activated protein (MAP) kinase activation, and stimulation of DNA synthesis. A mutant of activated H-RAS, H-RASV12C40 (where C40 indicates cysteine-40), was identified that was defective for MAP kinase activation and stimulation of DNA synthesis, but retained the ability to induce membrane ruffling. Another mutant of activated H-RAS, H-RASV12S35 (where S35 indicates serine-35), which activates MAP kinase, was defective for stimulation of membrane ruffling and induction of DNA synthesis. Expression of both mutants resulted in a stimulation of DNA synthesis that was comparable to that induced by H-RASV12. These results indicate that membrane ruffling and activation of MAP kinase represent distinct RAS effector pathways and that input from both pathways is required for the mitogenic activity of RAS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joneson, T -- White, M A -- Wigler, M H -- Bar-Sagi, D -- CA 55360/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 9;271(5250):810-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, State University of New York at Stony Brook 11794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8628998" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Division ; Cell Line ; Cell Membrane/*ultrastructure ; DNA/biosynthesis ; Enzyme Activation ; GTP-Binding Proteins/genetics/metabolism ; Microinjections ; Mutation ; Plasmids ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-raf ; Rats ; Signal Transduction ; rac GTP-Binding Proteins ; ras Proteins/genetics/*metabolism
    Print ISSN: 0036-8075
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  • 9
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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
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  • 10
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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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  • 11
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    Modulation of virulence factor expression by pathogen target cell contact (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-30
    Description: Upon contact with the eukaryotic cell, Yersinia pseudotuberculosis increased the rate of transcription of virulence genes (yop), as determined by in situ monitoring of light emission from individual bacteria expressing luciferase under the control of the yopE promoter. The microbe-host interaction triggered export of LcrQ, a negative regulator of Yop expression, via the Yop-type III secretion system. The intracellular concentration of LcrQ was thereby lowered, resulting in increased expression of Yops. These results suggest a key role for the type III secretion system of pathogenic bacteria to coordinate secretion with expression of virulence factors after physical contact with the target cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pettersson, J -- Nordfelth, R -- Dubinina, E -- Bergman, T -- Gustafsson, M -- Magnusson, K E -- Wolf-Watz, H -- New York, N.Y. -- Science. 1996 Aug 30;273(5279):1231-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Molecular Biology, University of Umea, S-901 87 Umea, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8703058" target="_blank"〉PubMed〈/a〉
    Keywords: *Bacterial Adhesion ; Bacterial Outer Membrane Proteins/biosynthesis/*genetics/secretion ; Bacterial Proteins/genetics/*secretion ; Calcium/metabolism ; Culture Media ; Cytosol/metabolism ; *Gene Expression Regulation, Bacterial ; HeLa Cells ; Humans ; Mutation ; Up-Regulation ; Virulence/*genetics ; Yersinia pseudotuberculosis/genetics/metabolism/*pathogenicity
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  • 12
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    Cooperative DNA binding and sequence-selective recognition conferred by the STAT amino-terminal domain (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-09
    Description: STAT proteins (signal transducers and activators of transcription) activate distinct target genes despite having similar DNA binding preferences. The transcriptional specificity of STAT proteins was investigated on natural STAT binding sites near the interferon-gamma gene. These sites are arranged in multiple copies and required cooperative interactions for STAT binding. The conserved amino-terminal domain of STAT proteins was required for cooperative DNA binding, although this domain was not essential for dimerization or binding to a single site. Cooperative binding interactions enabled the STAT proteins to recognize variations of the consensus site. These sites can be specific for the different STAT proteins and may function to direct selective transcriptional activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, X -- Sun, Y L -- Hoey, T -- New York, N.Y. -- Science. 1996 Aug 9;273(5276):794-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tularik, Two Corporate Drive, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8670419" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Cell Line ; DNA/*metabolism ; DNA-Binding Proteins/chemistry/immunology/*metabolism ; Interferon-gamma/genetics ; Introns ; Molecular Sequence Data ; Mutation ; Oligodeoxyribonucleotides/metabolism ; Promoter Regions, Genetic ; STAT1 Transcription Factor ; STAT4 Transcription Factor ; Sequence Deletion ; Signal Transduction ; Trans-Activators/chemistry/immunology/*metabolism ; *Transcriptional Activation
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  • 13
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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
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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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    Functional evidence for indirect recognition of G.U in tRNA(Ala) by alanyl-tRNA synthetase (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-12
    Description: The structural features of the G.U wobble pair in Escherichia coli alanine transfer RNA (tRNA(Ala)) that are associated with aminoacylation by alanyl-tRNA synthetase (AlaRS) were investigated in vivo for wild-type tRNA(Ala) and mutant tRNAs with G.U substitutions. tRNA(Ala) with G.U, C.A, or G.A gave similar amounts of charged tRNA(Ala) and supported viability of E. coli lacking chromosomal tRNA(Ala) genes. tRNA(Ala) with G.C was inactive. Recognition of G.U by AlaRS thus requires more than the functional groups on G.U in a regular helix and may involve detection of a helical distortion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gabriel, K -- Schneider, J -- McClain, W H -- GM42123/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 12;271(5246):195-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bacteriology, University of Wisconsin, Madison 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8539617" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine-tRNA Ligase/*metabolism ; Anticodon ; Base Composition ; Base Sequence ; Escherichia coli/genetics/growth & development ; Genes, Bacterial ; Guanine/chemistry ; Molecular Sequence Data ; Mutation ; Nucleic Acid Conformation ; Plasmids ; RNA, Transfer, Ala/chemistry/genetics/*metabolism ; Uracil/chemistry
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  • 15
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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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  • 16
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Checkpoints take the next step (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-01-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carr, A M -- New York, N.Y. -- Science. 1996 Jan 19;271(5247):314-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Cell Mutation Unit, Sussex University, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8553064" target="_blank"〉PubMed〈/a〉
    Keywords: Ataxia Telangiectasia Mutated Proteins ; *Cell Cycle ; *Cell Cycle Proteins ; Checkpoint Kinase 2 ; *DNA Damage ; DNA Replication ; DNA-Binding Proteins ; Humans ; *Mitosis ; Mutation ; Phosphorylation ; Protein Kinases/genetics/*metabolism ; *Protein-Serine-Threonine Kinases ; Proteins/genetics/metabolism ; Saccharomyces cerevisiae/cytology/metabolism ; *Saccharomyces cerevisiae Proteins ; Schizosaccharomyces/cytology/metabolism ; Signal Transduction ; Tumor Suppressor Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    Sterol esterification in yeast: a two-gene process (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-31
    Description: Unesterified sterol modulates the function of eukaryotic membranes. In human cells, sterol is esterified to a storage form by acyl-coenzyme A (CoA): cholesterol acyl transferase (ACAT). Here, two genes are identified, ARE1 and ARE2, that encode ACAT-related enzymes in yeast. The yeast enzymes are 49 percent identical to each other and exhibit 23 percent identity to human ACAT. Deletion of ARE2 reduced sterol ester levels to approximately 25 percent of normal levels, whereas disruption of ARE1 did not affect sterol ester biosynthesis. Deletion of both genes resulted in a viable cell with undetectable esterified sterol. Measurements of [14C]acetate incorporation into saponified lipids indicated down-regulation of sterol biosynthesis in the are1 are2 mutant cells. With the use of a consensus sequence to the yeast and human genes, an additional number of the ACAT gene family was identified in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, H -- Bard, M -- Bruner, D A -- Gleeson, A -- Deckelbaum, R J -- Aljinovic, G -- Pohl, T M -- Rothstein, R -- Sturley, S L -- GM 50237/GM/NIGMS NIH HHS/ -- HG00861/HG/NHGRI NIH HHS/ -- R01 AI38598/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 May 31;272(5266):1353-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Human Nutrition, Columbia University College of Physicians and Surgeons, New York, 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650549" target="_blank"〉PubMed〈/a〉
    Keywords: Acetates/metabolism ; Acyltransferases/chemistry/*genetics/metabolism ; Amino Acid Sequence ; Base Sequence ; Cell Membrane/metabolism ; Cholesterol Esters/metabolism ; Cyclin-Dependent Kinase 8 ; *Cyclin-Dependent Kinases ; DNA, Complementary/genetics ; Ergosterol/metabolism ; Esterification ; *Genes, Fungal ; Homeostasis ; Humans ; Molecular Sequence Data ; Mutation ; Oleic Acid ; Oleic Acids/metabolism ; Saccharomyces cerevisiae/*genetics/metabolism ; Saccharomyces cerevisiae Proteins ; Sterol O-Acyltransferase/*genetics/metabolism ; Sterols/*metabolism ; Transformation, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    A docking receptor for HDL cholesterol esters (1996)
    American Association for the Advancement of Science (AAAS)
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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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    A permease-oxidase complex involved in high-affinity iron uptake in yeast (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-03-15
    Description: Iron must cross biological membranes to reach essential intracellular enzymes. Two proteins in the plasma membrane of yeast--a multicopper oxidase, encoded by the FET3 gene, and a permease, encoded by the FTR1 gene--were shown to mediate high-affinity iron uptake. FET3 expression was required for FTR1 protein to be transported to the plasma membrane. FTR1 expression was required for apo-FET3 protein to be loaded with copper and thus acquire oxidase activity. FTR1 protein also played a direct role in iron transport. Mutations in a conserved sequence motif of FTR1 specifically blocked iron transport.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stearman, R -- Yuan, D S -- Yamaguchi-Iwai, Y -- Klausner, R D -- Dancis, A -- New York, N.Y. -- Science. 1996 Mar 15;271(5255):1552-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institutes of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8599111" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Biological Transport ; Carrier Proteins/chemistry/*genetics/*metabolism ; Cell Membrane/metabolism ; *Ceruloplasmin ; Copper/metabolism/pharmacology ; Endoplasmic Reticulum/metabolism ; Ferric Compounds/metabolism ; Ferritins/chemistry/metabolism ; Ferrous Compounds/metabolism ; Genes, Fungal ; Golgi Apparatus/metabolism ; Iron/*metabolism ; Membrane Transport Proteins/chemistry/*genetics/*metabolism ; Models, Biological ; Molecular Sequence Data ; Multienzyme Complexes/*metabolism ; Mutation ; Open Reading Frames ; Oxidation-Reduction ; Oxidoreductases/*metabolism ; Saccharomyces cerevisiae/genetics/*metabolism ; *Saccharomyces cerevisiae Proteins ; Transformation, Genetic
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  • 22
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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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  • 23
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    Structural basis of ligand discrimination by two related RNA aptamers resolved by NMR spectroscopy (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-05-31
    Description: In a previous study, an RNA aptamer for the specific recognition of arginine was evolved from a parent sequence that bound citrulline specifically. The two RNAs differ at only 3 positions out of 44. The solution structures of the two aptamers complexed to their cognate amino acids have now been determined by two-dimensional nuclear magnetic resonance spectroscopy. Both aptamers contain two asymmetrical internal loops that are not well ordered in the free RNA but that fold into a compact structure upon ligand binding. Those nucleotides common to both RNAs include a conserved cluster of purine residues, three of which form an uneven plane containing a G:G pair, and two other residues nearly perpendicular to that surface. Two of the three variant nucleotides are stacked on the cluster of purines and form a triple contact to the amino acid side chain, whereas the edge of the third variant nucleotide is capping the binding pocket.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Y -- Kochoyan, M -- Burgstaller, P -- Westhof, E -- Famulok, M -- New York, N.Y. -- Science. 1996 May 31;272(5266):1343-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre de Biochimie Structurale (CBS), Unite Mixte de Recherche, CNRS 9955, Montpellier, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650546" target="_blank"〉PubMed〈/a〉
    Keywords: Arginine/chemistry/*metabolism ; Base Composition ; Base Sequence ; Citrulline/chemistry/*metabolism ; Crystallography, X-Ray ; Hydrogen Bonding ; Ligands ; Magnetic Resonance Spectroscopy ; Models, Molecular ; Molecular Sequence Data ; Mutation ; *Nucleic Acid Conformation ; RNA/*chemistry/genetics/*metabolism
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  • 24
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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)
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    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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  • 25
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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)
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    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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  • 26
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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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    Molecular genetic insights into cardiovascular disease (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-03
    Description: The recent application of molecular genetic tools to inherited forms of cardiovascular disease has provided important insight into the molecular mechanisms underlying cardiac arrhythmias, cardiomyopathies, and vascular diseases. These studies point to defects in ion channels, contractile proteins, structural proteins, and signaling molecules as key players in disease pathogenesis. Genetic testing is now available for a subset of inherited cardiovascular diseases, and new mechanism-based therapies may be available in the near future. This remarkable progress and the implications it may have for more common forms of cardiovascular disease are reviewed here.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keating, M T -- Sanguinetti, M C -- New York, N.Y. -- Science. 1996 May 3;272(5262):681-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Utah, Salt Lake City, 84112, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614827" target="_blank"〉PubMed〈/a〉
    Keywords: Arrhythmias, Cardiac/diagnosis/*genetics ; Cardiomyopathies/diagnosis/*genetics ; Contractile Proteins/genetics ; Genetic Predisposition to Disease ; Genetic Testing ; Humans ; Ion Channels/genetics ; Mutation ; Myocardium/metabolism ; Prognosis ; Risk Factors ; Vascular Diseases/diagnosis/*genetics
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    Control of C. elegans larval development by neuronal expression of a TGF-beta homolog (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-22
    Description: The Caenorhabditis elegans dauer larva is specialized for dispersal without growth and is formed under conditions of overcrowding and limited food. The daf-7 gene, required for transducing environmental cues that support continuous development with plentiful food, encodes a transforming growth factor-beta (TGF-beta) superfamily member. A daf-7 reporter construct is expressed in the ASI chemosensory neurons. Dauer-inducing pheromone inhibits daf-7 expression and promotes dauer formation, whereas food reactivates daf-7 expression and promotes recovery from the dauer state. When the food/pheromone ratio is high, the level of daf-7 mRNA peaks during the L1 larval stage, when commitment to non-dauer development is made.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ren, P -- Lim, C S -- Johnsen, R -- Albert, P S -- Pilgrim, D -- Riddle, D L -- HD11239/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1389-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Program and Division of Biological Sciences, 311 Tucker Hall, University of Missouri, Columbia, MO 65211, USA. riddle@biosci.mbp.missouri.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8910282" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Caenorhabditis elegans/genetics/*growth & development/metabolism ; *Caenorhabditis elegans Proteins ; Genes, Helminth ; Genes, Reporter ; Green Fluorescent Proteins ; Helminth Proteins/chemistry/genetics/*physiology ; Humans ; Larva/growth & development/metabolism ; Ligands ; Luminescent Proteins/genetics ; Molecular Sequence Data ; Mutation ; Neurons, Afferent/*metabolism ; Phenotype ; Pheromones/pharmacology ; Temperature ; Transforming Growth Factor beta/chemistry/genetics/*physiology ; Transgenes
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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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    Kap104p: a karyopherin involved in the nuclear transport of messenger RNA binding proteins (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-25
    Description: A cytosolic yeast karyopherin, Kap104p, was isolated and shown to function in the nuclear import of a specific class of proteins. The protein bound directly to repeat-containing nucleoporins and to a cytosolic pool of two nuclear messenger RNA (mRNA) binding proteins, Nab2p and Nab4p. Depletion of Kap104p resulted in a rapid shift of Nab2p from the nucleus to the cytoplasm without affecting the localization of other nuclear proteins tested. This finding suggests that the major function of Kap104p lies in returning mRNA binding proteins to the nucleus after mRNA export.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aitchison, J D -- Blobel, G -- Rout, M P -- New York, N.Y. -- Science. 1996 Oct 25;274(5287):624-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, Howard Hughes Medical Institute, Rockefeller University, 1230 York Avenue, New York, NY 10021, USA. blobel@rockvax.rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8849456" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Biological Transport ; Carrier Proteins/chemistry/isolation & purification/*metabolism ; Cell Nucleus/*metabolism ; Cytosol/chemistry/metabolism ; Fungal Proteins/*metabolism ; *Karyopherins ; Membrane Proteins/metabolism ; Molecular Sequence Data ; Mutation ; Nuclear Envelope/metabolism ; *Nuclear Pore Complex Proteins ; Nuclear Proteins/*metabolism ; *Nucleocytoplasmic Transport Proteins ; RNA, Messenger/genetics/metabolism ; RNA-Binding Proteins/*metabolism ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/*metabolism ; *Saccharomyces cerevisiae Proteins ; Temperature ; beta Karyopherins
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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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    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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    A new turn (or two) for twist (1996)
    American Association for the Advancement of Science (AAAS)
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    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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    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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    New 'Alzheimer's mouse' produced (1996)
    American Association for the Advancement of Science (AAAS)
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    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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    KUZ, a conserved metalloprotease-disintegrin protein with two roles in Drosophila neurogenesis (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-30
    Description: During neurogenesis in Drosophila both neurons and nonneuronal cells are produced from a population of initially equivalent cells. The kuzbanian (kuz) gene described here is essential for the partitioning of neural and nonneuronal cells during development of both the central and peripheral nervous systems in Drosophila. Mosaic analyses indicated that kuz is required for cells to receive signals inhibiting the neural fate. These analyses further revealed that the development of a neuron requires a kuz-mediated positive signal from neighboring cells. The kuz gene encodes a metalloprotease-disintegrin protein with a highly conserved bovine homolog, raising the possibility that kuz homologs may act in similar processes during mammalian neurogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rooke, J -- Pan, D -- Xu, T -- Rubin, G M -- New York, N.Y. -- Science. 1996 Aug 30;273(5279):1227-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06536, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8703057" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cloning, Molecular ; Disintegrins/chemistry/genetics/*physiology ; Drosophila/cytology/embryology/*genetics/physiology ; *Drosophila Proteins ; *Genes, Insect ; Metalloendopeptidases/chemistry/genetics/*physiology ; Molecular Sequence Data ; Mosaicism ; Mutation ; Nervous System/embryology ; Neurons/*cytology ; Photoreceptor Cells, Invertebrate/cytology/embryology
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    Control of the gene optomotor-blind in Drosophila wing development by decapentaplegic and wingless (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-03-15
    Description: Diffusible factors of several protein families control appendage outgrowth and patterning in both insects and vertebrates. In Drosophila wing development, the gene decapentaplegic (dpp) is expressed along the anteroposterior compartment boundary. Early wingless (wg) expression is involved in setting up the dorsoventral boundary. Interaction between dpp- and wg-expressing cells promotes appendage outgrowth. Here, it is shown that optomotor-blind (omb) expression is required for distal wing development and is controlled by both dpp and wg. Ectopic omb expression can lead to the growth of additional wings. Thus, omb is essential for wing development and is controlled by two signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grimm, S -- Pflugfelder, G O -- New York, N.Y. -- Science. 1996 Mar 15;271(5255):1601-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Theodor-Boveri-Institut (Biozentrum), Lehrstuhl fur Genetik, Universitat Wurzburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8599120" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA-Binding Proteins/*genetics/physiology ; Drosophila/*genetics/growth & development ; *Drosophila Proteins ; *Gene Expression Regulation, Developmental ; Genes, Insect ; Insect Hormones/*genetics/physiology ; Larva/genetics/growth & development ; Mutation ; Nerve Tissue Proteins/*genetics/physiology ; Phenotype ; Proto-Oncogene Proteins/*genetics/physiology ; Signal Transduction ; *T-Box Domain Proteins ; Wings, Animal/*growth & development ; Wnt1 Protein
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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)
    Details
    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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    Structure of the FKBP12-rapamycin complex interacting with the binding domain of human FRAP (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-12
    Description: Rapamycin, a potent immunosuppressive agent, binds two proteins: the FK506-binding protein (FKBP12) and the FKBP-rapamycin-associated protein (FRAP). A crystal structure of the ternary complex of human FKBP12, rapamycin, and the FKBP12-rapamycin-binding (FRB) domain of human FRAP at a resolution of 2.7 angstroms revealed the two proteins bound together as a result of the ability of rapamycin to occupy two different hydrophobic binding pockets simultaneously. The structure shows extensive interactions between rapamycin and both proteins, but fewer interactions between the proteins. The structure of the FRB domain of FRAP clarifies both rapamycin-independent and -dependent effects observed for mutants of FRAP and its homologs in the family of proteins related to the ataxia-telangiectasia mutant gene product, and it illustrates how a small cell-permeable molecule can mediate protein dimerization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Choi, J -- Chen, J -- Schreiber, S L -- Clardy, J -- CA59021/CA/NCI NIH HHS/ -- GM38625/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jul 12;273(5272):239-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Baker Laboratory, Cornell University, Ithaca, NY 14853-1301, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662507" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Carrier Proteins/chemistry/genetics/*metabolism ; Crystallography, X-Ray ; DNA-Binding Proteins/chemistry/*metabolism ; Heat-Shock Proteins/chemistry/*metabolism ; Humans ; *Immunophilins ; Models, Molecular ; Mutation ; *Phosphotransferases (Alcohol Group Acceptor) ; Polyenes/*chemistry/*metabolism ; *Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Recombinant Proteins/chemistry/metabolism ; Sirolimus ; TOR Serine-Threonine Kinases ; Tacrolimus Binding Proteins
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    Circadian rhythms in cultured mammalian retina (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-19
    Description: Many retinal functions are circadian, but in most instances the location of the clock that drives the rhythm is not known. Cultured neural retinas of the golden hamster (Mesocricetus auratus) exhibited circadian rhythms of melatonin synthesis for at least 5 days at 27 degrees celsius. The rhythms were entrained by light cycles applied in vitro and were free-running in constant darkness. Retinas from hamsters homozygous for the circadian mutation tau, which shortens the free-running period of the circadian activity rhythm by 4 hours, showed a shortened free-running period of melatonin synthesis. The mammalian retina contains a genetically programmed circadian oscillator that regulates its synthesis of melatonin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tosini, G -- Menaker, M -- HD13162/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1996 Apr 19;272(5260):419-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Virginia, Charlottesville, VA 22903, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8602533" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Clocks ; *Circadian Rhythm/genetics ; Cricetinae ; Culture Techniques ; Darkness ; Genes ; Light ; Melatonin/*biosynthesis ; Mesocricetus ; Mutation ; Retina/metabolism/*physiology ; Temperature
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Flies unmask evolutionary warfare between the sexes (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morell, V -- New York, N.Y. -- Science. 1996 May 17;272(5264):953-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638139" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Drosophila/genetics/*physiology ; Female ; Genes, Insect ; Male ; Mutation ; Reproduction ; Sex Characteristics ; Sexual Behavior, Animal
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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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  • 43
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Sperm protein makes its mark upon the worm embryo (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roush, W -- New York, N.Y. -- Science. 1996 Jan 5;271(5245):33.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8539595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*embryology/genetics ; *Caenorhabditis elegans Proteins ; *Embryonic Development ; Female ; Fertilization ; Genes, Helminth ; Helminth Proteins/genetics/*physiology ; Male ; Mutation ; *Nuclear Proteins ; Oocytes/physiology ; Spermatozoa/*chemistry/physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    HERG sequence correction (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trudeau, M C -- Warmke, J W -- Ganetzky, B -- Robertson, G A -- New York, N.Y. -- Science. 1996 May 24;272(5265):1087.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638148" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Humans ; Mutation ; Potassium Channels/*genetics ; *Potassium Channels, Inwardly Rectifying
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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  • 48
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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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    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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  • 50
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    Cell killing by the Drosophila gene reaper (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-09
    Description: The reaper gene (rpr) is important for the activation of apoptosis in Drosophila. To investigate whether rpr expression is sufficient to induce apoptosis, transgenic flies were generated that express rpr complementary DNA or the rpr open reading frame in cells that normally live. Transcription of rpr from a heat-inducible promoter rapidly caused wide-spread ectopic apoptosis and organismal death. Ectopic overexpression of rpr in the developing retina resulted in eye ablation. The occurrence of cell death was highly sensitive to the dosage of the transgene. Because cell death induced by the protein encoded by rpr (RPR) could be blocked by the baculovirus p35 protein, RPR appears to activate a death program mediated by a ced-3/ICE (interleukin-1 converting enzyme)-like protease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, K -- Tahaoglu, E -- Steller, H -- New York, N.Y. -- Science. 1996 Feb 9;271(5250):805-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cutaneous Biology Research Center, Massachusetts General Hospital, Charlestown 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8628996" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; *Apoptosis ; Caspase 1 ; Cysteine Endopeptidases/metabolism ; DNA, Complementary/genetics ; Drosophila/cytology/embryology/*genetics ; *Drosophila Proteins ; Gene Dosage ; Gene Expression ; *Genes, Insect ; Hot Temperature ; Inhibitor of Apoptosis Proteins ; Mutation ; Open Reading Frames ; Peptides/*genetics/physiology ; Photoreceptor Cells, Invertebrate/cytology ; Transgenes ; Viral Proteins/genetics/physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Evidence that Spt6p controls chromatin structure by a direct interaction with histones (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-07
    Description: Genetic analysis has implicated SPT6, an essential gene of Saccharomyces cerevisiae, in the control of chromatin structure. Mutations in SPT6 and particular mutations in histone genes are able to overcome transcriptional defects in strains lacking the Snf/Swi protein complex. Here it is shown that an spt6 mutation causes changes in chromatin structure in vivo. In addition, both in vivo and in vitro experiments provide evidence that Spt6p interacts directly with histones and primarily with histone H3. Consistent with these findings, Spt6p is capable of nucleosome assembly in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bortvin, A -- Winston, F -- GM32967/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jun 7;272(5267):1473-6.〈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/8633238" target="_blank"〉PubMed〈/a〉
    Keywords: Chromatin/chemistry/genetics/metabolism/*ultrastructure ; DNA, Fungal/metabolism ; Fungal Proteins/genetics/metabolism/*physiology ; Histones/chemistry/genetics/*metabolism ; Humans ; Mutation ; Nuclear Proteins/genetics/metabolism/*physiology ; Nucleosomes/metabolism ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/*genetics/metabolism ; *Saccharomyces cerevisiae Proteins ; Transcription, Genetic ; Transcriptional Elongation Factors
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    Gene perplexes epilepsy researchers (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Brien, C -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1672.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596927" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chromosome Mapping ; Chromosomes, Human, Pair 21/*genetics ; Cystatin B ; Cystatins/*genetics ; Cysteine Proteinase Inhibitors/*genetics ; Epilepsies, Myoclonic/*genetics ; Female ; Humans ; Male ; Mutation ; Pedigree ; RNA, Messenger/genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Evidence for physical and functional association between EMB-5 and LIN-12 in Caenorhabditis elegans (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-05
    Description: The Caenorhabditis elegans LIN-12 and GLP-1 proteins are members of the LIN-12/Notch family of receptors for intercellular signals that specify cell fate. Evidence presented here suggests that the intracellular domains of LIN-12 and GLP-1 interact with the C. elegans EMB-5 protein and that the emb-5 gene functions in the same pathway as the lin-12 and glp-1 genes. EMB-5 is similar in sequence to a yeast protein that controls chromatin structure. Hence, a direct consequence of LIN-12 or GLP-1 activation may be an alteration of chromatin structure that produces changes in transcriptional activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hubbard, E J -- Dong, Q -- Greenwald, I -- GM37602/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jul 5;273(5271):112-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, Columbia University College of Physicians and Surgeons, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658178" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*cytology/embryology/genetics/*metabolism ; *Caenorhabditis elegans Proteins ; Cell Lineage ; Chromatin/metabolism ; Gene Expression Regulation, Developmental ; Genes, Helminth ; Helminth Proteins/genetics/*metabolism ; Meiosis ; Membrane Proteins/genetics/*metabolism ; Mitosis ; Mutation ; Receptors, Notch ; *Signal Transduction ; Temperature ; Transcription Factors/genetics/*metabolism
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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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    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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    Initiation of runaway cell death in an Arabidopsis mutant by extracellular superoxide (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-09-27
    Description: Reactive oxygen intermediates (ROIs) regulate apoptosis during normal development and disease in animals. ROIs are also implicated in hypersensitive resistance responses of plants against pathogens. Arabidopsis lsd1 mutants exhibited impaired control of cell death in the absence of pathogen and could not control the spread of cell death once it was initiated. Superoxide was necessary and sufficient to initiate lesion formation; it accumulated before the onset of cell death and subsequently in live cells adjacent to spreading lsd1 lesions. Thus, runaway cell death seen in lsd1 plants reflected abnormal accumulation of superoxide and lack of responsiveness to signals derived from it.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jabs, T -- Dietrich, R A -- Dangl, J L -- New York, N.Y. -- Science. 1996 Sep 27;273(5283):1853-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Delbruck Laboratory, Carl von Linne Weg 10, 50829 Koln, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8791589" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Arabidopsis/*cytology/genetics/metabolism ; Cell Membrane/enzymology ; Enzyme Inhibitors/pharmacology ; Gene Expression Regulation, Plant ; Genes, Plant ; Glutathione Transferase/genetics/metabolism ; Mutation ; NADH, NADPH Oxidoreductases/antagonists & inhibitors/metabolism ; NADPH Oxidase ; Onium Compounds/pharmacology ; Peroxidases/genetics/metabolism ; Plant Leaves/cytology/metabolism ; RNA, Messenger/genetics/metabolism ; RNA, Plant/genetics/metabolism ; Reactive Oxygen Species/metabolism ; Superoxide Dismutase/genetics ; Superoxides/*metabolism
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Streetcar carries evolution modelers around roadblocks (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, N -- New York, N.Y. -- Science. 1996 Mar 8;271(5254):1365-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596907" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Game Theory ; Genes ; Genetics, Population ; Humans ; *Models, Biological ; Models, Genetic ; Mutation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    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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    Identification of an asymmetrically localized sensor histidine kinase responsible for temporally and spatially regulated transcription (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-25
    Description: Caulobacter crescentus undergoes asymmetric cell division, resulting in a stalked cell and a motile swarmer cell. The genes encoding external components of the flagellum are expressed in the swarmer compartment of the predivisional cell through the localized activation of the transcription factor FlbD. The mechanisms responsible for the temporal and spatial activation of FlbD were determined through identification of FlbE, a histidine kinase required for FlbD activity. FlbE is asymmetrically distributed in the predivisional cell. It is located at the pole of the stalked compartment and at the site of cell division in the swarmer compartment. These findings suggest that FlbE and FlbD are activated in response to a morphological change in the cell resulting from cell division events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wingrove, J A -- Gober, J W -- GM-07104/GM/NIGMS NIH HHS/ -- GM48417/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Oct 25;274(5287):597-601.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry and the Molecular Biology Institute, University of California, Los Angeles, CA 90095-1569, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8849449" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/genetics/*metabolism ; Caulobacter crescentus/cytology/*genetics/physiology ; Cell Division ; DNA-Binding Proteins/genetics/*metabolism ; Gene Expression Regulation, Bacterial ; Genes, Bacterial ; Mutation ; Phosphorylation ; Promoter Regions, Genetic ; Protein Kinases/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Transcription Factors/genetics/*metabolism ; *Transcription, Genetic
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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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    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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    Molecular pathways controlling heart development (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-05-03
    Description: Heart formation requires complex interactions among cells from multiple embryonic origins. Recent studies have begun to reveal the genetic pathways that control cardiac morphogenesis. Many of the genes within these pathways are conserved across vast phylogenetic distances, which has allowed cardiac development to be dissected in organisms ranging from flies to mammals. Studies of cardiac development have also revealed the molecular defects underlying several congenital cardiac malformations in humans and may ultimately provide opportunities for genetic testing and intervention.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olson, E N -- Srivastava, D -- New York, N.Y. -- Science. 1996 May 3;272(5262):671-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Oncology, University of Texas Southwestern Medical Center, Dallas, 75235-9148, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614825" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; *Gene Expression Regulation, Developmental ; Genes ; Genes, Regulator ; Heart/*embryology ; Heart Conduction System/embryology ; Heart Defects, Congenital/embryology/*genetics/pathology ; Humans ; Morphogenesis ; Mutation ; Myocardium/cytology ; Neural Crest/cytology ; Transcription Factors/physiology ; Transcription, Genetic
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    Worm genes imply a master clock (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1996 May 17;272(5264):949-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638138" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics ; Animals ; Biological Clocks/*genetics ; Caenorhabditis elegans/*genetics/physiology ; *Genes, Helminth ; Longevity/genetics ; Mutation
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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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    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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    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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    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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    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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    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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    Selector genes, polymorphisms, and evolution (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tautz, D -- New York, N.Y. -- Science. 1996 Jan 12;271(5246):160-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Zoologisches Institut, Universitat Munchen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8539613" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; DNA-Binding Proteins/*genetics ; Drosophila/drug effects/*genetics ; *Drosophila Proteins ; Ether/pharmacology ; *Genes, Homeobox ; Genes, Insect ; *Genes, Regulator ; Homeodomain Proteins/*genetics ; Homeostasis ; Mutation ; *Polymorphism, Genetic ; *Transcription Factors
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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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    Visualization of slow axonal transport in vivo (1996)
    American Association for the Advancement of Science (AAAS)
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    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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    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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    Diffusional mobility of Golgi proteins in membranes of living cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-09
    Description: The mechanism by which Golgi membrane proteins are retained within the Golgi complex in the midst of a continuous flow of protein and lipid is not yet understood. The diffusional mobilities of mammalian Golgi membrane proteins fused with green fluorescent protein from Aequorea victoria were measured in living HeLa cells with the fluorescence photobleaching recovery technique. The diffusion coefficients ranged from 3 x 10(-9) square centimeters per second to 5 x 10(-9) square centimeters per second, with greater than 90 percent of the chimeric proteins mobile. Extensive lateral diffusion of the chimeric proteins occurred between Golgi stacks. Thus, the chimeras diffuse rapidly and freely in Golgi membranes, which suggests that Golgi targeting and retention of these molecules does not depend on protein immobilization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cole, N B -- Smith, C L -- Sciaky, N -- Terasaki, M -- Edidin, M -- Lippincott-Schwartz, J -- R37 AI14584/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 9;273(5276):797-801.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, Building 18T, 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/8670420" target="_blank"〉PubMed〈/a〉
    Keywords: Aluminum Compounds/pharmacology ; Diffusion ; Endoplasmic Reticulum/metabolism ; Fluorides/pharmacology ; Golgi Apparatus/*metabolism ; Green Fluorescent Proteins ; HeLa Cells ; Humans ; Intracellular Membranes/metabolism ; Luminescent Proteins ; Mannosidases/*metabolism ; Membrane Proteins/*metabolism ; Microscopy, Confocal ; Mutation ; N-Acetyllactosamine Synthase/*metabolism ; Receptors, Peptide/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism
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    Mechanosensation and the DEG/ENaC ion channels (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corey, D P -- Garcia-Anoveros, J -- New York, N.Y. -- Science. 1996 Jul 19;273(5273):323-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8685718" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Caenorhabditis elegans/genetics/*physiology ; Genes, Helminth ; Helminth Proteins/chemistry/genetics/*physiology ; Molecular Sequence Data ; Muscle Contraction ; Mutation ; Phenotype ; Sensation/genetics/*physiology ; Sodium Channels/chemistry/genetics/*physiology ; Touch/genetics/physiology
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    Uncoupling of GTP binding from target stimulation by a single mutation in the transducin alpha subunit (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-08
    Description: Glutamic acid-203 of the alpha subunit of transducin (alphaT) resides within a domain that undergoes a guanosine triphosphate (GTP)-induced conformational change that is essential for effector recognition. Changing the glutamic acid to an alanine in bovine alpha(T) yielded an alpha subunit (alpha(T)E203A) that was fully dependent on rhodopsin for GTP-guanosine diphosphate (GDP) exchange and showed GTP hydrolytic activity similar to that measured for wild-type alpha(T). However, unlike the wild-type protein, the GDP-bound form of alpha(T)E203A was constitutively active toward the effector of transducin, the cyclic guanosine monophosphate phosphodiesterase. Thus, the alpha(T)E203A mutant represents a short-circuited protein switch that no longer requires GTP for the activation of the effector target phosphodiesterase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mittal, R -- Erickson, J W -- Cerione, R A -- New York, N.Y. -- Science. 1996 Mar 8;271(5254):1413-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Cornell University, Ithaca, NY 14853-6401, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596913" target="_blank"〉PubMed〈/a〉
    Keywords: 3',5'-Cyclic-GMP Phosphodiesterases/*metabolism ; Adenosine Diphosphate Ribose/metabolism ; Alanine/chemistry ; Animals ; Base Sequence ; Cattle ; Enzyme Activation ; Glutamic Acid/chemistry ; Guanosine 5'-O-(3-Thiotriphosphate)/metabolism ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/*metabolism ; Molecular Sequence Data ; Mutation ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Recombinant Fusion Proteins ; Rhodopsin/metabolism ; Transducin/chemistry/genetics/*metabolism
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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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  • 83
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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)
    Details
    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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    Structure of the p53 tumor suppressor bound to the ankyrin and SH3 domains of 53BP2 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-08
    Description: Mutations in the p53 tumor suppressor are among the most frequently observed genetic alterations in human cancer and map to the 200-amino acid core domain of the protein. The core domain contains the sequence-specific DNA binding activity and the in vitro 53BP2 protein binding activity of p53. The crystal structure of the p53 core domain bound to the 53BP2 protein, which contains an SH3 (Src homology 3) domain and four ankyrin repeats, revealed that (i) the SH3 domain binds the L3 loop of p53 in a manner distinct from that of previously characterized SH3-polyproline peptide complexes, and (ii) an ankyrin repeat, which forms an L-shaped structure consisting of a beta hairpin and two alpha helices, binds the L2 loop of p53. The structure of the complex shows that the 53BP2 binding site on the p53 core domain consists of evolutionarily conserved regions that are frequently mutated in cancer and that it overlaps the site of DNA binding. The six most frequently observed p53 mutations disrupt 53BP2 binding in vitro. The structure provides evidence that the 53BP2-p53 complex forms in vivo and may have a critical role in the p53 pathway of tumor suppression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gorina, S -- Pavletich, N P -- CA65698/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Nov 8;274(5289):1001-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cellular Biochemistry and Biophysics 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/8875926" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Ankyrins/*chemistry ; Apoptosis Regulatory Proteins ; Binding Sites ; Carrier Proteins/*chemistry/metabolism ; Crystallography, X-Ray ; DNA/metabolism ; Humans ; Hydrogen Bonding ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Neoplasms/genetics ; Protein Binding ; *Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/chemistry/metabolism ; Tumor Suppressor Protein p53/*chemistry/genetics/metabolism ; *src Homology Domains
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  • 85
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    A mouse model of familial hypertrophic cardiomyopathy (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 86
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    Pycnodysostosis, a lysosomal disease caused by cathepsin K deficiency (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-30
    Description: Pycnodysostosis, an autosomal recessive osteochondrodysplasia characterized by osteosclerosis and short stature, maps to chromosome 1q21. Cathepsin K, a cysteine protease gene that is highly expressed in osteoclasts, localized to the pycnodysostosis region. Nonsense, missense, and stop codon mutations in the gene encoding cathepsin K were identified in patients. Transient expression of complementary DNA containing the stop codon mutation resulted in messenger RNA but no immunologically detectable protein. Thus, pycnodysostosis results from gene defects in a lysosomal protease with highest expression in osteoclasts. These findings suggest that cathepsin K is a major protease in bone resorption, providing a possible rationale for the treatment of disorders such as osteoporosis and certain forms of arthritis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gelb, B D -- Shi, G P -- Chapman, H A -- Desnick, R J -- R01 DK31775/DK/NIDDK NIH HHS/ -- R01 HL44816/HL/NHLBI NIH HHS/ -- R37 DK34045/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Aug 30;273(5279):1236-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics and Division of Pediatric Cardiology, Mount Sinai School of Medicine, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8703060" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Bone Matrix/metabolism ; Bone Resorption ; Cathepsin K ; Cathepsins/deficiency/*genetics/metabolism ; Chromosome Mapping ; Chromosomes, Human, Pair 1 ; Codon, Terminator ; Dinucleoside Phosphates/genetics ; Humans ; Lysosomal Storage Diseases/enzymology/*genetics ; Lysosomes/*enzymology ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Mutation ; Osteochondrodysplasias/enzymology/*genetics ; Osteoclasts/*enzymology ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 87
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    CKI1, a histidine kinase homolog implicated in cytokinin signal transduction (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-08
    Description: Although cytokinin plays a central role in plant development, little is known about cytokinin signal transduction. Five Arabidopsis thaliana mutants that exhibit typical cytokinin responses, including rapid cell division and shoot formation in tissue culture in the absence of exogenous cytokinin, were isolated by activation transferred DNA tagging. A gene, CKI1, which was tagged in four of the five mutants and induced typical cytokinin responses after introduction and overexpression in plants, was cloned. CKI1 encodes a protein similar to the two-component regulators. These results suggest that CKI1 is involved in cytokinin signal transduction, possibly as a cytokinin receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kakimoto, T -- New York, N.Y. -- Science. 1996 Nov 8;274(5289):982-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Graduate School of Science, Osaka University, Toyonaka, Osaka 560, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8875940" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis/genetics/*physiology ; *Arabidopsis Proteins ; Cloning, Molecular ; Cytokinins/pharmacology/*physiology ; DNA, Bacterial/genetics ; DNA, Complementary/genetics ; DNA, Plant/genetics ; Ethylenes/metabolism ; Genes, Plant ; Molecular Sequence Data ; Mutation ; Open Reading Frames ; Plant Proteins/chemistry/metabolism ; Polymorphism, Restriction Fragment Length ; Protein Kinases/chemistry/genetics/*physiology ; *Receptors, Cell Surface ; Sequence Homology, Amino Acid ; *Signal Transduction ; Transformation, Genetic
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  • 88
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    PKD2, a gene for polycystic kidney disease that encodes an integral membrane protein (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-31
    Description: A second gene for autosomal dominant polycystic kidney disease was identified by positional cloning. Nonsense mutations in this gene (PKD2) segregated with the disease in three PKD2 families. The predicted 968-amino acid sequence of the PKD2 gene product has six transmembrane spans with intracellular amino- and carboxyl-termini. The PKD2 protein has amino acid similarity with PKD1, the Caenorhabditis elegans homolog of PKD1, and the family of voltage-activated calcium (and sodium) channels, and it contains a potential calcium-binding domain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mochizuki, T -- Wu, G -- Hayashi, T -- Xenophontos, S L -- Veldhuisen, B -- Saris, J J -- Reynolds, D M -- Cai, Y -- Gabow, P A -- Pierides, A -- Kimberling, W J -- Breuning, M H -- Deltas, C C -- Peters, D J -- Somlo, S -- DK02015/DK/NIDDK NIH HHS/ -- DK48383/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 May 31;272(5266):1339-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Renal Division, Department of Medicine and Molecular Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650545" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Caenorhabditis elegans/chemistry/genetics ; Calcium Channels/chemistry/genetics ; Chromosome Mapping ; Chromosomes, Human, Pair 4 ; Cloning, Molecular ; Consensus Sequence ; Crystallography, X-Ray ; Female ; Glycosylation ; Humans ; Male ; Membrane Proteins/chemistry/*genetics/physiology ; Molecular Sequence Data ; Mutation ; Pedigree ; Phenotype ; Polycystic Kidney, Autosomal Dominant/*genetics ; Polymorphism, Single-Stranded Conformational ; Proteins/chemistry/genetics ; Sodium Channels/chemistry/genetics ; TRPP Cation Channels
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 89
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    Fly gene discovery gets at root of branching structures (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roush, W -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2011.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8984660" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Patterning ; *Drosophila Proteins ; Drosophila melanogaster/embryology/*genetics ; Fibroblast Growth Factors/chemistry ; Gene Expression Regulation, Developmental ; *Genes, Insect ; Insect Proteins/chemistry/*genetics/metabolism/physiology ; Larva/growth & development ; Morphogenesis ; Mutation ; *Protein-Tyrosine Kinases ; Receptors, Fibroblast Growth Factor/genetics/metabolism ; Trachea/embryology
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  • 90
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    Hedgehog's patterning call is patched through, smoothly (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roush, W -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1304-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966601" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Body Patterning ; Carcinoma, Basal Cell/genetics/therapy ; Hedgehog Proteins ; Humans ; Membrane Proteins/genetics/*metabolism ; Mutation ; Proteins/*metabolism ; Receptors, Cell Surface/*metabolism/physiology ; *Receptors, G-Protein-Coupled ; Signal Transduction ; Skin Neoplasms/genetics/therapy ; *Trans-Activators
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  • 91
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    Interaction between Wingless and Notch signaling pathways mediated by dishevelled (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-29
    Description: In Drosophila, the Wingless and Notch signaling pathways function in m any of the same developmental patterning events. Genetic analysis demonstrates that the dishevelled gene, which encodes a molecule previously implicated in implementation of the Winglass signal, interacts antagonistically with Notch and one of its known ligands, Delta. A direct physical interaction between Dishevelled and the Notch carboxyl terminus, distal to the cdc10/ankyrin repeats, suggests a mechanism for this interaction. It is proposed that Dishevelled, in addition to transducing the Wingless signal, blocks Notch signaling directly, thus providing a molecular mechanism for the inhibitory cross talk observed between these pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Axelrod, J D -- Matsuno, K -- Artavanis-Tsakonas, S -- Perrimon, N -- New York, N.Y. -- Science. 1996 Mar 29;271(5257):1826-32.〈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/8596950" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Clone Cells ; Drosophila/genetics/growth & development/*metabolism ; *Drosophila Proteins ; Genes, Insect ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins/antagonists & inhibitors/genetics/*metabolism ; Molecular Sequence Data ; Mutation ; Phenotype ; *Phosphoproteins ; Proteins/genetics/*metabolism ; Proto-Oncogene Proteins/genetics/*metabolism ; Pupa/metabolism ; Receptors, Notch ; *Signal Transduction ; Wings, Animal/cytology/growth & development ; Wnt1 Protein
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  • 92
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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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  • 93
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    A neural tetraspanin, encoded by late bloomer, that facilitates synapse formation (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-29
    Description: Upon contacting its postsynaptic target, a neuronal growth cone transforms into a presynaptic terminal. A membrane component on the growth cone that facilitates synapse formation was identified by means of a complementary DNA-based screen followed by genetic analysis. The late bloomer (lbl) gene in Drosophila encodes a member of the tetraspanin family of cell surface proteins. LBL protein is transiently expressed on motor axons, growth cones, and terminal arbors. In lbl mutant embryos, the growth cone of the RP3 motoneuron contacts its target muscles, but synapse formation is delayed and neighboring motoneurons display an increase in ectopic sprouting.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kopczynski, C C -- Davis, G W -- Goodman, C S -- New York, N.Y. -- Science. 1996 Mar 29;271(5257):1867-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California, Berkeley 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596956" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Axons/metabolism/ultrastructure ; Cloning, Molecular ; Drosophila/embryology/genetics/physiology ; *Drosophila Proteins ; *Genes, Insect ; Membrane Proteins/chemistry/genetics/*physiology ; Molecular Sequence Data ; Motor Neurons/cytology/metabolism/*physiology ; Muscles/innervation ; Mutation ; Nerve Tissue Proteins/chemistry/genetics/*physiology ; Neuromuscular Junction/*physiology ; Presynaptic Terminals/*physiology/ultrastructure ; Signal Transduction
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  • 94
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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)
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    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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  • 95
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    New virus variant killed Serengeti cats (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-02-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morell, V -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):596.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571120" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Distemper/transmission/*virology ; Distemper Virus, Canine/classification/*genetics ; Dogs ; *Genome, Viral ; Humans ; Lions/*virology ; Mutation ; Species Specificity ; Tanzania
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  • 96
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    Guiding neurons to the cortex (1996)
    American Association for the Advancement of Science (AAAS)
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    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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  • 97
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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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    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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  • 98
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    Rapid degradation of the G1 cyclin Cln2 induced by CDK-dependent phosphorylation (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-15
    Description: Cyclins regulate the major cell cycle transitions in eukaryotes through association with cyclin-dependent protein kinases (CDKs). In yeast, G1 cyclins are essential, rate-limiting activators of cell cycle initiation. G1-specific accumulation of one G1 cyclin, Cln2, results from periodic gene expression coupled with rapid protein turnover. Site-directed mutagenesis of CLN2 revealed that its phosphorylation provides a signal that promotes rapid degradation. Cln2 phosphorylation is dependent on the Cdc28 protein kinase, the CDK that it activates. These findings suggest that Cln2 is rendered self-limiting by virtue of its ability to activate its cognate CDK subunit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lanker, S -- Valdivieso, M H -- Wittenberg, C -- GM43487/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Mar 15;271(5255):1597-601.〈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/8599119" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; CDC28 Protein Kinase, S cerevisiae/*metabolism ; Cyclins/genetics/*metabolism ; Enzyme Activation ; Fungal Proteins/genetics/metabolism ; *G1 Phase ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Mutation ; Phenotype ; Phosphorylation ; Saccharomyces cerevisiae/cytology/metabolism ; Saccharomyces cerevisiae Proteins
    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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  • 99
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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
    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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  • 100
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    Green light for steroid hormones (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Russell, D W -- New York, N.Y. -- Science. 1996 Apr 19;272(5260):370-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas 75235-9046, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8602524" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Oxo-5-alpha-Steroid 4-Dehydrogenase/chemistry ; Arabidopsis/genetics/*growth & development/metabolism ; *Arabidopsis Proteins ; Brassinosteroids ; Cholestanols/*metabolism ; Cytochrome P-450 Enzyme System/genetics/metabolism ; *Genes, Plant ; Light ; Mutation ; Plant Growth Regulators/biosynthesis/*metabolism ; Plant Proteins/chemistry/*genetics/metabolism ; Steroids, Heterocyclic/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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