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  • Mice  (137)
  • Cloning, Molecular  (45)
  • Cell & Developmental Biology
  • Chemistry
  • Inorganic Chemistry
  • Polymer and Materials Science
  • American Association for the Advancement of Science (AAAS)  (176)
  • 1990-1994  (176)
  • 1965-1969
  • 1993  (176)
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  • 1990-1994  (176)
  • 1965-1969
Year
  • 1
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    Sea urchin egg receptor for sperm: sequence similarity of binding domain and hsp70 (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-05
    Description: Fertilization depends on cell surface recognition proteins that interact and thereby mediate binding and subsequent fusion of the sperm and egg. Overlapping complementary DNA's encoding the egg plasma membrane receptor for sperm from the sea urchin Strongylocentrotus purpuratus were cloned and sequenced. Analysis of the deduced primary structure suggests that the receptor is a transmembrane protein with a short cytoplasmic domain. This domain showed no sequence similarity to known protein sequences. In contrast, the extracellular, sperm binding domain of the receptor did show sequence similarity to the heat shock protein 70 (hsp70) family of proteins. Recombinant protein representing this portion of the receptor bound to the sperm protein, binding, and also inhibited fertilization in a species-specific manner; beads coated with the protein became specifically bound to acrosome-reacted sperm. These data provide a basis for detailed investigations of molecular interactions that occur in gamete recognition and egg activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Foltz, K R -- Partin, J S -- Lennarz, W J -- HD18590/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1421-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of California, Santa Barbara 93106.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8383878" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cloning, Molecular ; Female ; Fertilization ; Heat-Shock Proteins/*genetics ; Humans ; Male ; Molecular Sequence Data ; Ovum/physiology ; Receptors, Cell Surface/*genetics/metabolism ; Recombinant Proteins/metabolism ; Restriction Mapping ; Sea Urchins ; Sequence Homology, Amino Acid ; Sperm-Ovum Interactions ; Spermatozoa/cytology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Origin recognition complex (ORC) in transcriptional silencing and DNA replication in S. cerevisiae (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-17
    Description: In Saccharomyces cerevisiae, the HMR-E silencer blocks site-specific interactions between proteins and their recognition sequences in the vicinity of the silencer. Silencer function is correlated with the firing of an origin of replication at HMR-E. An essential gene with a role in transcriptional silencing was identified by means of a screen for mutations affecting expression of HMR. This gene, known as ORC2, was shown to encode a component of the origin recognition complex that binds yeast origins of replication. A temperature-sensitive mutation in ORC2 disrupted silencing in cells grown at the permissive temperature. At the restrictive temperature, the orc2-1 mutation caused cell cycle arrest at a point in the cell cycle indicative of blocks in DNA replication. The orc2-1 mutation also resulted in the enhanced mitotic loss of a plasmid, suggestive of a defect in replication. These results provide strong evidence for an in vivo role of ORC in both chromosomal replication and silencing, and provide a link between the mechanism of silencing and DNA replication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Foss, M -- McNally, F J -- Laurenson, P -- Rine, J -- GM31105/GM/NIGMS NIH HHS/ -- P30ES01896-12/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1993 Dec 17;262(5141):1838-44.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266071" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Cell Cycle ; Cloning, Molecular ; *DNA Replication ; DNA, Fungal/genetics/metabolism ; *DNA-Binding Proteins ; Fungal Proteins/chemistry/*genetics/metabolism ; *Gene Expression Regulation, Fungal ; *Genes, Fungal ; Molecular Sequence Data ; Mutation ; Origin Recognition Complex ; Phenotype ; Plasmids ; *Replicon ; Repressor Proteins/chemistry/*genetics/metabolism ; Saccharomyces cerevisiae/cytology/*genetics/metabolism ; Saccharomyces cerevisiae Proteins ; Transcription, Genetic
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  • 3
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    Rate and mechanism of nonhomologous recombination during a single cycle of retroviral replication (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-08
    Description: Oncogenes discovered in retroviruses such as Rous sarcoma virus were generated by transduction of cellular proto-oncogenes into the viral genome. Several different kinds of junctions between the viral and proto-oncogene sequences have been found in different viruses. A system of retrovirus vectors and a protocol that mimicked this transduction during a single cycle of retrovirus replication was developed. The transduction involved the formation of a chimeric viral-cellular RNA, strand switching of the reverse transcription growing point from an infectious retrovirus to the chimeric RNA, and often a subsequent deletion during the rest of viral DNA synthesis. A short region of sequence identity was frequently used for the strand switching. The rate of this process was about 0.1 to 1 percent of the rate of homologous retroviral recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Temin, H M -- CA-07175/CA/NCI NIH HHS/ -- CA-22443/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 8;259(5092):234-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McArdle Laboratory for Cancer Research, University of Wisconsin-Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8421784" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Cinnamates ; *DNA Replication ; DNA, Viral/chemistry/genetics ; Drug Resistance/genetics ; Genes, Viral ; Genetic Vectors ; Hygromycin B/analogs & derivatives ; Kinetics ; Mice ; Molecular Sequence Data ; Moloney murine leukemia virus/genetics ; Neomycin ; Plasmids ; *Proto-Oncogenes ; RNA, Viral/analysis/genetics ; *Recombination, Genetic ; Repetitive Sequences, Nucleic Acid ; Retroviridae/*genetics/physiology ; Transfection ; *Virus Replication
    Print ISSN: 0036-8075
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  • 4
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    Mutations in the glucose-6-phosphatase gene that cause glycogen storage disease type 1a (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-22
    Description: Glycogen storage disease (GSD) type 1a is caused by the deficiency of D-glucose-6-phosphatase (G6Pase), the key enzyme in glucose homeostasis. Despite both a high incidence and morbidity, the molecular mechanisms underlying this deficiency have eluded characterization. In the present study, the molecular and biochemical characterization of the human G6Pase complementary DNA, its gene, and the expressed protein, which is indistinguishable from human microsomal G6Pase, are reported. Several mutations in the G6Pase gene of affected individuals that completely inactivate the enzyme have been identified. These results establish the molecular basis of this disease and open the way for future gene therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lei, K J -- Shelly, L L -- Pan, C J -- Sidbury, J B -- Chou, J Y -- New York, N.Y. -- Science. 1993 Oct 22;262(5133):580-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211187" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA, Complementary/genetics ; Exons ; Glucose-6-Phosphatase/*genetics/metabolism ; Glycogen Storage Disease Type I/enzymology/*genetics ; Glycosylation ; Humans ; Liver/enzymology ; Mice ; Molecular Sequence Data ; *Mutation ; Protein Conformation ; Transfection
    Print ISSN: 0036-8075
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  • 5
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    Expression cloning and signaling properties of the rat glucagon receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-12
    Description: Glucagon and the glucagon receptor are a primary source of control over blood glucose concentrations and are especially important to studies of diabetes in which the loss of control over blood glucose concentrations clinically defines the disease. A complementary DNA clone for the glucagon receptor was isolated by an expression cloning strategy, and the receptor protein was expressed in several kidney cell lines. The cloned receptor bound glucagon and caused an increase in the intracellular concentration of adenosine 3', 5'-monophosphate (cAMP). The cloned glucagon receptor also transduced a signal that led to an increased concentration of intracellular calcium. The glucagon receptor is similar to the calcitonin and parathyroid hormone receptors. It can transduce signals leading to the accumulation of two different second messengers, cAMP and calcium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jelinek, L J -- Lok, S -- Rosenberg, G B -- Smith, R A -- Grant, F J -- Biggs, S -- Bensch, P A -- Kuijper, J L -- Sheppard, P O -- Sprecher, C A -- New York, N.Y. -- Science. 1993 Mar 12;259(5101):1614-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ZymoGenetics Inc., Seattle, WA 98105.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8384375" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/pharmacology ; Cell Line ; Cloning, Molecular ; Cricetinae ; Cyclic AMP/metabolism ; Glucagon/metabolism/*pharmacology ; Kidney ; Kinetics ; Liver/*metabolism ; Molecular Sequence Data ; Rats ; Receptors, Gastrointestinal Hormone/genetics/metabolism/*physiology ; Receptors, Glucagon ; *Signal Transduction ; Transfection
    Print ISSN: 0036-8075
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  • 6
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    The secretory granule matrix: a fast-acting smart polymer (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-12
    Description: The secretory granule matrix is a miniature biopolymer that consists of a charged polymer network that traps peptides and transmitters when it condenses and releases them on exocytotic decondensation. Models of exocytotic fusion have treated this matrix as a short circuit and have neglected its electrical contributions. This matrix responded to negative voltages by swelling, which was accompanied by a large increase in conductance, and to positive voltages by condensing. Thus, the matrix resembled a diode. The swollen matrix exerted large pressures on the order of 12 bar. The responses took place within milliseconds of the application of the electric field. These findings suggest that matrix decondensation, and therefore product release, is controlled by potential gradients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nanavati, C -- Fernandez, J M -- New York, N.Y. -- Science. 1993 Feb 12;259(5097):963-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, Mayo Clinic, Rochester, MN 55905.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8438154" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytoplasmic Granules/*chemistry/physiology ; Electric Conductivity ; Electrochemistry ; Exocytosis ; Mast Cells/*ultrastructure ; Membrane Potentials ; Mice ; Polymers/*chemistry
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  • 7
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    Inhibition of Rev-mediated HIV-1 expression by an RNA binding protein encoded by the interferon-inducible 9-27 gene (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-26
    Description: Interferon inhibits expression of human immunodeficiency virus type-1 (HIV-1) through unknown mechanisms. A gene inducible by interferon-alpha (IFN-alpha) and interferon-gamma (IFN-gamma) was isolated by screening of a human complementary DNA library for proteins binding to the Rev-responsive element (RRE) of HIV-1. The product of this gene, RBP9-27, was shown to bind RNA in vitro and to inhibit HIV-1 expression after transfection into human cells. RBP9-27 primarily inhibited Rev-dependent posttranscriptional steps of viral gene expression. Thus, RBP9-27 is a cellular factor that antagonizes Rev function. These results suggest an interferon-induced antiviral mechanism operating through the induction of RNA binding proteins such as RBP9-27. Elucidation of RBP9-27 function may lead to a better understanding of the mechanism of interferon action during HIV-1 infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Constantoulakis, P -- Campbell, M -- Felber, B K -- Nasioulas, G -- Afonina, E -- Pavlakis, G N -- N0-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 26;259(5099):1314-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Retrovirus Section, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7680491" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cloning, Molecular ; *Gene Expression Regulation, Viral ; Genes, env ; *Genes, rev ; HIV-1/*genetics ; Humans ; Interferons/pharmacology ; *Membrane Proteins ; Molecular Sequence Data ; Oligodeoxyribonucleotides/chemistry ; RNA-Binding Proteins/*genetics ; Regulatory Sequences, Nucleic Acid
    Print ISSN: 0036-8075
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  • 8
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    Disappearance of the lymphoid system in Bcl-2 homozygous mutant chimeric mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-17
    Description: The bcl-2 proto-oncogene can prevent the death of many cell types. Mice were generated that were chimeric for the homozygous inactivation of bcl-2. Lymphocytes without Bcl-2 differentiated into phenotypically mature cells. However, in vitro, the mature T cells that lacked Bcl-2 had shorter life-spans and increased sensitivity to glucocorticoids and gamma-irradiation. In contrast, stimulation of CD3 inhibited the death of these cells. T and B cells with no Bcl-2 disappeared from the bone marrow, thymus, and periphery by 4 weeks of age. Thus, Bcl-2 was dispensable for lymphocyte maturation, but was required for a stable immune system after birth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakayama, K -- Negishi, I -- Kuida, K -- Shinkai, Y -- Louie, M C -- Fields, L E -- Lucas, P J -- Stewart, V -- Alt, F W -- AI 15322/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 17;261(5128):1584-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8372353" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3/immunology ; Apoptosis ; B-Lymphocytes/cytology/*immunology ; Base Sequence ; Bone Marrow/immunology ; Bone Marrow Cells ; Cell Line ; Chimera ; Homozygote ; Humans ; Lymphoid Tissue/cytology/immunology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Proto-Oncogene Proteins/genetics/*physiology ; Proto-Oncogene Proteins c-bcl-2 ; Proto-Oncogenes ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/cytology/*immunology
    Print ISSN: 0036-8075
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  • 9
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    Microbial competition: Escherichia coli mutants that take over stationary phase cultures (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-19
    Description: Many microorganisms, including Escherichia coli, can survive extended periods of starvation. The properties of cells that survived prolonged incubation in stationary phase were studied by mixture of 10-day-old (aged) cultures with 1-day-old (young) cultures of the same strain of Escherichia coli. Mutants from the aged cultures that could grow eventually took over the population, which resulted in the death of the cells from the young cultures. This phenotype was conferred by mutations in rpoS, which encodes a putative stationary phase-specific sigma factor. These rapid population shifts have implications for the studies of microbial evolution and ecology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zambrano, M M -- Siegele, D A -- Almiron, M -- Tormo, A -- Kolter, R -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1757-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7681219" target="_blank"〉PubMed〈/a〉
    Keywords: Acridine Orange ; Alleles ; Amino Acid Sequence ; Cloning, Molecular ; Escherichia coli/*genetics/*growth & development/physiology ; Hydrogen Peroxide/metabolism ; Molecular Sequence Data ; *Mutation ; Peroxidase/metabolism ; Phenotype ; Sigma Factor/chemistry/*genetics ; Staining and Labeling ; Time Factors
    Print ISSN: 0036-8075
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  • 10
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    Induction of G alpha i2-specific antisense RNA in vivo inhibits neonatal growth (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-14
    Description: Guanosine triphosphate-binding regulatory proteins (G proteins) are key elements in transmembrane signaling and have been implicated as regulators of more complex biological processes such as differentiation and development. The G protein G alpha i2 is capable of mediating the inhibitory control of adenylylcyclase and regulates stem cell differentiation to primitive endoderm. Here an antisense RNA to G alpha i2 was expressed in a hybrid RNA construct whose expression was both tissue-specific and induced at birth. Transgenic mice in which the antisense construct was expressed displayed a lack of normal development in targeted organs that correlated with the absence of G alpha i2. The loss of G alpha i2 expression in adipose tissue of the transgenic mice was correlated with a rise in basal levels of adenosine 3',5'-monophosphate (cAMP) and the loss of receptor-mediated inhibition of adenylylcyclase. These data expand our understanding of G protein function in vivo and demonstrate the necessity for G alpha i2 in the development of liver and fat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moxham, C M -- Hod, Y -- Malbon, C C -- New York, N.Y. -- Science. 1993 May 14;260(5110):991-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Pharmacology, State University of New York (SUNY)/Stony Brook 11794-8651.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493537" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*growth & development/metabolism ; Animals ; Animals, Newborn/growth & development ; Base Sequence ; Body Weight ; GTP-Binding Proteins/biosynthesis/genetics/*physiology ; Growth/drug effects/*physiology ; Kidney/growth & development/metabolism ; Liver/*growth & development/metabolism ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Phosphoenolpyruvate Carboxykinase (GTP)/genetics ; RNA, Antisense/*genetics ; Transfection
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  • 11
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    New technique offers a window on bacteria's secret weapons (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1993 Jan 29;259(5095):595.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430305" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Bacterial/genetics/isolation & purification ; *Genes, Bacterial ; Mice ; Salmonella typhimurium/genetics/*pathogenicity ; Virulence/genetics
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  • 12
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    A genetic linkage map of the mouse: current applications and future prospects (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-01
    Description: Technological advances have made possible the development of high-resolution genetic linkage maps for the mouse. These maps in turn offer exciting prospects for understanding mammalian genome evolution through comparative mapping, for developing mouse models of human disease, and for identifying the function of all genes in the organism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Copeland, N G -- Jenkins, N A -- Gilbert, D J -- Eppig, J T -- Maltais, L J -- Miller, J C -- Dietrich, W F -- Weaver, A -- Lincoln, S E -- Steen, R G -- HG00198/HG/NHGRI NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 1;262(5130):57-66.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211130" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Chromosome Mapping ; Cloning, Molecular ; Crosses, Genetic ; Female ; Genetic Markers ; *Genome ; Human Genome Project ; Humans ; Male ; Mice/*genetics ; Multigene Family ; Muridae/*genetics ; Mutation ; Neoplasms/genetics
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  • 13
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    Shutdown of class switch recombination by deletion of a switch region control element (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-12
    Description: Upon activation, B lymphocytes can change the class of the antibody they express by immunoglobulin class switch recombination. Cytokines can direct this recombination to distinct classes by the specific activation of repetitive recombinogenic DNA sequences, the switch regions. Recombination to a particular switch region (s gamma 1) was abolished in mice that were altered to lack sequences that are 5' to the s gamma 1 region. This result directly implicates the functional importance of 5' switch region flanking sequences in the control of class switch recombination. Mutant mice exhibit a selective agammaglobulinemia and may be useful in the assessment of the biological importance of immunoglobulin G1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jung, S -- Rajewsky, K -- Radbruch, A -- New York, N.Y. -- Science. 1993 Feb 12;259(5097):984-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8438159" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Base Sequence ; Cell Line ; Chimera ; Drug Resistance/genetics ; Embryo, Mammalian ; *Gene Deletion ; Immunoglobulin G/genetics ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin Switch Region/*genetics ; Interleukin-4/pharmacology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutagenesis ; Neomycin ; *Recombination, Genetic ; Stem Cells
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  • 14
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    Uncovering of functional alternative CTLA-4 counter-receptor in B7-deficient mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-05
    Description: B7 delivers a costimulatory signal through CD28, resulting in interleukin-2 secretion and T cell proliferation. Blockade of this pathway results in T cell anergy. The in vivo role of B7 was evaluated with B7-deficient mice. These mice had a 70 percent decrease in costimulation of the response to alloantigen. Despite lacking B7 expression, activated B cells from these mice bound CTLA-4 and GL1 monoclonal antibody, demonstrating that alternative CTLA-4 ligand or ligands exist. These receptors are functionally important because the residual allogenic mixed lymphocyte responses were blocked by CTLA4Ig. Characterization of these CTLA-4 ligands should lead to strategies for manipulating the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freeman, G J -- Borriello, F -- Hodes, R J -- Reiser, H -- Hathcock, K S -- Laszlo, G -- McKnight, A J -- Kim, J -- Du, L -- Lombard, D B -- CA 40216/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Nov 5;262(5135):907-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematologic Malignancies, Dana-Farber Cancer Institute, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7694362" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antigens, CD ; Antigens, CD80/genetics/*immunology/metabolism ; Antigens, Differentiation/immunology/*metabolism ; B-Lymphocytes/*immunology ; Base Sequence ; CTLA-4 Antigen ; Cell Line ; *Immunoconjugates ; Interleukin-2/secretion ; Isoantigens/immunology ; Lymphocyte Activation ; Lymphocyte Culture Test, Mixed ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; T-Lymphocytes/*immunology ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    The role of TH1 and TH2 cells in a rodent malaria infection (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-25
    Description: CD4+ T cells play a major role in protective immunity against the blood stage of malaria, but the mechanism of protection is unclear. By adoptive transfer of cloned T cell lines, direct evidence is provided that both TH1 and TH2 subsets of CD4+ T cells can protect mice against Plasmodium chabaudi chabaudi infection. TH1 cells protect by a nitric oxide-dependent mechanism, whereas TH2 cells protect by the enhancement and accelerated production of specific immunoglobulin G1 antibody.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taylor-Robinson, A W -- Phillips, R S -- Severn, A -- Moncada, S -- Liew, F Y -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1931-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Laboratories for Experimental Parasitology, University of Glasgow, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8100366" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Protozoan/biosynthesis ; Arginine/analogs & derivatives/pharmacology ; CD4-Positive T-Lymphocytes/*immunology ; Cell Line ; Female ; Immunoglobulin G/*biosynthesis ; Lymphocyte Depletion ; Malaria/*immunology ; Mice ; Mice, Inbred Strains ; Nitrates/blood ; Nitric Oxide/*metabolism ; Plasmodium chabaudi/*immunology ; T-Lymphocyte Subsets/*immunology ; omega-N-Methylarginine
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    A new five-year plan for the U.S. Human Genome Project (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Collins, F -- Galas, D -- New York, N.Y. -- Science. 1993 Oct 1;262(5130):43-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Center for Human Genome Research, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211127" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomedical Research ; Chromosome Mapping ; Ethics, Medical ; Federal Government ; Financing, Government ; Genetic Diseases, Inborn ; Genetic Markers ; Genetic Techniques ; Government Agencies ; *Human Genome Project/economics/legislation & jurisprudence ; Humans ; Industry ; International Cooperation ; Internationality ; Mice ; National Institutes of Health (U.S.) ; Research ; Sequence Analysis, DNA ; United States
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  • 17
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    Generation of allospecific natural killer cells by stimulation across a polymorphism of HLA-C (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-21
    Description: The cytotoxicity of human natural killer (NK) cells is modulated by the major histocompatibility complex human leukocyte antigen (HLA)-C molecules on the surface of the target cell. Alloreactive NK cells specific for the NK-1 alloantigen could be reproducibly generated from individuals that were homozygous for HLA-C with asparagine at residue 77 and lysine at residue 80 [HLA-C(Asn77,Lys80)] by stimulation with target cells that were homozygous for HLA-C(Ser77,Asn80); the reciprocal stimulation yielded NK cells specific for the NK-2 alloantigen. However, neither homozygous target cell stimulated the generation of alloreactive NK cells from heterozygous individuals. Thus, these data reveal an unanticipated difference between human NK alloreactivity defined by this system and murine "hybrid resistance."〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Colonna, M -- Brooks, E G -- Falco, M -- Ferrara, G B -- Strominger, J L -- CA 47554/CA/NCI NIH HHS/ -- KO8 AI01064/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 May 21;260(5111):1121-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunogenetics, Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493555" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Base Sequence ; Cell Line ; *Cytotoxicity, Immunologic ; Genotype ; HLA-C Antigens/genetics/*immunology ; Heterozygote ; Homozygote ; Humans ; Isoantigens/*immunology ; Killer Cells, Natural/*immunology ; Mice ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Polymorphism, Genetic
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  • 18
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    Systemic gene expression after intravenous DNA delivery into adult mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-09
    Description: Direct gene transfer into adult animals resulting in generalized or tissue-specific expression would facilitate rapid analysis of transgene effects and allow precise in vivo manipulation of biologic processes at the molecular level. A single intravenous injection of expression plasmid:cationic liposome complexes into adult mice efficiently transfected virtually all tissues. In addition to vascular endothelial cells, most of the extravascular parenchymal cells present in many tissues including the lung, spleen, lymph nodes, and bone marrow expressed the transgene without any apparent treatment-related toxicity. The transgene was still expressed in large numbers of cells in multiple tissues for at least 9 weeks after a single injection. Expression could be targeted to specific tissues and cell types, depending on the promoter element used.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, N -- Liggitt, D -- Liu, Y -- Debs, R -- New York, N.Y. -- Science. 1993 Jul 9;261(5118):209-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Institute, University of California, San Francisco 94143-0128.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7687073" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Bone Marrow/metabolism ; Chloramphenicol O-Acetyltransferase/genetics ; Cystic Fibrosis/genetics ; Cystic Fibrosis Transmembrane Conductance Regulator ; Cytomegalovirus/genetics ; Female ; *Gene Expression ; Injections, Intravenous ; Liposomes ; Liver/metabolism ; Lung/metabolism ; Lung Neoplasms/genetics ; Lymphoid Tissue/metabolism ; Membrane Proteins/genetics ; Mice ; Mice, Inbred ICR ; Mice, Transgenic ; Molecular Sequence Data ; Myocardium/metabolism ; Oligodeoxyribonucleotides ; Phosphatidylethanolamines/chemistry ; Plasmids ; Quaternary Ammonium Compounds ; *Transfection
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  • 19
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    Binding of L-selectin to the vascular sialomucin CD34 (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-15
    Description: The adhesive interactions between leukocyte L-selectin and the endothelium are involved in the migration of lymphocytes through peripheral lymph nodes and of neutrophils to sites of inflammation. A recombinant L-selectin stains high endothelial venules (HEVs) in lymph nodes and recognizes sulfated carbohydrates found on two endothelial glycoproteins, Sgp50 and Sgp90. Amino acid sequencing of purified Sgp90 revealed a protein core identical to that CD34, a sialomucin expressed on hematopoietic stem cells and endothelium. A polyclonal antiserum to recombinant murine CD34 stains peripheral lymph node endothelium and recognizes Sgp90 that is functionally bound by L-selectin. Thus, an HEV glycoform of CD34 can function as a ligand for L-selectin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baumheter, S -- Singer, M S -- Henzel, W -- Hemmerich, S -- Renz, M -- Rosen, S D -- Lasky, L A -- GM 23547/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 15;262(5132):436-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Genentech, Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7692600" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Antigens, CD/*metabolism ; Antigens, CD34 ; Cell Adhesion Molecules/*metabolism ; Clusterin ; Endothelium, Vascular/*metabolism ; Glycoproteins/*metabolism ; L-Selectin ; Lymph Nodes/*blood supply ; Mice ; *Molecular Chaperones ; Molecular Sequence Data ; Mucins/*metabolism ; Recombinant Proteins/metabolism ; Sialomucins
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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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    Immunology. Interfering with interferon (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1693-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456294" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Deletion ; Interferon-gamma/genetics/*immunology ; Mice ; Mice, Mutant Strains ; Receptors, Interferon/genetics ; Virus Diseases/immunology
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  • 21
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    Resistance of MHC class I-deficient mice to experimental systemic lupus erythematosus (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-07-02
    Description: Experimental systemic lupus erythematosus (SLE) can be induced in mice by immunization with a human monoclonal antibody to DNA that bears a common idiotype (16/6Id). These mice generate antibodies to 16/6Id, antibodies to DNA, and antibodies directed against nuclear antigens. Subsequently, manifestations of SLE develop, including leukopenia, proteinuria, and immune complex deposits in the kidney. In contrast, after immunization with 16/6Id, mice lacking major histocompatibility complex (MHC) class I molecules generated antibodies to 16/6Id but did not generate antibodies to DNA or to nuclear antigen. Furthermore, they did not develop any of the above clinical manifestations. These results reveal an unexpected function of MHC class I in the induction of autoimmune SLE.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mozes, E -- Kohn, L D -- Hakim, F -- Singer, D S -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):91-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8316860" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Antinuclear/immunology ; Antibodies, Monoclonal/immunology ; Histocompatibility Antigens Class I/*immunology ; Immunity, Innate ; Immunization ; Immunoglobulin Idiotypes/immunology ; Lupus Erythematosus, Systemic/*immunology ; Mice
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  • 22
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    Fusion between transcription factor CBF beta/PEBP2 beta and a myosin heavy chain in acute myeloid leukemia (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-20
    Description: The pericentric inversion of chromosome 16 [inv(16)(p13q22)] is a characteristic karyotypic abnormality associated with acute myeloid leukemia, most commonly of the M4Eo subtype. The 16p and 16q breakpoints were pinpointed by yeast artificial chromosome and cosmid cloning, and the two genes involved in this inversion were identified. On 16q the inversion occurred near the end of the coding region for CBF beta, also known as PEBP2 beta, a subunit of a heterodimeric transcription factor regulating genes expressed in T cells; on 16p a smooth muscle myosin heavy chain (SMMHC) gene (MYH11) was interrupted. In six of six inv(16) patient samples tested, an in-frame fusion messenger RNA was demonstrated that connected the first 165 amino acids of CBF beta with the tail region of SMMHC. The repeated coiled coil of SMMHC may result in dimerization of the CBF beta fusion protein, which in turn would lead to alterations in transcriptional regulation and contribute to leukemic transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, P -- Tarle, S A -- Hajra, A -- Claxton, D F -- Marlton, P -- Freedman, M -- Siciliano, M J -- Collins, F S -- CA55164/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Aug 20;261(5124):1041-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8351518" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; *Chromosome Inversion ; *Chromosomes, Human, Pair 16 ; Cloning, Molecular ; Core Binding Factor Alpha 1 Subunit ; Core Binding Factor beta Subunit ; Core Binding Factors ; Cosmids ; DNA-Binding Proteins/*genetics ; Humans ; In Situ Hybridization, Fluorescence ; Leukemia, Myelomonocytic, Acute/*genetics ; Molecular Sequence Data ; Muscle, Smooth/chemistry ; Myosins/*genetics ; *Neoplasm Proteins ; Polymerase Chain Reaction ; Protein Multimerization ; Restriction Mapping ; Transcription Factor AP-2 ; Transcription Factors/*genetics
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  • 23
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    A wingless-dependent polar coordinate system in Drosophila imaginal discs (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-22
    Description: The patterning of the imaginal discs in Drosophila melanogaster is a progressive process that, like the patterning of the larval epidermis during embryogenesis, requires the activity of segment polarity genes. One segment polarity gene, wingless, encodes a homolog of the mouse proto-oncogene Wnt-1 and plays a prominent role in the patterning of the larval epidermis and the imaginal discs. However, whereas the function of wingless in the embryo is initially associated with a pattern of stripes along the anteroposterior axis that are part of a Cartesian coordinate system, it is shown here that during imaginal development wingless is associated with a pattern of sectors that provide references for a polar coordinate system homologous to that postulated in a well-known model for the regeneration of insect and vertebrate limbs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couso, J P -- Bate, M -- Martinez-Arias, A -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1993 Jan 22;259(5094):484-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Cambridge, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8424170" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila melanogaster/embryology/*genetics/growth & development ; Embryo, Nonmammalian/cytology/physiology ; Gene Expression ; Larva ; Mice ; Phenotype ; Protein-Tyrosine Kinases/genetics ; Proto-Oncogene Proteins/genetics ; Proto-Oncogenes ; Sequence Homology, Nucleic Acid ; Wings, Animal ; Wnt Proteins ; Wnt1 Protein ; *Zebrafish Proteins ; beta-Galactosidase/genetics
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  • 24
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    T cell receptor specificity and diabetes in nonobese diabetic mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bendelac, A -- New York, N.Y. -- Science. 1993 Dec 3;262(5139):1582-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8248809" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diabetes Mellitus, Type 1/*immunology ; Mice ; Mice, Inbred NOD ; Mice, Transgenic ; Receptors, Antigen, T-Cell, alpha-beta/*genetics
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  • 25
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    Identification of the von Hippel-Lindau disease tumor suppressor gene (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-28
    Description: A gene discovered by positional cloning has been identified as the von Hippel-Lindau (VHL) disease tumor suppressor gene. A restriction fragment encompassing the gene showed rearrangements in 28 of 221 VHL kindreds. Eighteen of these rearrangements were due to deletions in the candidate gene, including three large nonoverlapping deletions. Intragenic mutations were detected in cell lines derived from VHL patients and from sporadic renal cell carcinomas. The VHL gene is evolutionarily conserved and encodes two widely expressed transcripts of approximately 6 and 6.5 kilobases. The partial sequence of the inferred gene product shows no homology to other proteins, except for an acidic repeat domain found in the procyclic surface membrane glycoprotein of Trypanosoma brucei.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Latif, F -- Tory, K -- Gnarra, J -- Yao, M -- Duh, F M -- Orcutt, M L -- Stackhouse, T -- Kuzmin, I -- Modi, W -- Geil, L -- New York, N.Y. -- Science. 1993 May 28;260(5112):1317-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunobiology, National Cancer Institute-Frederick Cancer Research and Development Center (NCI-FCRDC), Frederick, MD 21702-1201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493574" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Carcinoma, Renal Cell/genetics ; Chromosomes, Human, Pair 3 ; Cloning, Molecular ; Gene Deletion ; *Genes, Tumor Suppressor ; Humans ; Kidney Neoplasms/genetics ; Membrane Glycoproteins/chemistry/*genetics ; Molecular Sequence Data ; Mutation ; Open Reading Frames ; Pedigree ; Polymorphism, Genetic ; Tumor Cells, Cultured ; von Hippel-Lindau Disease/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 26
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    Induction by EGF and interferon-gamma of tyrosine phosphorylated DNA binding proteins in mouse liver nuclei (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-24
    Description: Intraperitoneal injection of epidermal growth factor (EGF) into mice resulted in the appearance in liver nuclei of three tyrosine phosphorylated proteins (84, 91, and 92 kilodaltons) within minutes after administration of EGF. Administration of interferon-gamma (IFN-gamma) resulted in the appearance in liver nuclei of two tyrosine phosphorylated proteins (84 and 91 kilodaltons). The 84- and 91-kilodalton proteins detected after either EGF or IFN-gamma administration were identified as the IFN-gamma activation factors (GAF). Furthermore, gel shift analysis revealed that these GAF proteins, detected after either EGF or IFN-gamma administration, specifically bound to the sis-inducible element of the c-fos promoter. Thus, GAF proteins participate in nuclear signaling in both IFN-gamma and EGF pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ruff-Jamison, S -- Chen, K -- Cohen, S -- HD-00700/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 24;261(5129):1733-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8378774" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Nucleus/drug effects/*metabolism ; DNA-Binding Proteins/*metabolism ; Epidermal Growth Factor/*pharmacology ; Genes, fos ; Interferon-Stimulated Gene Factor 3 ; Interferon-gamma/*pharmacology ; Liver/drug effects/metabolism ; Mice ; Molecular Sequence Data ; Phosphorylation ; Promoter Regions, Genetic ; STAT1 Transcription Factor ; *Trans-Activators ; Transcription Factors/*metabolism ; Tyrosine/*metabolism
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  • 27
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    Molecular mapping and detoxification of the lipid A binding site by synthetic peptides (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-15
    Description: Endotoxin [lipopolysaccharide (LPS)], the major antigen of the outer membrane of Gram-negative bacteria, consists of a variable-size carbohydrate chain that is covalently linked to N,O-acylated beta-1,6-D-glucosamine disaccharide 1,4'-bisphosphate (lipid A). The toxic activity of LPS resides in the lipid A structure. The structural features of synthetic peptides that bind to lipid A with high affinity, detoxify LPS in vitro, and prevent LPS-induced cytokine release and lethality in vivo were defined. The binding thermodynamics were comparable to that of an antigen-antibody reaction. Such synthetic peptides may provide a strategy for prophylaxis and treatment of LPS-mediated diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rustici, A -- Velucchi, M -- Faggioni, R -- Sironi, M -- Ghezzi, P -- Quataert, S -- Green, B -- Porro, M -- New York, N.Y. -- Science. 1993 Jan 15;259(5093):361-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biosynth Research Laboratories, Siena, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8420003" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding, Competitive ; Bordetella pertussis/chemistry ; Escherichia coli/chemistry ; Hydrogen-Ion Concentration ; Limulus Test ; Lipid A/chemistry/*metabolism/toxicity ; Lipopolysaccharides/chemistry/*metabolism/toxicity ; Mice ; Mice, Inbred BALB C ; Micelles ; Microscopy, Electron ; Molecular Sequence Data ; Peptides/chemical synthesis/chemistry/*metabolism ; Polymyxin B/chemistry/*metabolism ; Protein Conformation ; Temperature
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    Reversal of left-right asymmetry: a situs inversus mutation (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-30
    Description: A recessive mutation was identified in a family of transgenic mice that resulted in a reversal of left-right polarity (situs inversus) in 100 percent of the homozygous transgenic mice tested. Sequences that flanked the transgenic integration site were cloned and mapped to mouse chromosome 4, between the Tsha and Hxb loci. During early embryonic development, the direction of postimplantation turning, one of the earliest manifestations of left-right asymmetry, was reversed in homozygous transgenic embryos. This insertional mutation identifies a gene that controls embryonic turning and visceral left-right polarity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yokoyama, T -- Copeland, N G -- Jenkins, N A -- Montgomery, C A -- Elder, F F -- Overbeek, P A -- HD25340/HD/NICHD NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):679-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8480178" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Chromosome Mapping ; Cloning, Molecular ; Embryonic and Fetal Development/*genetics ; Female ; *Genes, Recessive ; Homozygote ; Male ; Mice ; Mice, Transgenic ; Mutagenesis, Insertional ; Situs Inversus/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The mice that roared (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1993 Nov 19;262(5137):1211.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235648" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression/*physiology ; Animals ; Brain/*metabolism ; Mice ; Mice, Knockout ; Receptors, Serotonin/genetics/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Cyclic ADP-ribose in beta cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Islam, M S -- Larsson, O -- Berggren, P O -- New York, N.Y. -- Science. 1993 Oct 22;262(5133):584-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211188" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Diphosphate Ribose/*analogs & derivatives/pharmacology/physiology ; Animals ; Calcium/*metabolism ; Cyclic ADP-Ribose ; Inositol Phosphates/pharmacology ; Islets of Langerhans/drug effects/*metabolism ; Mice ; Mice, Obese ; Microsomes/drug effects/metabolism ; Second Messenger Systems
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 31
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    Cyclic ADP-ribose and pancreatic beta cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Islam, M S -- Larsson, O -- Berggren, P O -- New York, N.Y. -- Science. 1993 Dec 3;262(5139):1499.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8248793" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Diphosphate Ribose/*analogs & derivatives/pharmacology ; Animals ; Cyclic ADP-Ribose ; Glucose/*pharmacology ; Islets of Langerhans/*drug effects ; Mice ; Mice, Obese
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  • 32
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    Requirement for a GTPase-activating protein in vesicle budding from the endoplasmic reticulum (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-05
    Description: The binding and hydrolysis of guanosine triphosphate (GTP) by the small GTP-binding protein Sar1p is required to form transport vesicles from the endoplasmic reticulum (ER) in Saccharomyces cerevisiae. Experiments revealed that an interaction between Sar1p and the Sec23p subunit of an oligomeric protein is also required for vesicle budding. The isolated Sec23p subunit and the oligomeric complex stimulated guanosine triphosphatase (GTPase) activity of Sar1p 10- to 15-fold but did not activate two other small GTP-binding proteins involved in vesicle traffic (Ypt1p and ARF). Activation of GTPase was inhibited by an antibody to Sec23p but not by an antibody that inhibits the budding activity of the other subunit of the Sec23p complex. Also, activation was thermolabile in pure samples of Sec23p that were isolated from two independent sec23 mutant strains. It appears that Sec23p represents a new class of GTPase-activating protein because its sequence shows no similarity to any known member of this family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoshihisa, T -- Barlowe, C -- Schekman, R -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1466-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8451644" target="_blank"〉PubMed〈/a〉
    Keywords: COP-Coated Vesicles ; Cloning, Molecular ; Endoplasmic Reticulum/*metabolism/ultrastructure ; Fungal Proteins/genetics/metabolism ; GTP-Binding Proteins/genetics/*metabolism ; GTPase-Activating Proteins ; Genes, Fungal ; Kinetics ; Macromolecular Substances ; *Monomeric GTP-Binding Proteins ; Mutagenesis ; Proteins/*metabolism ; Saccharomyces cerevisiae/genetics/*metabolism ; *Saccharomyces cerevisiae Proteins ; Spheroplasts/metabolism ; Vesicular Transport Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Enzyme may blunt cocaine's action (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morell, V -- New York, N.Y. -- Science. 1993 Mar 26;259(5103):1828.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456310" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Catalytic/*therapeutic use ; Antibodies, Monoclonal/*therapeutic use ; *Cocaine/immunology/metabolism ; Humans ; Mice ; Substance-Related Disorders/*drug therapy
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Pushing at the envelope (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jasny, B R -- New York, N.Y. -- Science. 1993 Oct 1;262(5130):11.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211115" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Genetic Testing ; Genetic Therapy ; *Human Genome Project ; Humans ; Mice
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    GDNF: a glial cell line-derived neurotrophic factor for midbrain dopaminergic neurons (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-21
    Description: A potent neurotrophic factor that enhances survival of midbrain dopaminergic neurons was purified and cloned. Glial cell line-derived neurotrophic factor (GDNF) is a glycosylated, disulfide-bonded homodimer that is a distantly related member of the transforming growth factor-beta superfamily. In embryonic midbrain cultures, recombinant human GDNF promoted the survival and morphological differentiation of dopaminergic neurons and increased their high-affinity dopamine uptake. These effects were relatively specific; GDNF did not increase total neuron or astrocyte numbers nor did it increase transmitter uptake by gamma-aminobutyric-containing and serotonergic neurons. GDNF may have utility in the treatment of Parkinson's disease, which is marked by progressive degeneration of midbrain dopaminergic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, L F -- Doherty, D H -- Lile, J D -- Bektesh, S -- Collins, F -- New York, N.Y. -- Science. 1993 May 21;260(5111):1130-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Synergen, Inc., Boulder, CO 80301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Astrocytes/cytology/drug effects ; Base Sequence ; Cell Differentiation/drug effects ; Cell Line ; Cell Survival/drug effects ; Cells, Cultured ; Cloning, Molecular ; Dopamine/*biosynthesis ; Glial Cell Line-Derived Neurotrophic Factor ; Humans ; Mesencephalon/cytology/*drug effects/metabolism ; Molecular Sequence Data ; Molecular Weight ; *Nerve Growth Factors ; Nerve Tissue Proteins/chemistry/genetics/isolation & purification/*pharmacology ; Neuroglia/*metabolism ; Neurons/cytology/*drug effects/metabolism ; Parkinson Disease/drug therapy ; Rats
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    T cell receptor specificity and diabetes in nonobese diabetic mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, S -- New York, N.Y. -- Science. 1993 Dec 3;262(5139):1582.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8267784" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diabetes Mellitus, Type 1/*immunology ; Mice ; Mice, Inbred NOD ; Mice, Transgenic ; Receptors, Antigen, T-Cell, alpha-beta/*genetics
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    The pluses of subtraction (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myers, R M -- New York, N.Y. -- Science. 1993 Feb 12;259(5097):942-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of California, San Francisco 94143-0444.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8094900" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; DNA/*chemistry ; DNA Probes ; Female ; Gene Deletion ; Humans ; Male ; Nucleic Acid Hybridization/*methods ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length
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    Progression to diabetes in nonobese diabetic (NOD) mice with transgenic T cell receptors (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-19
    Description: The T cell receptor (TCR) requirements in the pathogenesis of insulin-dependent diabetes were examined with transgenic NOD mice bearing nondisease-related TCR alpha and beta chains. In both TCR beta and TCR alpha beta transgenic NOD mice the beta chain transgene was expressed by 〉 98% of peripheral T cells. The alpha chain transgene was also highly expressed. Insulitis developed in both sets of transgenic animals with most of the lymphocytes in the lesion expressing the transgenic beta chain and with depletion of the endogenous TCR V beta genes. Nonetheless, NOD animals transgenic for TCR beta and TCR alpha beta developed diabetes similar to controls. Thus, skewing the TCR repertoire did not diminish autoimmune susceptibility in NOD mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lipes, M A -- Rosenzweig, A -- Tan, K N -- Tanigawa, G -- Ladd, D -- Seidman, J G -- Eisenbarth, G S -- New York, N.Y. -- Science. 1993 Feb 19;259(5098):1165-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joslin Diabetes Center, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8267690" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/physiology ; Animals ; Base Sequence ; Crosses, Genetic ; Diabetes Mellitus, Type 2/genetics/immunology/*physiopathology ; Female ; Gene Rearrangement, T-Lymphocyte ; Islets of Langerhans/immunology/pathology ; Male ; Mice ; Mice, Inbred NOD/*physiology ; Mice, Transgenic ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Pancreatic Diseases/genetics/immunology/pathology ; Polymerase Chain Reaction/methods ; Receptors, Antigen, T-Cell, alpha-beta/genetics/*physiology ; T-Lymphocytes/*immunology/pathology
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    A strategy for prophylactic vaccination against HIV (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salk, J -- Bretscher, P A -- Salk, P L -- Clerici, M -- Shearer, G M -- New York, N.Y. -- Science. 1993 May 28;260(5112):1270-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute for Biological Studies, San Diego, CA 92138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8098553" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines ; Acquired Immunodeficiency Syndrome/immunology/*prevention & control ; Adjuvants, Immunologic ; Animals ; CD4-Positive T-Lymphocytes/immunology ; Cytokines/immunology ; HIV Antibodies/biosynthesis ; HIV Antigens/immunology ; HIV Infections/immunology/*prevention & control ; Haplorhini ; Humans ; Immunity, Cellular ; Immunologic Memory ; Mice ; T-Lymphocytes, Cytotoxic/immunology ; *Vaccination
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 40
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    Tumor rejection after direct costimulation of CD8+ T cells by B7-transfected melanoma cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-15
    Description: A variety of tumors are potentially immunogenic but do not stimulate an effective anti-tumor immune response in vivo. Tumors may be capable of delivering antigen-specific signals to T cells, but may not deliver the costimulatory signals necessary for full activation of T cells. Expression of the costimulatory ligand B7 on melanoma cells was found to induce the rejection of a murine melanoma in vivo. This rejection was mediated by CD8+ T cells; CD4+ T cells were not required. These results suggest that B7 expression renders tumor cells capable of effective antigen presentation, leading to their eradication in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Townsend, S E -- Allison, J P -- CA57986/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 15;259(5093):368-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7678351" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens, CD80 ; Antigens, Surface/genetics/*immunology ; CD4-Positive T-Lymphocytes/immunology ; Cross Reactions ; Female ; Gene Expression Regulation ; Genetic Vectors ; Ligands ; *Lymphocyte Activation ; Melanoma/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Nude ; T-Lymphocytes, Regulatory/*immunology ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 41
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    Helper T cells without CD4: control of leishmaniasis in CD4-deficient mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: Expression of either the CD4 or CD8 glycoproteins discriminates two functionally distinct lineages of T lymphocytes. A null mutation in the gene encoding CD4 impairs the development of the helper cell lineage that is normally defined by CD4 expression. Infection of CD4-null mice with Leishmania has revealed a population of functional helper T cells that develops despite the absence of CD4. These CD8- alpha beta T cell receptor+ T cells are major histocompatibility complex class II-restricted and produce interferon-gamma when challenged with parasite antigens. These results indicate that T lymphocyte lineage commitment and peripheral function need not depend on the function of CD4.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Locksley, R M -- Reiner, S L -- Hatam, F -- Littman, D R -- Killeen, N -- AI30663/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1448-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco 94143-0654.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8367726" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/genetics/*immunology ; Antigens, CD8/immunology ; Antigens, Protozoan/immunology ; B-Lymphocytes/immunology ; Base Sequence ; CD4-CD8 Ratio ; Histocompatibility Antigens Class II/immunology ; Hypersensitivity, Delayed ; Interferon-gamma/biosynthesis/immunology ; Leishmania tropica/*immunology ; Leishmaniasis, Cutaneous/*immunology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Oligodeoxyribonucleotides ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; T-Lymphocytes/immunology ; T-Lymphocytes, Helper-Inducer/*immunology
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    Methylation and imprinting: from host defense to gene regulation? (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barlow, D P -- New York, N.Y. -- Science. 1993 Apr 16;260(5106):309-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology, Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8469984" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA/genetics/*metabolism ; *Dosage Compensation, Genetic ; Embryo, Mammalian/metabolism ; Fathers ; Female ; *Gene Expression Regulation ; Insulin-Like Growth Factor II/genetics ; Male ; Methylation ; Mice ; Models, Genetic ; Mothers ; Oocytes/metabolism ; Receptor, IGF Type 2/genetics ; Spermatozoa/metabolism
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    Regulation by heme of mitochondrial protein transport through a conserved amino acid motif (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-01-22
    Description: A conserved motif, termed the heme regulatory motif (HRM), was identified in the presequences of the erythroid delta-aminolevulinate synthase precursors and was shown to be involved in hemin inhibition of transport of these proteins into mouse mitochondria in vitro. When the HRM was inserted into the presequence of the ornithine transcarbamoylase precursor, a normally unregulated mitochondrial protein, it conferred hemin inhibition on the transport of the chimeric protein. The conserved cysteine within the HRM was shown by site-directed mutagenesis to be required for hemin inhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lathrop, J T -- Timko, M P -- 5 RO1 DK33304-06/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 22;259(5094):522-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Virginia, Charlottesville 22901.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8424176" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Aminolevulinate Synthetase/genetics/*metabolism ; Amino Acid Sequence ; Animals ; Biological Transport/drug effects ; Chickens ; Enzyme Precursors/*metabolism ; Erythrocytes/*enzymology ; Heme/*pharmacology ; Humans ; Intracellular Membranes/drug effects/metabolism ; Mice ; Mice, Inbred DBA ; Mitochondria, Liver/drug effects/*metabolism ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Regulatory Sequences, Nucleic Acid ; Sequence Homology, Amino Acid
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    Interleukin-2 receptor gamma chain: a functional component of the interleukin-4 receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-17
    Description: The interleukin-2 (IL-2) receptor gamma chain (IL-2R gamma) is an essential component of high- and intermediate-affinity IL-2 receptors. IL-2R gamma was demonstrated to be a component of the IL-4 receptor on the basis of chemical cross-linking data, the ability of IL-2R gamma to augment IL-4 binding affinity, and the requirement for IL-2R gamma in IL-4-mediated phosphorylation of insulin receptor substrate-1. The observation that IL-2R gamma is a functional component of the IL-4 receptor, together with the finding that IL-2R gamma associates with the IL-7 receptor, begins to elucidate why deficiency of this common gamma chain (gamma c) has a profound effect on lymphoid function and development, as seen in X-linked severe combined immunodeficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Russell, S M -- Keegan, A D -- Harada, N -- Nakamura, Y -- Noguchi, M -- Leland, P -- Friedmann, M C -- Miyajima, A -- Puri, R K -- Paul, W E -- New York, N.Y. -- Science. 1993 Dec 17;262(5141):1880-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Pulmonary and Molecular Immunology, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266078" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Cell Line, Transformed ; Genetic Linkage ; Humans ; Insulin Receptor Substrate Proteins ; Interleukin-4/metabolism ; L Cells (Cell Line) ; Mice ; Molecular Sequence Data ; Phosphoproteins/metabolism ; Phosphorylation ; Receptors, Interleukin-2/chemistry/genetics/*metabolism ; Receptors, Interleukin-4 ; Receptors, Mitogen/chemistry/genetics/*metabolism ; Severe Combined Immunodeficiency/genetics/immunology ; Signal Transduction ; Transfection ; X Chromosome
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    Naked DNA points way to vaccines (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1691-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456293" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Viral/*genetics/therapeutic use ; Influenza A virus/*genetics/immunology ; Mice ; Nucleoproteins/genetics/immunology ; Orthomyxoviridae Infections/*prevention & control ; *RNA-Binding Proteins ; Transfection ; Viral Core Proteins/genetics/immunology ; Viral Vaccines/*genetics
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    Regulation of V(D)J recombination activator protein RAG-2 by phosphorylation (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-14
    Description: Antigen receptor genes are assembled by site-specific DNA rearrangement. The recombination activator genes RAG-1 and RAG-2 are essential for this process, termed V(D)J rearrangement. The activity and stability of the RAG-2 protein have now been shown to be regulated by phosphorylation. In fibroblasts RAG-2 was phosphorylated predominantly at two serine residues, one of which affected RAG-2 activity in vivo. The threonine at residue 490 was phosphorylated by p34cdc2 kinase in vitro; phosphorylation at this site in vivo was associated with rapid degradation of RAG-2. Instability was transferred to chimeric proteins by a 90-residue portion of RAG-2. Mutation of the p34cdc2 phosphorylation site of the tumor suppressor protein p53 conferred a similar phenotype, suggesting that this association between phosphorylation and degradation is a general mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, W C -- Desiderio, S -- CA16519/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 May 14;260(5110):953-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493533" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; CDC2 Protein Kinase/metabolism ; Cell Line ; *DNA-Binding Proteins ; *Gene Rearrangement ; Humans ; Mice ; Molecular Sequence Data ; Mutation ; Nuclear Proteins ; Phosphorylation ; Proteins/chemistry/genetics/*metabolism ; Receptors, Antigen/*genetics ; Recombinant Fusion Proteins/metabolism ; Transfection ; Tumor Suppressor Protein p53/genetics
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  • 47
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    Presentation of a viral T cell epitope expressed in the CDR3 region of a self immunoglobulin molecule (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-08
    Description: Synthetic peptides corresponding to microbial epitopes stimulate T cell immunity but their immunogenicity is poor and their half-lives are short. A viral epitope inserted into the complementarity-determining region 3 (CDR3) loop of the heavy chain of a self immunoglobulin (Ig) molecule was generated from the Ig context and was presented by I-Ed class II molecules to virus-specific, CD4+ T cells. Chimeric Ig-peptide was presented 100 to 1000 times more efficiently than free synthetic peptide and was able to prime virus-specific T cells in vivo. These features suggest that antigenized Ig can provide an improved and safe vaccine for the presentation of microbial and other peptides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zaghouani, H -- Steinman, R -- Nonacs, R -- Shah, H -- Gerhard, W -- Bona, C -- AI13013/AI/NIAID NIH HHS/ -- AI18316/AI/NIAID NIH HHS/ -- AI24460/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Jan 8;259(5092):224-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7678469" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigen-Presenting Cells/*immunology ; Antigens, Viral/*immunology ; Arsenic/immunology ; *Arsenicals ; Base Sequence ; CD4-Positive T-Lymphocytes/immunology ; DNA/genetics ; Epitopes/*immunology ; Hemagglutinin Glycoproteins, Influenza Virus ; Hemagglutinins, Viral/genetics/immunology ; Histocompatibility Antigens Class II/immunology ; Immunoglobulin Heavy Chains/genetics/immunology ; Immunoglobulin Variable Region/genetics/immunology ; Immunoglobulins/genetics/*immunology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Mutagenesis ; Receptors, Fc/immunology ; Recombinant Fusion Proteins/immunology ; Transfection
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  • 48
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    Rapid assessment of drug susceptibilities of Mycobacterium tuberculosis by means of luciferase reporter phages (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-07
    Description: Effective chemotherapy of tuberculosis requires rapid assessment of drug sensitivity because of the emergence of multidrug-resistant Mycobacterium tuberculosis. Drug susceptibility was assessed by a simple method based on the efficient production of photons by viable mycobacteria infected with specific reporter phages expressing the firefly luciferase gene. Light production was dependent on phage infection, expression of the luciferase gene, and the level of cellular adenosine triphosphate. Signals could be detected within minutes after infection of virulent M. tuberculosis with reporter phages. Culture of conventional strains with antituberculosis drugs, including isoniazid or rifampicin, resulted in extinction of light production. In contrast, light signals after luciferase reporter phage infection of drug-resistant strains continued to be produced. Luciferase reporter phages may help to reduce the time required for establishing antibiotic sensitivity of M. tuberculosis strains from weeks to days and to accelerate screening for new antituberculosis drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jacobs, W R Jr -- Barletta, R G -- Udani, R -- Chan, J -- Kalkut, G -- Sosne, G -- Kieser, T -- Sarkis, G J -- Hatfull, G F -- Bloom, B R -- AI27235/AI/NIAID NIH HHS/ -- AI28927/AI/NIAID NIH HHS/ -- UO1AI30189/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 May 7;260(5109):819-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Albert Einstein College of Medicine, Bronx, NY 10461.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8484123" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Antitubercular Agents/*pharmacology ; Cloning, Molecular ; Drug Resistance, Microbial ; Luciferases/genetics/metabolism ; *Luminescent Measurements ; Microbial Sensitivity Tests/*methods ; Mycobacteriophages/genetics ; Mycobacterium/genetics/metabolism ; Mycobacterium bovis/drug effects/genetics/metabolism ; Mycobacterium tuberculosis/*drug effects/genetics/metabolism
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    Rapid loss of CD4+ T cells in human-PBL-SCID mice by noncytopathic HIV isolates (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-30
    Description: Human immunodeficiency virus (HIV) isolates differ in cell tropism, replication, pathogenicity, and syncytial induction in vitro. CD4+ T cells were enumerated in severe combined immunodeficient mice transplanted with human peripheral blood leukocytes (hu-PBL-SCID mice) and infected with HIV isolates with different in vitro cytopathicity. Two noncytopathic, macrophage-tropic strains, HIV-1SF162 and HIV-2UC1, induced extensive CD4+ T cell depletion, whereas HIV-1SF33, which is highly cytopathic for T cells in vitro, caused little CD4+ T cell depletion at equivalent virus burden. In vitro cytopathicity assays therefore do not predict CD4 depletion in the hu-PBL-SCID model.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mosier, D E -- Gulizia, R J -- MacIsaac, P D -- Torbett, B E -- Levy, J A -- AI24499/AI/NIAID NIH HHS/ -- AI29182/AI/NIAID NIH HHS/ -- AI30238/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):689-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8097595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *CD4-Positive T-Lymphocytes/immunology/microbiology ; Cytopathogenic Effect, Viral ; HIV Infections/*immunology/microbiology ; HIV-1/*pathogenicity/physiology ; HIV-2/*pathogenicity/physiology ; Humans ; Leukocyte Count ; Lymphopenia/*immunology ; Mice ; Mice, SCID ; Polymerase Chain Reaction ; T-Lymphocyte Subsets/immunology/microbiology ; Virus Replication
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    Generation of a mouse strain that produces immunoglobulin kappa chains with human constant regions (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-19
    Description: Humanized antibodies are highly efficient as immunotherapeutic reagents and have many advantages over rodent antibodies. A mouse strain was generated by gene targeting to replace the mouse kappa light chain constant (C) region gene with the human C kappa gene. Mice homozygous for the replacement mutation (C kappa R) produced normal concentrations of serum antibodies, most of which carry chimeric kappa light chains, and mounted normal immune responses to hapten-protein conjugates. This technology provides a feasible option for the generation of high-affinity humanized antibodies by means of the powerful somatic hypermutation-selection mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zou, Y R -- Gu, H -- Rajewsky, K -- New York, N.Y. -- Science. 1993 Nov 19;262(5137):1271-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235658" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/*immunology ; Base Sequence ; Gene Rearrangement ; *Genes, Immunoglobulin ; Humans ; Immunoglobulin Constant Regions/*biosynthesis/genetics ; Immunoglobulin Isotypes/biosynthesis ; Immunoglobulin kappa-Chains/*biosynthesis/genetics ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Mutation ; Polymerase Chain Reaction ; Recombinant Fusion Proteins/biosynthesis ; Stem Cells ; Transfection
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    Neuronal differentiation rescued by implantation of Weaver granule cell precursors into wild-type cerebellar cortex (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-16
    Description: The migration of postmitotic neurons away from compact, germinal zones is a critical step in neuronal differentiation in the developing brain. To study the molecular signals necessary for cerebellar granule cell migration in situ, precursor cells from the neurological mutant mouse weaver, an animal with phenotypic defects in migration, were implanted into the external germinal layer (EGL) of wild-type cerebellar cortex. In this region, labeled weaver precursor cells of the EGL progressed through all stages of granule neuron differentiation, including the extension of parallel fibers, migration through the molecular and Purkinje cell layers, positioning in the internal granule cell layer, and extension of dendrites. Thus, the weaver gene acts nonautonomously in vivo, and local cell interactions may induce early steps in neuronal differentiation that are required for granule cell migration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gao, W Q -- Hatten, M E -- New York, N.Y. -- Science. 1993 Apr 16;260(5106):367-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8469990" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Movement ; Cerebellar Cortex/*cytology ; Genes ; Mice ; Mice, Neurologic Mutants ; Microscopy, Fluorescence ; Models, Neurological ; Neurons/*cytology/physiology/transplantation ; Phenotype ; Stem Cell Transplantation ; Stem Cells/*cytology/physiology
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    Increased activity of L-type Ca2+ channels exposed to serum from patients with type I diabetes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-02
    Description: Type I diabetes [insulin-dependent diabetes mellitus (IDDM)] is an autoimmune disease associated with the destruction of pancreatic beta cells. Serum from patients with IDDM increased L-type calcium channel activity of insulin-producing cells and of GH3 cells derived from a pituitary tumor. The subsequent increase in the concentration of free cytoplasmic Ca2+ ([Ca2+]i) was associated with DNA fragmentation typical of programmed cell death or apoptosis. These effects of the serum were prevented by adding a blocker of voltage-activated L-type Ca2+ channels. When the serum was depleted of immunoglobulin M (IgM), it no longer affected [Ca2+]i. An IgM-mediated increase in Ca2+ influx may thus be part of the autoimmune reaction associated with IDDM and contribute to the destruction of beta cells in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Juntti-Berggren, L -- Larsson, O -- Rorsman, P -- Ammala, C -- Bokvist, K -- Wahlander, K -- Nicotera, P -- Dypbukt, J -- Orrenius, S -- Hallberg, A -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):86-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rolf Luft Center for Diabetes Research, Department of Endocrinology, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7686306" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Pyridinecarboxylic acid, ; 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ; ester/pharmacology ; Animals ; Apoptosis ; Calcium/*metabolism ; Calcium Channels/drug effects/*metabolism ; DNA Damage ; Diabetes Mellitus, Type 1/*immunology ; Humans ; Immunoglobulin M/*physiology ; Islets of Langerhans/drug effects/*metabolism ; Membrane Potentials ; Mice ; Pituitary Neoplasms/metabolism ; Tumor Cells, Cultured ; Verapamil/pharmacology
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    Cure of xenografted human carcinomas by BR96-doxorubicin immunoconjugates (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-09
    Description: Immunoconjugates (BR96-DOX) were prepared between chimeric monoclonal antibody BR96 and the anticancer drug doxorubicin. The monoclonal antibody binds an antigen related to Lewis Y that is abundantly expressed at the surface of cells from many human carcinomas; it has a high degree of tumor selectivity and is internalized after binding. BR96-DOX induced complete regressions and cures of xenografted human lung, breast, and colon carcinomas growing subcutaneously in athymic mice and cured 70 percent of mice bearing extensive metastases of a human lung carcinoma. Also, BR96-DOX cured 94 percent of athymic rats with subcutaneous human lung carcinoma, even though the rats, like humans and in contrast to mice, expressed the BR96 target antigen in normal tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trail, P A -- Willner, D -- Lasch, S J -- Henderson, A J -- Hofstead, S -- Casazza, A M -- Firestone, R A -- Hellstrom, I -- Hellstrom, K E -- New York, N.Y. -- Science. 1993 Jul 9;261(5118):212-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, NJ 08543.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8327892" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/administration & dosage/immunology/*therapeutic use ; Antigens, Neoplasm/immunology ; Antigens, Surface/immunology ; Breast Neoplasms/drug therapy ; Colonic Neoplasms/drug therapy ; Doxorubicin/administration & dosage/*therapeutic use ; Humans ; Immunotoxins/administration & dosage/*therapeutic use ; Lung Neoplasms/drug therapy ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplasms, Experimental/*drug therapy ; Rats ; Rats, Nude
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    Interleukin-7: a cofactor for V(D)J rearrangement of the T cell receptor beta gene (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-02
    Description: The diversity of the T cell receptor repertoire is generated by rearrangement of gene elements in immature thymocytes. To identify a thymic signal that induces this rearrangement, a variety of agents were tested for their ability to induce rearrangement of the T cell receptor beta gene in suspensions of thymocytes from mouse embryos at day 14 of gestation. Of 16 agents tested, only interleukin-7 (IL-7) induced V(D)J gene rearrangement and sustained expression of the RAG-1 and RAG-2 genes, which are known to control rearrangement. These data implicate IL-7, a cytokine that is abundantly expressed in embryonic thymus, in driving gene rearrangement during early T cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muegge, K -- Vila, M P -- Durum, S K -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):93-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biological Carcinogenesis and Development Program, Program Resources Inc./Dyncorp, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7686307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Cell Survival/drug effects ; Cells, Cultured ; *DNA-Binding Proteins ; Gene Expression ; *Gene Rearrangement, beta-Chain T-Cell Antigen Receptor ; Genes, RAG-1 ; Hematopoietic Cell Growth Factors/pharmacology ; Interleukin-7/*pharmacology ; Ionomycin/pharmacology ; Mice ; Molecular Sequence Data ; Organ Culture Techniques ; Proteins/genetics ; Stem Cell Factor ; T-Lymphocytes/cytology/*immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Thymus Gland/embryology/immunology ; Tumor Cells, Cultured
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    Requirement for CD8+ cells in T cell receptor peptide-induced clonal unresponsiveness (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-01
    Description: T cell receptor (TCR) vaccination in rats prevents the development of experimental allergic encephalomyelitis (EAE), an animal model of multiple sclerosis. The mechanism of this potential immunotherapy was examined by vaccinating mice with an immunogenic peptide fragment of the variable region of the TCR V beta 8.2 gene. Another immunogen that usually induces an immune response mediated by V beta 8.2+ T cells was subsequently inhibited because specific clonal unresponsiveness (anergy) had been induced. Depletion of CD8+ cells before TCR peptide vaccination blocked such inhibition. Thus, the clonal anergy was dependent on CD8+ T cells, and such immunoregulatory T cells may participate in the normal course of EAE.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gaur, A -- Ruberti, G -- Haspel, R -- Mayer, J P -- Fathman, C G -- AI 27989/AI/NIAID NIH HHS/ -- DK 39959/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):91-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8418501" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/administration & dosage ; Antigens, CD8/*immunology ; Encephalomyelitis, Autoimmune, Experimental/*immunology/prevention & control ; Lymph Nodes/immunology ; Lymphocyte Activation ; Lymphocyte Depletion ; Mice ; Mice, Inbred DBA ; Mice, Inbred Strains ; Receptors, Antigen, T-Cell/*immunology ; T-Lymphocyte Subsets/*immunology ; T-Lymphocytes/*immunology ; *Vaccines
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    Interleukin-2 receptor gamma chain: a functional component of the interleukin-7 receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-17
    Description: The interleukin-2 receptor gamma chain (IL-2R gamma) is a necessary component of functional IL-2 receptors. IL-2R gamma mutations result in X-linked severe combined immunodeficiency (XSCID) in humans, a disease characterized by the presence of few or no T cells. In contrast, SCID patients with IL-2 deficiency and IL-2-deficient mice have normal numbers of T cells, suggesting that IL-2R gamma is part of more than one cytokine receptor. By using chemical cross-linking, IL-2R gamma was shown to be physically associated with the IL-7 receptor. The presence of IL-2R gamma augmented both IL-7 binding affinity and the efficiency of internalization of IL-7. These findings may help explain the defects of XSCID. Given its role in more than one cytokine receptor system, the common gamma chain (gamma c) is proposed as the designation for IL-2R gamma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noguchi, M -- Nakamura, Y -- Russell, S M -- Ziegler, S F -- Tsang, M -- Cao, X -- Leonard, W J -- New York, N.Y. -- Science. 1993 Dec 17;262(5141):1877-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Pulmonary and Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266077" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Cell Line ; Genetic Linkage ; Interleukin-7/*metabolism ; L Cells (Cell Line) ; Mice ; Receptors, Interleukin/chemistry/genetics/*metabolism ; Receptors, Interleukin-2/chemistry/genetics/*metabolism ; Receptors, Interleukin-7 ; Severe Combined Immunodeficiency/genetics/immunology ; T-Lymphocytes/immunology ; Transfection ; X Chromosome
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    Neuroprotective effects of glutamate antagonists and extracellular acidity (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-04
    Description: Glutamate antagonists protect neurons from hypoxic injury both in vivo and in vitro, but in vitro studies have not been done under the acidic conditions typical of hypoxia-ischemia in vivo. Consistent with glutamate receptor antagonism, extracellular acidity reduced neuronal death in murine cortical cultures that were deprived of oxygen and glucose. Under these acid conditions, N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate-kainate antagonists further reduced neuronal death, such that some neurons tolerated prolonged oxygen and glucose deprivation almost as well as did astrocytes. Neuroprotection induced by this combination exceeded that induced by glutamate antagonists alone, suggesting that extracellular acidity has beneficial effects beyond the attenuation of ionotropic glutamate receptor activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaku, D A -- Giffard, R G -- Choi, D W -- NS 01425/NS/NINDS NIH HHS/ -- NS 26907/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 4;260(5113):1516-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8389056" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death/drug effects ; Cell Hypoxia/physiology ; Cells, Cultured ; Cerebral Cortex/cytology ; *Excitatory Amino Acid Antagonists ; Extracellular Space/*metabolism ; Glucose/deficiency ; *Hydrogen-Ion Concentration ; L-Lactate Dehydrogenase/metabolism ; Mice ; Nerve Degeneration/drug effects ; Neurons/*drug effects/enzymology ; Receptors, AMPA ; Receptors, Kainic Acid ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors
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    Molecular mechanism of transcription-repair coupling (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-04-02
    Description: Lesions in the transcribed strand block transcription and are repaired more rapidly than lesions in the nontranscribed (coding) strand which do not block RNA polymerase (RNAP). It has been shown previously that in Escherichia coli the mfd (mutation frequency decline) gene is necessary for strand-specific repair. The mfd gene was cloned and sequenced and the Mfd protein was purified and used to reconstitute strand-specific repair in a completely defined system. The mfd gene encodes a protein of 130 kilodaltons and contains the so-called "helicase motifs," a leucine zipper motif, and regions of sequence similarity to UvrB and RecG proteins. The Mfd protein was shown to (i) displace RNAP stalled at a lesion in an adenosine triphosphate-dependent reaction, (ii) bind to the damage recognition subunit (UvrA) of the excision nuclease, and (iii) stimulate the repair of the transcribed strand only when transcription is taking place. Thus, Mfd appears to target the transcribed strand for repair by recognizing a stalled RNAP and actively recruiting the repair enzyme to the transcription blocking lesion as it dissociates the stalled RNAP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selby, C P -- Sancar, A -- New York, N.Y. -- Science. 1993 Apr 2;260(5104):53-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill 27599.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8465200" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacterial Proteins/chemistry/*genetics/metabolism ; Base Sequence ; Binding Sites ; Cloning, Molecular ; *DNA Helicases ; DNA Repair/*genetics ; DNA, Bacterial/metabolism ; DNA-Directed RNA Polymerases/metabolism ; Endodeoxyribonucleases/metabolism ; Escherichia coli/*genetics ; *Escherichia coli Proteins ; Leucine Zippers ; Molecular Sequence Data ; Multienzyme Complexes/chemistry/genetics ; Mutation/genetics ; Transcription Factors/chemistry/*genetics/metabolism ; *Transcription, Genetic
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    'Bubble boy' paradox resolved (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nowak, R -- New York, N.Y. -- Science. 1993 Dec 17;262(5141):1818.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266068" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Genetic Linkage ; Humans ; Mice ; Mutation ; Receptors, Interleukin/chemistry/genetics/metabolism ; Receptors, Interleukin-2/*chemistry/genetics/metabolism ; Receptors, Interleukin-4 ; Receptors, Interleukin-7 ; Receptors, Mitogen/*chemistry/genetics/metabolism ; Severe Combined Immunodeficiency/genetics/*immunology ; X Chromosome
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Organic synthesis of prostaglandins: advancing biology (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noyori, R -- Suzuki, M -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):44-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Nagoya University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8418493" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Animals ; Antineoplastic Agents/chemical synthesis/therapeutic use ; Epoprostenol/pharmacology ; Leukemia L1210/metabolism ; Mice ; Molecular Structure ; Prostaglandins/*chemical synthesis/metabolism/therapeutic use ; Receptors, Prostaglandin/physiology ; Tumor Cells, Cultured
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    Transgenic mice display a class (switching) act (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aldhous, P -- New York, N.Y. -- Science. 1993 Nov 19;262(5137):1212-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235650" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantibodies/biosynthesis/immunology ; B-Lymphocytes/*immunology ; *Genes, Immunoglobulin ; *Immunoglobulin Class Switching ; Immunoglobulins/biosynthesis ; Mice ; Mice, Knockout ; Mice, Transgenic/*genetics/immunology ; Recombinant Fusion Proteins/biosynthesis/immunology
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    Imanishi-Kari says her new data shows she was right (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Travis, J -- New York, N.Y. -- Science. 1993 May 21;260(5111):1073-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biomedical Research ; Gene Rearrangement ; *Genes, Immunoglobulin ; History, 20th Century ; Hybridomas ; Immunoglobulin Idiotypes/*genetics ; Information Dissemination ; Mice ; Mice, Transgenic ; Scientific Misconduct
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    Antagonism of catecholamine receptor signaling by expression of cytoplasmic domains of the receptors (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-05
    Description: The actions of many hormones and neurotransmitters are mediated by the members of a superfamily of receptors coupled to heterotrimeric guanine nucleotide-binding proteins (G proteins). These receptors are characterized by a highly conserved topographical arrangement in which seven transmembrane domains are connected by intracellular and extracellular loops. The interaction between these receptors and G proteins is mediated in large part by the third intracellular loop of the receptor. Coexpression of the third intracellular loop of the alpha 1B-adrenergic receptor with its parent receptor inhibited receptor-mediated activation of phospholipase C. The inhibition extended to the closely related alpha 1C-adrenergic receptor subtype, but not the phospholipase C-coupled M1 muscarinic acetylcholine receptor nor the adenylate cyclase-coupled D1A dopamine receptor. These results suggest that the receptor-G protein interface may represent a target for receptor antagonist drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luttrell, L M -- Ostrowski, J -- Cotecchia, S -- Kendall, H -- Lefkowitz, R J -- HL16037/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1453-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8383880" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Cloning, Molecular ; Cyclic AMP/metabolism ; Cytoplasm/metabolism ; GTP-Binding Proteins/*metabolism ; Globins/genetics ; Glutathione Transferase/genetics/metabolism ; Humans ; Inositol Phosphates/metabolism ; Kinetics ; Molecular Sequence Data ; Muscarinic Antagonists ; Oligodeoxyribonucleotides ; Plasmids ; Protein Structure, Secondary ; Receptors, Adrenergic, alpha/genetics/*metabolism ; Receptors, Dopamine D1/antagonists & inhibitors/genetics/*metabolism ; Receptors, Muscarinic/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Transfection ; Type C Phospholipases/metabolism
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    Inhibition of viral replication by interferon-gamma-induced nitric oxide synthase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: Interferons (IFNs) induce antiviral activity in many cell types. The ability of IFN-gamma to inhibit replication of ectromelia, vaccinia, and herpes simplex-1 viruses in mouse macrophages correlated with the cells' production of nitric oxide (NO). Viral replication was restored in IFN-gamma-treated macrophages exposed to inhibitors of NO synthase. Conversely, epithelial cells with no detectable NO synthesis restricted viral replication when transfected with a complementary DNA encoding inducible NO synthase or treated with organic compounds that generate NO. In mice, an inhibitor of NO synthase converted resolving ectromelia virus infection into fulminant mousepox. Thus, induction of NO synthase can be necessary and sufficient for a substantial antiviral effect of IFN-gamma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karupiah, G -- Xie, Q W -- Buller, R M -- Nathan, C -- Duarte, C -- MacMicking, J D -- CA43610/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1445-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7690156" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/*biosynthesis/metabolism ; Animals ; Arginine/analogs & derivatives/pharmacology ; Cell Line ; Cells, Cultured ; Ectromelia virus/drug effects/*physiology ; Ectromelia, Infectious/microbiology ; Enzyme Induction ; Female ; Humans ; Interferon-gamma/*pharmacology ; Macrophages/*microbiology ; Mice ; Mice, Inbred C57BL ; Nitric Oxide/metabolism/pharmacology ; Nitric Oxide Synthase ; Simplexvirus/drug effects/physiology ; Transfection ; Vaccinia virus/drug effects/physiology ; *Virus Replication/drug effects ; omega-N-Methylarginine
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    Developmental regulation of neural response to FGF-1 and FGF-2 by heparan sulfate proteoglycan (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-02
    Description: Murine neural precursor cells and cell lines derived from them are stimulated by members of the heparin-binding fibroblast growth factor (FGF) family. The activity of FGF is regulated by heparan sulfate proteoglycans (HSPGs), and this interaction is an essential prerequisite for the binding of growth factor to the signal transducing receptors. Messenger RNA for FGF-2 was detectable in the neuroepithelium at embryonic day 9, and the HSPGs produced by these cells at this time preferentially bound FGF-2. However, at embryonic day 11, when messenger RNA for FGF-1 was first detectable, there was a switch in the binding specificity of the HSPG to FGF-1. Thus, a single species of HSPG undergoes a rapid, tightly controlled change in growth factor-binding specificity concomitant with the temporal expression of the FGFs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nurcombe, V -- Ford, M D -- Wildschut, J A -- Bartlett, P F -- New York, N.Y. -- Science. 1993 Apr 2;260(5104):103-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7682010" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Culture Media, Conditioned ; Epithelium/chemistry/embryology ; Fibroblast Growth Factor 1/genetics/*pharmacology ; Fibroblast Growth Factor 2/genetics/*pharmacology ; Gene Expression ; Gestational Age ; Heparan Sulfate Proteoglycans ; Heparitin Sulfate/*pharmacology ; Mice ; Molecular Weight ; Nervous System/chemistry/*embryology/metabolism ; Neurons/cytology ; Polysaccharide-Lyases/metabolism ; Proteoglycans/*pharmacology ; RNA, Messenger/analysis ; Signal Transduction/physiology ; Stem Cells/cytology
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    Mice lacking TdT: mature animals with an immature lymphocyte repertoire (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-27
    Description: In adult animals, template-independent (or N) nucleotides are frequently added during the rearrangement of variable (V), diversity (D), and joining (J) segments of lymphocyte receptor genes, greatly enhancing junctional diversity. Receptor genes from adult mice carrying a mutation in the terminal deoxynucleotidyl transferase (TdT) gene have few N nucleotides, providing proof that this enzyme is essential for creating diversity. Unlike those from normal adults, receptor genes from adult mutant mice show extensive evidence of homology-directed recombination, suggesting that TdT blocks this process. Thus, switch-on of the TdT gene during the first week after birth provokes an even greater expansion of lymphocyte receptor diversity than had previously been thought.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gilfillan, S -- Dierich, A -- Lemeur, M -- Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1993 Aug 27;261(5125):1175-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes du CNRS, Institut de Chimie Biologique, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8356452" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA Nucleotidylexotransferase/genetics/*metabolism ; Gene Rearrangement, B-Lymphocyte ; Gene Rearrangement, T-Lymphocyte ; *Genes, Immunoglobulin ; Immunoglobulin Joining Region/genetics ; Immunoglobulin Variable Region/genetics ; Lymphocytes/*immunology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Nucleotides/*metabolism ; Receptors, Antigen, T-Cell/*genetics ; Recombination, Genetic
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    Differential T cell costimulatory requirements in CD28-deficient mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-30
    Description: T cell receptor stimulation without costimulation is insufficient for the induction of an optimal immune response. It is thought that engagement of the CD28 molecule with its ligand B7 provides an essential costimulatory signal without which full activation of T cells cannot occur. A mouse strain with a defective CD28 gene was established. Development of T and B cells in the CD28-deficient mice appeared normal. However, T lymphocytes derived from CD28-/- mutant mice had impaired responses to lectins. Lectin stimulation did not trigger interleukin-2 (IL-2) production, IL-2 receptor alpha expression was significantly decreased, and exogenous IL-2 only partially rescued the CD28 defect. Basal immunoglobulin (Ig) concentrations in CD28-deficient mice were about one-fifth of those found in wild-type controls, with low titers of IgG1 and IgG2b but an increase in IgG2a. In addition, activity of T helper cells in CD28-/- mice was reduced and immunoglobulin class switching was diminished after infection with vesicular stomatitis virus. However, cytotoxic T cells could still be induced and the mice showed delayed-type hypersensitivity after infection with lymphocytic choriomeningitis virus. Thus, CD28 is not required for all T cell responses in vivo, suggesting that alternative costimulatory pathways may exist.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shahinian, A -- Pfeffer, K -- Lee, K P -- Kundig, T M -- Kishihara, K -- Wakeham, A -- Kawai, K -- Ohashi, P S -- Thompson, C B -- Mak, T W -- New York, N.Y. -- Science. 1993 Jul 30;261(5121):609-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Biophysics and Immunology, University of Toronto, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7688139" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/blood ; Antigens, CD/genetics/*immunology ; Antigens, CD28 ; Antigens, CD80 ; Antigens, Differentiation, T-Lymphocyte/genetics/*immunology ; Antigens, Surface/immunology ; B-Lymphocytes/immunology ; Concanavalin A/pharmacology ; Immunoglobulins/blood ; Interleukin-2/biosynthesis/pharmacology ; *Lymphocyte Activation ; Lymphocytic Choriomeningitis/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Mutant Strains ; Mutation ; Receptors, Interleukin-2/metabolism ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Helper-Inducer/immunology ; Vesicular stomatitis Indiana virus/immunology ; Virus Diseases/immunology
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    Multiple defects of immune cell function in mice with disrupted interferon-gamma genes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-19
    Description: Interferon-gamma (IFN-gamma) is a pleiotrophic cytokine with immunomodulatory effects on a variety of immune cells. Mice with a targeted disruption of the IFN-gamma gene were generated. These mice developed normally and were healthy in the absence of pathogens. However, mice deficient in IFN-gamma had impaired production of macrophage antimicrobial products and reduced expression of macrophage major histocompatibility complex class II antigens. IFN-gamma-deficient mice were killed by a sublethal dose of the intracellular pathogen Mycobacterium bovis. Splenocytes exhibited uncontrolled proliferation in response to mitogen and alloantigen. After a mixed lymphocyte reaction, T cell cytolytic activity was enhanced against allogeneic target cells. Resting splenic natural killer cell activity was reduced in IFN-gamma-deficient mice. Thus, IFN-gamma is essential for the function of several cell types of the murine immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dalton, D K -- Pitts-Meek, S -- Keshav, S -- Figari, I S -- Bradley, A -- Stewart, T A -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1739-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genentech Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456300" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cytotoxicity, Immunologic ; Histocompatibility Antigens Class II/immunology ; *Immunity ; Interferon-gamma/*genetics/physiology ; Isoantigens/immunology ; Killer Cells, Natural/immunology ; Lymphocyte Culture Test, Mixed ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Mycobacterium bovis ; Nitric Oxide/metabolism ; Spleen/cytology/immunology ; T-Lymphocytes/immunology ; Transfection ; Tuberculosis/immunology
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    A stimulating new approach to cancer treatment (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-01-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Travis, J -- New York, N.Y. -- Science. 1993 Jan 15;259(5093):310-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7678350" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD80 ; Antigens, Surface/*genetics ; *Genetic Therapy ; Humans ; *Immunotherapy ; Killer Cells, Natural/*immunology ; Mice ; Neoplasms/*therapy
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    The Caenorhabditis elegans unc-17 gene: a putative vesicular acetylcholine transporter (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-30
    Description: Mutations in the unc-17 gene of the nematode Caenorhabditis elegans produce deficits in neuromuscular function. This gene was cloned and complementary DNAs were sequenced. On the basis of sequence similarity to mammalian vesicular transporters of biogenic amines and of localization to synaptic vesicles of cholinergic neurons in C. elegans, unc-17 likely encodes the vesicular transporter of acetylcholine. Mutations that eliminated all unc-17 gene function were lethal, suggesting that the acetylcholine transporter is essential. Molecular analysis of unc-17 mutations will allow the correlation of specific parts of the gene (and the protein) with observed functional defects. The mutants will also be useful for the isolation of extragenic suppressors, which could identify genes encoding proteins that interact with UNC-17.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alfonso, A -- Grundahl, K -- Duerr, J S -- Han, H P -- Rand, J B -- R01 GM038679/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 30;261(5121):617-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular and Cell Biology, Oklahoma Medical Research Foundation, Oklahoma City 73104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8342028" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*metabolism ; Alleles ; Amino Acid Sequence ; Animals ; Caenorhabditis elegans/chemistry/cytology/*genetics ; *Caenorhabditis elegans Proteins ; Carrier Proteins/analysis/chemistry/*genetics ; Cloning, Molecular ; *Genes, Helminth ; Helminth Proteins/analysis/chemistry/*genetics ; *Membrane Transport Proteins ; Molecular Sequence Data ; Mutation ; Neurons/*chemistry ; Parasympathetic Nervous System/chemistry ; Phenotype ; Sequence Alignment ; Synaptic Vesicles/*chemistry ; Vesicular Acetylcholine Transport Proteins ; *Vesicular Transport Proteins
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    Inhibition of transcriptional regulator Yin-Yang-1 by association with c-Myc (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-17
    Description: Yin-Yang-1 (YY1) regulates the transcription of many genes, including the oncogenes c-fos and c-myc. Depending on the context, YY1 acts as a transcriptional repressor, a transcriptional activator, or a transcriptional initiator. The yeast two-hybrid system was used to screen a human complementary DNA (cDNA) library for proteins that associate with YY1, and a c-myc cDNA was isolated. Affinity chromatography confirmed that YY1 associates with c-Myc but not with Max. In cotransfections, c-Myc inhibits both the repressor and the activator functions of YY1, which suggests that one way c-Myc acts is by modulating the activity of YY1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shrivastava, A -- Saleque, S -- Kalpana, G V -- Artandi, S -- Goff, S P -- Calame, K -- CA 38571/CA/NCI NIH HHS/ -- GM29361/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Dec 17;262(5141):1889-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, Columbia University College of Physicians and Surgeons, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266081" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adenovirus E1A Proteins/metabolism ; Animals ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Basic-Leucine Zipper Transcription Factors ; DNA-Binding Proteins/antagonists & inhibitors/genetics/*metabolism/pharmacology ; Erythroid-Specific DNA-Binding Factors ; Helix-Loop-Helix Motifs ; Humans ; Mice ; Proto-Oncogene Proteins c-myc/*metabolism/pharmacology ; Recombinant Fusion Proteins/metabolism ; Transcription Factors/antagonists & inhibitors/genetics/*metabolism/pharmacology ; Transfection ; Tumor Cells, Cultured ; Upstream Stimulatory Factors ; YY1 Transcription Factor ; *Zinc Fingers
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    Heterologous protection against influenza by injection of DNA encoding a viral protein (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-19
    Description: Cytotoxic T lymphocytes (CTLs) specific for conserved viral antigens can respond to different strains of virus, in contrast to antibodies, which are generally strain-specific. The generation of such CTLs in vivo usually requires endogenous expression of the antigen, as occurs in the case of virus infection. To generate a viral antigen for presentation to the immune system without the limitations of direct peptide delivery or viral vectors, plasmid DNA encoding influenza A nucleoprotein was injected into the quadriceps of BALB/c mice. This resulted in the generation of nucleoprotein-specific CTLs and protection from a subsequent challenge with a heterologous strain of influenza A virus, as measured by decreased viral lung titers, inhibition of mass loss, and increased survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ulmer, J B -- Donnelly, J J -- Parker, S E -- Rhodes, G H -- Felgner, P L -- Dwarki, V J -- Gromkowski, S H -- Deck, R R -- DeWitt, C M -- Friedman, A -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1745-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Research, Merck Research Laboratories, West Point, PA 19486.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456302" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA, Viral/*genetics/therapeutic use ; Gene Expression ; Genetic Vectors ; Histocompatibility Antigens Class I/immunology ; Immunization ; Influenza A virus/*genetics/immunology/isolation & purification ; Lung/microbiology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Muscles/metabolism ; Nucleoproteins/*genetics/*immunology ; Orthomyxoviridae Infections/microbiology/*prevention & control ; Plasmids ; *RNA-Binding Proteins ; T-Lymphocytes, Cytotoxic/immunology ; Transfection ; Viral Core Proteins/*genetics/*immunology ; Viral Vaccines/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Released form of CNTF receptor alpha component as a soluble mediator of CNTF responses (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-19
    Description: The alpha component of the receptor for ciliary neurotrophic factor (CNTF) differs from other known growth factor receptors in that it is anchored to cell membranes by a glycosylphosphatidylinositol linkage. One possible function of this type of linkage is to allow for the regulated release of this receptor component. Cell lines not normally responsive to CNTF responded to treatment with a combination of CNTF and a soluble form of the CNTF alpha receptor component. These findings not only demonstrate that the CNTF receptor alpha chain is a required component of the functional CNTF receptor complex but also reveal that it can function in soluble form as part of a heterodimeric ligand. Potential physiological roles for the soluble CNTF receptor are suggested by its presence in cerebrospinal fluid and by its release from skeletal muscle in response to peripheral nerve injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, S -- Aldrich, T H -- Ip, N Y -- Stahl, N -- Scherer, S -- Farruggella, T -- DiStefano, P S -- Curtis, R -- Panayotatos, N -- Gascan, H -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1736-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, Inc., Tarrytown, NY 10591.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7681218" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects ; Cell Division/drug effects ; Cell Membrane/metabolism ; Ciliary Neurotrophic Factor ; Cloning, Molecular ; Gene Expression ; Glycosylphosphatidylinositols/metabolism ; Growth Inhibitors/pharmacology ; Hematopoietic Stem Cells/cytology/drug effects ; Humans ; Interleukin-6/pharmacology ; Leukemia Inhibitory Factor ; Lymphokines/pharmacology ; Mice ; Muscle Denervation ; Muscles/innervation/metabolism ; Nerve Tissue Proteins/*pharmacology ; Phosphatidylinositol Diacylglycerol-Lyase ; Phosphoric Diester Hydrolases/metabolism ; Phosphotyrosine ; RNA, Messenger/genetics ; Rats ; Receptor, Ciliary Neurotrophic Factor ; Receptors, Cell Surface/chemistry/*physiology ; Signal Transduction/physiology ; Tumor Cells, Cultured ; Tyrosine/analogs & derivatives/metabolism
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    A faster walk along the genome (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aldhous, P -- New York, N.Y. -- Science. 1993 May 21;260(5111):1075.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493549" target="_blank"〉PubMed〈/a〉
    Keywords: *Base Sequence ; Cloning, Molecular ; DNA/*genetics ; Oligodeoxyribonucleotides/*genetics ; Sequence Analysis, DNA/*methods
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Development of mature CD8+ thymocytes: selection rather than instruction? (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-13
    Description: The role of major histocompatibility complex (MHC) molecules in T cell differentiation was investigated by comparison of thymocyte subpopulations in wild-type mice and beta 2-microglobulin (beta 2M) mutant mice deficient in MHC class I expression and mature CD8+ cells. On the basis of surface markers, glucocorticoid resistance, in vitro differentiation capacity, and absence in beta 2 M-l- mice, CD4intermediateCD8hi cells with high expression of alpha beta T cell receptor (TCR alpha beta) were identified as having been positively selected by MHC class I for development into mature CD8+ T cells. Activated CD4intCD8hi cells bearing intermediate rather than high amounts of TCR were present in both wild-type and beta 2M-l- animals. These data suggest that recognition of MHC class I molecules is required for full maturation to CD8+ T cells, but not for receptor-initiated commitment to the CD8+ lineage, consistent with a stochastic (selection) model of thymocyte development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van Meerwijk, J P -- Germain, R N -- New York, N.Y. -- Science. 1993 Aug 13;261(5123):911-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Biology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8102208" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/analysis ; Antigens, CD8/*analysis ; CD4-Positive T-Lymphocytes/cytology/immunology ; Cell Differentiation ; Dexamethasone/pharmacology ; Histocompatibility Antigens Class I/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Phenotype ; Receptors, Antigen, T-Cell, alpha-beta/*analysis ; T-Lymphocyte Subsets/cytology/drug effects/*immunology
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    DNA sequence determination by hybridization: a strategy for efficient large-scale sequencing (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-11
    Description: The concept of sequencing by hybridization (SBH) makes use of an array of all possible n-nucleotide oligomers (n-mers) to identify n-mers present in an unknown DNA sequence. Computational approaches can then be used to assemble the complete sequence. As a validation of this concept, the sequences of three DNA fragments, 343 base pairs in length, were determined with octamer oligonucleotides. Possible applications of SBH include physical mapping (ordering) of overlapping DNA clones, sequence checking, DNA fingerprinting comparisons of normal and disease-causing genes, and the identification of DNA fragments with particular sequence motifs in complementary DNA and genomic libraries. The SBH techniques may accelerate the mapping and sequencing phases of the human genome project.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drmanac, R -- Drmanac, S -- Strezoska, Z -- Paunesku, T -- Labat, I -- Zeremski, M -- Snoddy, J -- Funkhouser, W K -- Koop, B -- Hood, L -- New York, N.Y. -- Science. 1993 Jun 11;260(5114):1649-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biological and Medical Research Division, Argonne National Laboratory, IL 60439.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8503011" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cloning, Molecular ; Humans ; Macaca mulatta ; Molecular Sequence Data ; *Nucleic Acid Hybridization ; Oligonucleotide Probes ; Sequence Analysis, DNA/*methods
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    WT1-mediated growth suppression of Wilms tumor cells expressing a WT1 splicing variant (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-24
    Description: A human Wilms tumor cell line (RM1) was developed to test the tumor suppressor activity of WT1, a zinc finger transcription factor that is expressed in the developing human kidney and is mutationally inactivated in a subset of Wilms tumors. Transfection of each of four wild-type WT1 isoforms suppressed the growth of RM1 cells. The endogenous WT1 transcript in these cells was devoid of exon 2 sequences, a splicing alteration that was also detected in varying amounts in all Wilms tumors tested but not in normal kidney. Production of this abnormal transcript, which encodes a functionally altered protein, may represent a distinct mechanism for inactivating WT1 in Wilms tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haber, D A -- Park, S -- Maheswaran, S -- Englert, C -- Re, G G -- Hazen-Martin, D J -- Sens, D A -- Garvin, A J -- CA37887/CA/NCI NIH HHS/ -- CA58596/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Dec 24;262(5142):2057-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics, Massachusetts General Hospital Cancer Center, Boston 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266105" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Division/genetics ; DNA-Binding Proteins/biosynthesis/*genetics/physiology ; Genes, Wilms Tumor/genetics/*physiology ; Humans ; Mice ; Mice, Nude ; Molecular Sequence Data ; Neoplasm Transplantation ; RNA, Messenger/genetics ; Tumor Cells, Cultured ; WT1 Proteins ; Wilms Tumor/*genetics/*pathology
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    mSlo, a complex mouse gene encoding "maxi" calcium-activated potassium channels (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-09
    Description: Complementary DNAs (cDNAs) from mSlo, a gene encoding calcium-activated potassium channels, were isolated from mouse brain and skeletal muscle, sequenced, and expressed in Xenopus oocytes. The mSlo-encoded channel resembled "maxi" or BK (high conductance) channel types; single channel conductance was 272 picosiemens with symmetrical potassium concentrations. Whole cell and single channel currents were blocked by charybdotoxin, iberiotoxin, and tetraethylammonium ion. A large number of variant mSlo cDNAs were isolated, indicating that several diverse mammalian BK channel types are produced by a single gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Butler, A -- Tsunoda, S -- McCobb, D P -- Wei, A -- Salkoff, L -- R01 NS24785-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 9;261(5118):221-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7687074" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Amino Acid Sequence ; Animals ; Calcium/metabolism/*pharmacology ; Charybdotoxin ; DNA/genetics ; Drosophila ; Electric Conductivity ; Large-Conductance Calcium-Activated Potassium Channels ; Membrane Proteins/chemistry/*genetics ; Mice ; Molecular Sequence Data ; Oocytes/metabolism ; Peptides/pharmacology ; Potassium/metabolism ; Potassium Channels/chemistry/drug effects/*genetics/metabolism ; *Potassium Channels, Calcium-Activated ; RNA/genetics ; RNA, Complementary ; Scorpion Venoms/pharmacology ; Sodium/metabolism ; Tetraethylammonium ; Tetraethylammonium Compounds/pharmacology ; Transcription, Genetic ; Xenopus
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    Ixr1, a yeast protein that binds to platinated DNA and confers sensitivity to cisplatin (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-30
    Description: Structure-specific recognition proteins (SSRPs) bind to DNA containing intrastrand cross-links formed by the anticancer drug cisplatin. A yeast gene encoding an SSRP, designated IXR1, was cloned and sequenced. The Ixr1 protein, a member of the high mobility group-box protein family, bound specifically to DNA modified with cisplatin but not inactive platinum compounds. A yeast strain with an inactivated IXR1 gene was half as sensitive to cisplatin and accumulated one-third as many platinum-DNA lesions after treatment with cisplatin as the parental strain. These findings suggest that SSRPs play a role in mediating the cytotoxicity of cisplatin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, S J -- Kellett, P J -- Lippard, S J -- New York, N.Y. -- Science. 1993 Jul 30;261(5121):603-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8342024" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cisplatin/*metabolism/*pharmacology ; Cloning, Molecular ; DNA/*metabolism ; *DNA Adducts ; DNA, Fungal/*metabolism ; *DNA-Binding Proteins ; Fungal Proteins/chemistry/genetics/*metabolism ; Genes, Fungal ; High Mobility Group Proteins/chemistry/genetics/*metabolism ; Molecular Sequence Data ; Saccharomyces cerevisiae/chemistry/drug effects/genetics/*metabolism ; *Saccharomyces cerevisiae Proteins
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    Identification of the SH3 domain of GAP as an essential sequence for Ras-GAP-mediated signaling (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-22
    Description: Guanosine triphosphatase activating protein (GAP) is an essential component of Ras signaling pathways. GAP functions in different cell types as a deactivator and a transmitter of cellular Ras signals. A domain (amino acids 275 to 351) encompassing the Src homology region 3 (SH3) of GAP was found to be essential for GAP signaling. A monoclonal antibody was used to block germinal vesicle breakdown (GVBD) induced by the oncogenic protein Ha-ras Lys12 in Xenopus oocytes. The monoclonal antibody, which was found to recognize the peptide containing amino acids 275 to 351 within the amino-terminal domain of GAP, did not modify the stimulation of the Ha-Ras-GTPase by GAP. Injection of peptides corresponding to amino acids 275 to 351 and 317 to 326 blocked GVBD induced by insulin or by Ha-Ras Lys12 but not that induced by progesterone. These findings confirm that GAP is an effector for Ras in Xenopus oocytes and that the SH3 domain is essential for signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duchesne, M -- Schweighoffer, F -- Parker, F -- Clerc, F -- Frobert, Y -- Thang, M N -- Tocque, B -- New York, N.Y. -- Science. 1993 Jan 22;259(5094):525-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rhone Poulenc Rorer, Centre de Recherche de Vitry-Alfortville, Vitry Sur Seine, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7678707" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal ; Cloning, Molecular ; Epitopes/analysis ; Escherichia coli/genetics ; GTP Phosphohydrolases/metabolism ; GTPase-Activating Proteins ; *Genes, ras ; Genes, src ; Glutathione Transferase/genetics/metabolism ; Oocytes/physiology ; Polymerase Chain Reaction/methods ; Proteins/*genetics/immunology/*metabolism ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; Sequence Homology, Amino Acid ; *Signal Transduction ; Xenopus ; ras GTPase-Activating Proteins
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    Formation of an Fe(III)-tyrosinate complex during biomineralization of H-subunit ferritin (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-05
    Description: An iron(III)-tyrosinate complex was identified in ferritin by ultraviolet-visible and resonance Raman spectroscopies. Previously, a specific amino acid side chain coordinated to iron in ferritin was not known. Ferritin protein was overexpressed in Escherichia coli from complementary DNA sequences of bullfrog red cell ferritin. The purple iron(III)-tyrosinate intermediate that formed during the first stages of iron uptake was replaced by the amber multinuclear iron(III)-oxo complexes of fully mineralized ferritin. Only the H subunit formed detectable amounts of the iron(III)-tyrosinate complex, which may explain the faster rates of iron biomineralization in H- compared to L-type ferritin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waldo, G S -- Ling, J -- Sanders-Loehr, J -- Theil, E C -- DK-20251/DK/NIDDK NIH HHS/ -- GM-18865/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):796-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, North Carolina State University, Raleigh 27695.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430332" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cloning, Molecular ; Erythrocytes/metabolism ; Escherichia coli/genetics ; Ferritins/chemistry/genetics/*metabolism ; Humans ; Macromolecular Substances ; Molecular Sequence Data ; Organometallic Compounds/*analysis ; Rana catesbeiana ; Recombinant Proteins/chemistry/metabolism ; Sequence Homology ; Spectrum Analysis, Raman ; Tyrosine/*analogs & derivatives/analysis
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    T cell activation antigen, CD26, as a cofactor for entry of HIV in CD4+ cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-24
    Description: The CD4 molecule is essential for binding HIV particles, but is not sufficient for efficient viral entry and infection. The cofactor was shown to be dipeptidyl peptidase IV (DPP IV), also known as CD26. This serine protease cleaves its substrates at specific motifs; such motifs area also highly conserved in the V3 loops of HIV-1, HIV-2, and related simian isolates. Entry of HIV-1 or HIV-2 into T lymphoblastoid and monocytoid cell lines was inhibited by a specific monoclonal antibody against DPP IV or specific peptide inhibitors of this protease. Coexpression of human CD4 and CD26 in murine NIH 3T3 cells rendered them permissive to infection by HIV-1 and HIV-2. These observations could provide the basis for developing simple and specific inhibitors of HIV and open a possibility for vaccine development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Callebaut, C -- Krust, B -- Jacotot, E -- Hovanessian, A G -- New York, N.Y. -- Science. 1993 Dec 24;262(5142):2045-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite de Virologie et Immunologie Cellulaire, UA CNRS, Institut Pasteur, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7903479" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Antibodies, Monoclonal ; Antigens, Differentiation, T-Lymphocyte/*physiology ; CD4-Positive T-Lymphocytes/*microbiology ; Cell Line ; Dipeptidyl Peptidase 4 ; Dipeptidyl-Peptidases and Tripeptidyl-Peptidases/antagonists & ; inhibitors/*physiology ; HIV Envelope Protein gp120/physiology ; HIV-1/*pathogenicity ; HIV-2/*pathogenicity ; HeLa Cells ; Humans ; L Cells (Cell Line) ; Leukocytes, Mononuclear/microbiology ; Mice ; Molecular Sequence Data ; Peptide Fragments/physiology ; Trypsin
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  • 83
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    Prevention of collagen-induced arthritis with an antibody to gp39, the ligand for CD40 (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-03
    Description: The ligand for the CD40 antigen is a 39-kilodalton protein, gp39, expressed on the surface of activated CD4+ T cells and is essential for thymus-dependent humoral immunity. The role of gp39-CD40 interactions in autoimmune disease was investigated in vivo with the use of an antibody that blocks their interactions (anti-gp39). Arthritis induced in mice by immunization with type II collagen was inhibited by anti-gp39. Anti-gp39 blocked the development of joint inflammation, serum antibody titers to collagen, the infiltration of inflammatory cells into the subsynovial tissue, and the erosion of cartilage and bone. Thus, interference with gp39-CD40 interactions may have therapeutic potential in the treatment of autoimmune disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Durie, F H -- Fava, R A -- Foy, T M -- Aruffo, A -- Ledbetter, J A -- Noelle, R J -- AI26296/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 3;261(5126):1328-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Dartmouth Medical School, Lebanon, NH 03756.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7689748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*immunology ; Antigens, CD/*immunology ; Antigens, CD40 ; Antigens, Differentiation, B-Lymphocyte/*immunology ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Arthritis, Experimental/immunology/pathology/prevention & control ; Arthritis, Rheumatoid/immunology/pathology/*prevention & control ; Autoimmune Diseases/immunology/pathology/*prevention & control ; CD40 Ligand ; Collagen/immunology ; Disease Models, Animal ; Immunization ; Immunoglobulin G/blood ; Joints/pathology ; Ligands ; Male ; Membrane Glycoproteins/*immunology ; Mice ; Mice, Inbred DBA
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    Learning how to suppress cancer (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1385-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8367721" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; *Genes, Tumor Suppressor ; Genes, p53 ; Genetic Engineering ; Genetic Therapy ; Humans ; Neoplasms/diagnosis/*genetics/therapy
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  • 85
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    Translocation of repetitive RNA sequences with the germ plasm in Xenopus oocytes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-10
    Description: Xlsirts are a family of interspersed repeat RNAs from Xenopus laevis that contain from 3 to 13 repeat units (each 79 to 81 nucleotides long) flanked by unique sequences. They are homologous to the mammalian Xist gene that is involved in X chromosome inactivation. Xlsirt RNA appears first in the mitochondrial cloud (Balbiani body) in stage 2 oocytes and is then translocated as island-like structures to the vegetal cortex at early stage 3 coincident with the localization of the germ plasm. Exogenous Xlsirt RNA injected into oocytes translocates to the location of the endogenous RNA at that particular stage. The Xlsirt RNA repeat sequences are required for translocation and can cause the translocation of heterologous unique RNAs to the vegetal cortex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kloc, M -- Spohr, G -- Etkin, L D -- New York, N.Y. -- Science. 1993 Dec 10;262(5140):1712-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas, M.D. Anderson Cancer Center, Houston 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7505061" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cells, Cultured ; Cloning, Molecular ; DNA, Complementary ; Female ; In Situ Hybridization ; Molecular Sequence Data ; Nucleic Acid Conformation ; Oocytes/*metabolism ; Oogenesis ; RNA/chemistry/*metabolism ; *Repetitive Sequences, Nucleic Acid ; Xenopus laevis
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  • 86
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    Induction of type I diabetes by interferon-alpha in transgenic mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-25
    Description: Type I diabetes is an autoimmune disease involving an interaction between an epigenetic event (possibly a viral infection), the pancreatic beta cells, and the immune system in a genetically susceptible host. The possibility that the type I interferons could mediate this interaction was tested with transgenic mice in which the insulin-producing beta cells expressed an interferon-alpha. These mice developed a hypoinsulinemic diabetes associated with a mixed inflammation centered on the islets. The inflammation and the diabetes were prevented with a neutralizing antibody to the interferon-alpha. Thus, the expression of interferon-alpha by the beta cells could be causal in the development of type I diabetes, which suggests a therapeutic approach to this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stewart, T A -- Hultgren, B -- Huang, X -- Pitts-Meek, S -- Hully, J -- MacLachlan, N J -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1942-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Endocrine Research, Genentech, Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8100367" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/therapeutic use ; CD4-CD8 Ratio ; CD4-Positive T-Lymphocytes ; Diabetes Mellitus, Type 1/*etiology/immunology/pathology ; Female ; Glucagon/analysis ; Insulin/analysis/blood ; Interferon-alpha/*biosynthesis/immunology ; Islets of Langerhans/immunology/*metabolism/pathology ; Leukocytes, Mononuclear ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neutralization Tests ; Somatostatin/analysis
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  • 87
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    U2AF homolog required for splicing in vivo (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-22
    Description: Several fission yeast temperature-sensitive mutants defective in pre-mRNA processing (prp- mutants) at the nonpermissive temperature have been identified. Here, the prp2+ gene has been cloned by its ability to complement the temperature-sensitive growth defect of a prp2- mutant. The gene also corrects the pre-mRNA splicing defect of prp2- mutants and encodes a 59-kilodalton polypeptide (PRP2). A molecular characterization indicates that PRP2 is a previously uncharacterized yeast splicing factor with extensive similarity to the mammalian splicing factor U2AF65. Thus, this study provides evidence that a U2AF homolog participates in RNA processing in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Potashkin, J -- Naik, K -- Wentz-Hunter, K -- R01GM47487/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 22;262(5133):573-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Molecular Biology, University of Health Sciences, Chicago Medical School, IL 60064.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211184" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cloning, Molecular ; Conserved Sequence ; DEAD-box RNA Helicases ; Fungal Proteins/chemistry/*genetics/metabolism ; Genes, Fungal ; Genetic Complementation Test ; Molecular Sequence Data ; *Nuclear Proteins ; RNA Precursors/*metabolism ; *RNA Splicing ; RNA, Fungal/metabolism ; Ribonucleoproteins/chemistry/*genetics/metabolism ; *Saccharomyces cerevisiae Proteins ; Schizosaccharomyces/*genetics ; Sequence Homology, Amino Acid
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  • 88
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    Protection against vaginal SIV transmission with microencapsulated vaccine (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-28
    Description: Although protection in animal models against intravenous challenges with simian immunodeficiency virus (SIV) has been reported, no previous vaccines have protected against a heterosexual route of infection. In this study, five of six macaques were protected against vaginal challenge when immunized with formalin-treated SIV in biodegradable microspheres by the intramuscular plus oral or plus intratracheal route. Oral immunization alone did not protect. After a second vaginal challenge, three of four intramuscularly primed and mucosally boosted macaques remained protected. The data suggest that protection against human immunodeficiency virus vaginal transmission could be provided by microsphere-based booster vaccines when used to immunize women who are systemically primed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, P A -- Compans, R W -- Gettie, A -- Staas, J K -- Gilley, R M -- Mulligan, M J -- Yamshchikov, G V -- Chen, D -- Eldridge, J H -- AI28147/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 May 28;260(5112):1323-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉New Mexico Regional Primate Research Laboratory, New Mexico State University, Holloman Air Force Base 88330.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493576" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Animals ; Antibodies, Viral/*analysis/biosynthesis ; Female ; Immunization, Secondary ; Injections, Intramuscular ; Macaca mulatta ; Mice ; Microspheres ; Simian Acquired Immunodeficiency Syndrome/immunology/*prevention & ; control/transmission ; Simian Immunodeficiency Virus/*immunology ; Trachea ; Vaccination ; Vagina/*immunology/microbiology ; *Viral Vaccines/administration & dosage
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  • 89
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    Switch of CD8 T cells to noncytolytic CD8-CD4- cells that make TH2 cytokines and help B cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-18
    Description: CD8+ T cells are a major defense against viral infections and intracellular parasites. Their production of interferon-gamma (IFN-gamma) and their cytolytic activity are key elements in the immune response to these pathogens. Mature mouse CD8+ T cells that were activated in the presence of interleukin-4 (IL-4) developed into a CD8-CD4- population that was not cytolytic and did not produce IFN-gamma. However, these CD8- cells produced large amounts of IL-4, IL-5, and IL-10 and helped activate resting B cells. Thus, CD8 effector functions are potentially diverse and could be exploited by infectious agents that switch off host protective cytolytic responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Erard, F -- Wild, M T -- Garcia-Sanz, J A -- Le Gros, G -- New York, N.Y. -- Science. 1993 Jun 18;260(5115):1802-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Allergy/Immunology, Ciba-Geigy Ltd., Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8511588" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/analysis ; Antigens, CD8/*analysis ; B-Lymphocytes/*immunology ; Cell Line ; Cells, Cultured ; Cytotoxicity, Immunologic ; Immunophenotyping ; Interleukin-10/biosynthesis ; Interleukin-2/pharmacology ; Interleukin-4/biosynthesis/pharmacology ; Interleukin-5/biosynthesis ; Interleukins/*biosynthesis ; Ionomycin/pharmacology ; *Lymphocyte Activation ; Membrane Glycoproteins/genetics ; Mice ; Perforin ; Pore Forming Cytotoxic Proteins ; T-Lymphocyte Subsets/*immunology ; T-Lymphocytes, Cytotoxic/immunology ; Tetradecanoylphorbol Acetate/pharmacology
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  • 90
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    Thymic selection of cytotoxic T cells independent of CD8 alpha-Lck association (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-17
    Description: The CD8 alpha cytoplasmic domain associates with p56lck, a nonreceptor protein-tyrosine kinase. The biological relevance of CD8 alpha-Lck association in T cell development was tested with transgenic mice generated to express a CD8 alpha molecule with two amino acid substitutions in its cytoplasmic domain, which abolishes the association of CD8 alpha with Lck. The CD8 alpha mutant was analyzed in a CD8-/- background and in the context of the transgenic 2C T cell receptor. The development and function of CD8+ T cells in these mice were apparently normal. Thus, CD8 alpha-Lck association is not necessary for positive selection, negative selection, or CD8-dependent cytotoxic function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, I T -- Limmer, A -- Louie, M C -- Bullock, E D -- Fung-Leung, W P -- Mak, T W -- Loh, D Y -- AI 155322-13/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 17;261(5128):1581-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, Genetics, and Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8372352" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/metabolism ; Antigens, CD8/immunology/*metabolism ; *Cytotoxicity, Immunologic ; Female ; Genes, MHC Class I ; Lymphocyte Culture Test, Mixed ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Receptors, Antigen, T-Cell ; T-Lymphocytes, Cytotoxic/*immunology
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  • 91
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    Colocalization of X-linked agammaglobulinemia and X-linked immunodeficiency genes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-16
    Description: Mice that bear the X-linked immunodeficiency (xid) mutation have a B lymphocyte-specific defect resulting in an inability to make antibody responses to polysaccharide antigens. A backcross of 1114 progeny revealed the colocalization of xid with Bruton's agammaglobulinemia tyrosine kinase (btk) gene, which is implicated in the human immune deficiency, X-linked agammaglobulinemia. Mice that carry xid have a missense mutation that alters a highly conserved arginine near the amino-terminus of the btk protein, Btk. Because this region of Btk lies outside any obvious kinase domain, the xid mutation may define another aspect of tyrosine kinase function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomas, J D -- Sideras, P -- Smith, C I -- Vorechovsky, I -- Chapman, V -- Paul, W E -- GM33160/GM/NIGMS NIH HHS/ -- HG00277/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 16;261(5119):355-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8332900" target="_blank"〉PubMed〈/a〉
    Keywords: Agammaglobulinemia/enzymology/*genetics/immunology ; Amino Acid Sequence ; Animals ; B-Lymphocytes/enzymology/immunology ; Base Sequence ; Chromosome Mapping ; Crosses, Genetic ; Female ; *Genes ; Genetic Linkage ; Immunologic Deficiency Syndromes/enzymology/*genetics/immunology ; Male ; Mice ; Mice, Inbred CBA ; Mice, Mutant Strains ; Molecular Sequence Data ; Muridae ; Mutation ; Protein-Tyrosine Kinases/chemistry/*genetics/metabolism ; *X Chromosome
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  • 92
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    Regulation of the human hsp70 promoter by p53 (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-01
    Description: The tumor suppressor p53 is a nuclear phosphoprotein with characteristics of a transcription factor. It displays sequence-specific DNA binding, contains a potent transactivation domain, and has been implicated as both a transcriptional activator and a repressor. Transcription of the human hsp70 gene is stimulated by adenovirus E1a protein. This E1a transactivation of the hsp70 promoter is mediated by CCAAT binding factor (CBF). It is demonstrated here that p53 both represses transcription from the human hsp70 promoter and also interacts with CBF. Thus, the repression of the hsp70 promoter by p53 may be mediated by direct protein-protein interaction with CBF. These results suggest that protein-protein interaction between p53 and specific transcription factors may be an additional mechanism by which p53 regulates gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Agoff, S N -- Hou, J -- Linzer, D I -- Wu, B -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):84-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Molecular Biology, and Cell Biology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8418500" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus E1A Proteins/metabolism ; Base Sequence ; CCAAT-Enhancer-Binding Proteins ; Chloramphenicol O-Acetyltransferase/genetics/metabolism ; Cloning, Molecular ; DNA-Binding Proteins/metabolism ; Electrophoresis, Polyacrylamide Gel ; Escherichia coli/genetics ; *Gene Expression Regulation ; Heat-Shock Proteins/biosynthesis/*genetics/isolation & purification ; Humans ; *Promoter Regions, Genetic ; Recombinant Fusion Proteins/isolation & purification/metabolism ; TATA Box ; Transcription Factors/metabolism ; *Transcription, Genetic ; Tumor Suppressor Protein p53/genetics/isolation & purification/*metabolism
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  • 93
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    IL-12: initiation cytokine for cell-mediated immunity (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scott, P -- AI30073/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 23;260(5107):496-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8097337" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Humans ; *Immunity, Cellular ; Interleukin-12 ; Interleukins/*immunology ; Macrophages/immunology ; Mice ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Helper-Inducer/cytology/*immunology
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  • 94
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    T cell development in mice that lack the zeta chain of the T cell antigen receptor complex (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-13
    Description: The zeta subunit of the T cell antigen receptor complex is required for targeting nascent receptor complexes to the cell surface and for receptor-mediated signal transduction. To examine the significance of the zeta subunit in T cell development, mice deficient for zeta expression were generated by gene targeting. These zeta-/- mice had few CD4+CD8+ thymocytes, and the generation of CD4+ and CD8+ single positive T cells was impaired but not completely abrogated. Peripheral T cells were present but were unusual in that they expressed small amounts of CD5 and few T cell receptors. Thus, zeta chain expression influences thymocyte differentiation but is not absolutely required for the generation of single positive T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Love, P E -- Shores, E W -- Johnson, M D -- Tremblay, M L -- Lee, E J -- Grinberg, A -- Huang, S P -- Singer, A -- Westphal, H -- New York, N.Y. -- Science. 1993 Aug 13;261(5123):918-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Development, National Institutes of Health (NIH), Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7688481" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/analysis ; Antigens, CD3/analysis ; Antigens, CD4/analysis ; Antigens, CD5 ; Antigens, CD8/analysis ; Cell Differentiation ; Membrane Proteins/genetics/*physiology ; Mice ; Mutation ; RNA, Messenger/genetics/metabolism ; Receptors, Antigen, T-Cell/genetics/*physiology ; Receptors, Antigen, T-Cell, alpha-beta/analysis ; T-Lymphocyte Subsets/*cytology/immunology ; Thymus Gland/cytology
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  • 95
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    Database contamination (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gersuk, V H -- Rose, T M -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):605.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8480168" target="_blank"〉PubMed〈/a〉
    Keywords: Cloning, Molecular ; DNA, Fungal ; Databases, Factual ; *Gene Library ; *Genome, Human ; Humans ; RNA, Fungal/genetics ; RNA, Transfer/genetics
    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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  • 96
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    Resistance of mice deficient in IL-4 to retrovirus-induced immunodeficiency syndrome (MAIDS) (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-08
    Description: The murine acquired immunodeficiency syndrome (MAIDS) is induced by a defective murine leukemia virus and has many symptoms similar to those found in patients infected with the human immunodeficiency virus. The presence of both B cells and CD4+ T cells is critical for the development of the disease. Furthermore, a Th2 cytokine response dominates during the progression of the disease. When interleukin-4 (IL-4)-deficient mice that are defective in Th2 cytokine responses were infected, there was no lethality, and the development of the T cell abnormalities associated with MAIDS was delayed. These data suggest that IL-4 or a Th2 response is involved in the development of retrovirus-induced immunodeficiency in mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kanagawa, O -- Vaupel, B A -- Gayama, S -- Koehler, G -- Kopf, M -- A130803/PHS HHS/ -- New York, N.Y. -- Science. 1993 Oct 8;262(5131):240-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Medicine, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211142" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA Primers ; Gene Products, gag/genetics ; Immunity, Innate ; Interleukin-2/biosynthesis ; Interleukin-4/biosynthesis/deficiency/genetics/*immunology ; Leukemia Virus, Murine/genetics ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Molecular Sequence Data ; Murine Acquired Immunodeficiency Syndrome/*immunology ; RNA, Messenger/analysis/genetics ; RNA, Viral/analysis/genetics ; T-Lymphocytes, Helper-Inducer/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
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    Identification of a mobile endogenous transposon in Arabidopsis thaliana (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-16
    Description: A mobile endogenous transposable element, Tag1, has been identified in the plant Arabidopsis thaliana. Tag1 was found in the nitrate transporter gene, CHL1, of a chlorate-resistant mutant present in a population of plants containing an active maize Ac transposon. Tag1 excises from the chl1 gene producing chlorate-sensitive revertants with Tag1 or Tag1-related elements at different loci. Tag1 and related elements are present in the Landsberg but not Columbia or Wassilewskija ecotypes of Arabidopsis. Thus, Tag1 provides a tool for the insertional mutagenesis of plant genes essential for biological processes of agronomic importance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsay, Y F -- Frank, M J -- Page, T -- Dean, C -- Crawford, N M -- 5T32CA09345-12/CA/NCI NIH HHS/ -- GM 40672/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 16;260(5106):342-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, San Diego, La Jolla 92093-0116.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8385803" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/drug effects/*genetics/metabolism ; Base Sequence ; Chlorates/pharmacology ; Cloning, Molecular ; DNA/chemistry/genetics ; *DNA Transposable Elements ; Drug Resistance ; *Genes, Plant ; Molecular Sequence Data ; Mutation ; Nitrates/metabolism ; Plants, Genetically Modified
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 98
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    Restoration of T cell development in RAG-2-deficient mice by functional TCR transgenes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-05
    Description: Introduction of TCR alpha transgene, TCR beta transgene, or both into RAG-2-/-mice differentially rescues T cell development. RAG-2-/- mice have small numbers of TCR-CD4-CD8-(double negative, DN) thymocytes that express CD3 gamma delta epsilon and zeta proteins intracellularly. Introduction of a TCR beta transgene, but not a TCR alpha transgene, into the RAG-2-/- background restored normal numbers of thymocytes. These cells were CD4+CD8+ (double positive, DP) and expressed small amounts of surface TCR beta chain dimers in association with CD3 gamma delta epsilon but not zeta. RAG-2-/- mice that expressed alpha and beta TCR transgenes developed both DP and single positive thymocytes. Thus, the TCR beta subunit, possibly in association with a novel CD3 complex, participates in the DN to the DP transition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shinkai, Y -- Koyasu, S -- Nakayama, K -- Murphy, K M -- Loh, D Y -- Reinherz, E L -- Alt, F W -- AI19807/AI/NIAID NIH HHS/ -- AI20047/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):822-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Children's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430336" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigens, CD3/analysis/*genetics ; Antigens, CD4/analysis ; Antigens, CD8/analysis ; Base Sequence ; Cell Membrane/immunology ; *DNA-Binding Proteins ; Electrophoresis, Polyacrylamide Gel ; Gene Expression ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Molecular Weight ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction/methods ; Proteins/*genetics ; Receptors, Antigen, T-Cell, alpha-beta/analysis/*genetics ; Receptors, Antigen, T-Cell, gamma-delta/analysis/*genetics ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes/*immunology ; Thymus Gland/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    Altered growth of human colon cancer cell lines disrupted at activated Ki-ras (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-02
    Description: Point mutations that activate the Ki-ras proto-oncogene are presented in about 50 percent of human colorectal tumors. To study the functional significance of these mutations, the activated Ki-ras genes in two human colon carcinoma cell lines, DLD-1 and HCT 116, were disrupted by homologous recombination. Compared with parental cells, cells disrupted at the activated Ki-ras gene were morphologically altered, lost the capacity for anchorage-independent growth, grew more slowly both in vitro and in nude mice, and showed reduced expression of c-myc. Thus, the activated Ki-ras gene plays a key role in colorectal tumorigenesis through altered cell differentiation and cell growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shirasawa, S -- Furuse, M -- Yokoyama, N -- Sasazuki, T -- New York, N.Y. -- Science. 1993 Apr 2;260(5104):85-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Kyushu University, Fukuoka, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8465203" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Differentiation ; Cell Division ; Codon ; Colonic Neoplasms/*genetics/pathology ; Gene Expression Regulation, Neoplastic ; Genes, myc/genetics ; Genes, ras/*genetics ; Humans ; Infant ; Mice ; Mice, Nude ; Molecular Sequence Data ; Mutagenesis, Insertional ; Nucleic Acid Hybridization ; Plasmids ; *Point Mutation ; Polymerase Chain Reaction ; Restriction Mapping ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    Selection of bacterial virulence genes that are specifically induced in host tissues (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-29
    Description: A genetic system was devised that positively selects for bacterial genes that are specifically induced when bacteria infect their host. With the pathogen Salmonella typhimurium, the genes identified by this selection show a marked induction in bacteria recovered from mouse spleen. Mutations in all ivi (in vivo-induced) genes that were tested conferred a defect in virulence. This genetic system was designed to be of general use in a wide variety of bacterial-host systems and has several applications in both vaccine and antimicrobial drug development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mahan, M J -- Slauch, J M -- Mekalanos, J J -- AI08245/AI/NIAID NIH HHS/ -- AI26289/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 29;259(5095):686-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430319" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Bacterial ; Cloning, Molecular ; Genes, Bacterial ; Mice ; Mice, Inbred BALB C ; Mutagenesis ; Recombinant Fusion Proteins/metabolism ; Salmonella Infections, Animal/microbiology ; Salmonella typhimurium/*genetics/*pathogenicity ; Virulence/*genetics ; beta-Galactosidase/genetics/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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