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  • Cells, Cultured
  • American Association for the Advancement of Science (AAAS)  (43)
  • American Meteorological Society
  • PANGAEA
  • 1995-1999  (43)
  • 1990-1994
  • 1985-1989
  • 1996  (43)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (43)
  • American Meteorological Society
  • PANGAEA
Years
  • 1995-1999  (43)
  • 1990-1994
  • 1985-1989
Year
  • 1
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    IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-02
    Description: Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. An inhibitory form of IRS-1 was observed in muscle and fat tissues from obese rats. These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hotamisligil, G S -- Peraldi, P -- Budavari, A -- Ellis, R -- White, M F -- Spiegelman, B M -- DK 42539/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):665-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Biology, Dana-Farber Cancer Institute, Boston, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571133" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/*metabolism ; Adipose Tissue/metabolism ; Animals ; Cells, Cultured ; Insulin/pharmacology ; Insulin Receptor Substrate Proteins ; Insulin Resistance/*physiology ; Male ; Mice ; Muscle, Skeletal/metabolism ; Obesity/*metabolism ; Phosphoproteins/metabolism/*physiology ; Phosphorylation ; Rats ; Rats, Zucker ; Receptor, Insulin/*antagonists & inhibitors/metabolism ; Serine/metabolism ; Signal Transduction ; Tumor Necrosis Factor-alpha/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    HIV-1 Langerhans' cell tropism associated with heterosexual transmission of HIV (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: Heterosexual transmission by vaginal intercourse accounts for most transmission of human immunodeficiency virus-type 1 (HIV-1) in Africa and Asia but is less important in the HIV-1 epidemics of the United States and Western Europe. Epithelial Langerhans' cells (LCs) represent a possible source of initial cell contact for vaginal infection. Fifteen primary isolates of HIV-1 from U.S. homosexuals and 18 HIV-1 isolates from Thailand heterosexuals were evaluated for growth in LCs of U.S. origin. All the viruses from the Thai heterosexuals, which were subtype E, grew more efficiently in the LCs than any of the viruses from the U.S. homosexuals, which are subtype B. These results suggest that LC tropism is associated with the efficiency of heterosexual transmission of HIV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soto-Ramirez, L E -- Renjifo, B -- McLane, M F -- Marlink, R -- O'Hara, C -- Sutthent, R -- Wasi, C -- Vithayasai, P -- Vithayasai, V -- Apichartpiyakul, C -- Auewarakul, P -- Pena Cruz, V -- Chui, D S -- Osathanondh, R -- Mayer, K -- Lee, T H -- Essex, M -- 5 D43 TW0004/TW/FIC NIH HHS/ -- CA 39805/CA/NCI NIH HHS/ -- HL 33774/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1291-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard AIDS Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638113" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cells, Cultured ; HIV Core Protein p24/analysis ; HIV Infections/*transmission/virology ; HIV-1/classification/*growth & development/isolation & purification ; Homosexuality, Male ; Humans ; Langerhans Cells/*virology ; Macrophages/virology ; Male ; Monocytes/virology ; *Sexual Behavior ; Sexually Transmitted Diseases, Viral/*transmission/virology ; T-Lymphocytes/virology ; Thailand ; United States ; Virus Replication
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Abnormal centrosome amplification in the absence of p53 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-22
    Description: The centrosome plays a vital role in mitotic fidelity, ensuring establishment of bipolar spindles and balanced chromosome segregation. Centrosome duplication occurs only once during the cell cycle and is therefore highly regulated. Here, it is shown that in mouse embryonic fibroblasts (MEFs) lacking the p53 tumor suppressor protein, multiple copies of functionally competent centrosomes are generated during a single cell cycle. In contrast, MEFs prepared from normal mice or mice deficient in the retinoblastoma tumor suppressor gene product do not display these abnormalities. The abnormally amplified centrosomes profoundly affect mitotic fidelity, resulting in unequal segregation of chromosomes. These observations implicate p53 in the regulation of centrosome duplication and suggest one possible mechanism by which the loss of p53 may cause genetic instability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukasawa, K -- Choi, T -- Kuriyama, R -- Rulong, S -- Vande Woude, G F -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1744-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, MD 21702-1201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596939" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood ; Cells, Cultured ; Centrosome/*metabolism ; Culture Media ; Fibroblasts ; Genes, Retinoblastoma ; Genes, p53 ; *Interphase ; Mice ; *Mitosis ; Spindle Apparatus/metabolism/ultrastructure ; Tumor Suppressor Protein p53/*physiology
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  • 4
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    Antigen presentation and T cell development in H2-M-deficient mice (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: HLA-DM (DM) facilitates peptide loading of major histocompatibility complex class II molecules in human cell lines. Mice lacking functional H2-M, the mouse equivalent of DM, have normal amounts of class II molecules at the cell surface, but most of these are associated with invariant chain-derived CLIP peptides. These mice contain large numbers of CD4+ T cells, which is indicative of positive selection in the thymus. Their CD4+ cells were unresponsive to self H2-M-deficient antigen-presenting cells (APCs) but were hyperreactive to wild-type APCs. H2-M-deficient APCs failed to elicit proliferative responses from wild-type T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fung-Leung, W P -- Surh, C D -- Liljedahl, M -- Pang, J -- Leturcq, D -- Peterson, P A -- Webb, S R -- Karlsson, L -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1278-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638109" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigen-Presenting Cells/*immunology ; Antigens, Differentiation, B-Lymphocyte/immunology/metabolism ; Base Sequence ; CD4-Positive T-Lymphocytes/*immunology ; Cells, Cultured ; Gene Targeting ; Histocompatibility Antigens Class II/genetics/*immunology/metabolism ; Isoantigens/immunology ; Lymphocyte Activation ; Mice ; Molecular Sequence Data ; Mutation
    Print ISSN: 0036-8075
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  • 5
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    Spread of synaptic depression mediated by presynaptic cytoplasmic signaling (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-17
    Description: Postsynaptic activity may modulate presynaptic functions by transsynaptic retrograde signals. At developing neuromuscular synapses in Xenopus nerve-muscle cultures, a brief increase in the cytosolic calcium ion (Ca2+) concentration in postsynaptic myocytes induced persistent depression of presynaptic transmitter secretion. This depression spread to distant synapses formed by the same neuron. Clearance of extracellular fluid did not prevent the spread of depression, and depression could not be induced by increasing the Ca2+ concentration in a nearby myocyte not in contact with the presynaptic neuron. Thus, the spread of depression is mediated by signaling in the presynaptic cytoplasm, rather than by a retrograde factor in the extracellular space.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cash, S -- Zucker, R S -- Poo, M M -- NS15114/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 May 17;272(5264):998-1001.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Columbia University, New York 10027, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638143" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Cells, Cultured ; Chelating Agents ; Cytoplasm/*metabolism ; Egtazic Acid/analogs & derivatives ; Evoked Potentials ; Muscles/cytology/innervation/physiology ; Neurites/physiology ; Neuromuscular Junction/metabolism/*physiology ; Photolysis ; Presynaptic Terminals/physiology ; *Signal Transduction ; Synapses/*physiology ; *Synaptic Transmission ; Ultraviolet Rays ; Xenopus
    Print ISSN: 0036-8075
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  • 6
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    Selective activation of NF-kappa B by nerve growth factor through the neurotrophin receptor p75 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-26
    Description: Nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) selectively bind to distinct members of the Trk family of tyrosine kinase receptors, but all three bind with similar affinities to the neurotrophin receptor p75 (p75NTR). The biological significance of neurotrophin binding to p75NTR in cells that also express Trk receptors has been difficult to ascertain. In the absence of TrkA, NGF binding to p75NGR activated the transcription factor nuclear factor kappa B (NF-kappa B) in rat Schwann cells. This activation was not observed in Schwann cells isolated from mice that lacked p75NTR. The effect was selective for NGF; NF-kappa B was not activated by BDNF or NT-3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carter, B D -- Kaltschmidt, C -- Kaltschmidt, B -- Offenhauser, N -- Bohm-Matthaei, R -- Baeuerle, P A -- Barde, Y A -- New York, N.Y. -- Science. 1996 Apr 26;272(5261):542-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiochemistry, Max-Planck Institute for Psychiatry, Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614802" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Brain-Derived Neurotrophic Factor ; Cell Nucleus/metabolism ; Cells, Cultured ; DNA/metabolism ; L Cells (Cell Line) ; Mice ; Molecular Sequence Data ; NF-kappa B/*metabolism ; Nerve Growth Factors/*metabolism/pharmacology ; Nerve Tissue Proteins/metabolism/pharmacology ; Neurotrophin 3 ; Proto-Oncogene Proteins/metabolism ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Nerve Growth Factor ; Receptor, trkA ; Receptors, Nerve Growth Factor/*metabolism ; Schwann Cells/*metabolism ; Signal Transduction/*physiology
    Print ISSN: 0036-8075
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  • 7
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    Binding of APC to the human homolog of the Drosophila discs large tumor suppressor protein (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-17
    Description: The adenomatous polyposis coli gene (APC) is mutated in familial adenomatous polyposis and in sporadic colorectal tumors, and its product binds to the adherens junction protein beta-catenin. Overexpression of APC blocks cell cycle progression. The APC-beta-catenin complex was shown to bind to DLG, the human homolog of the Drosophila discs large tumor suppressor protein. This interaction required the carboxyl-terminal region of APC and the DLG homology repeat region of DLG. APC colocalized with DLG at the lateral cytoplasm in rat colon epithelial cells and at the synapse in cultured hippocampal neurons. These results suggest that the APC-DLG complex may participate in regulation of both cell cycle progression and neuronal function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsumine, A -- Ogai, A -- Senda, T -- Okumura, N -- Satoh, K -- Baeg, G H -- Kawahara, T -- Kobayashi, S -- Okada, M -- Toyoshima, K -- Akiyama, T -- New York, N.Y. -- Science. 1996 May 17;272(5264):1020-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncogene Research, Institute for Microbial Diseases, Osaka University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638125" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Amino Acid Sequence ; Animals ; Cell Cycle ; Cells, Cultured ; Colon/chemistry/cytology ; Cytoskeletal Proteins/analysis/chemistry/*metabolism ; Drosophila ; *Drosophila Proteins ; Epithelial Cells ; Epithelium/chemistry ; Fluorescent Antibody Technique ; Hippocampus/chemistry/cytology ; Humans ; Insect Hormones/analysis/chemistry/*metabolism ; Mice ; Molecular Sequence Data ; Neurons/chemistry/cytology ; Protein Binding ; Recombinant Fusion Proteins/metabolism ; Synapses/chemistry ; *Trans-Activators ; *Tumor Suppressor Proteins ; beta Catenin
    Print ISSN: 0036-8075
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  • 8
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    Fertile results: bringing up baby (eggs) (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roush, W -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):594-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571119" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Culture Techniques ; Cells, Cultured ; Female ; Fertilization in Vitro ; Granulosa Cells/cytology/*physiology ; Mice ; Oocytes/cytology/*physiology ; *Oogenesis ; Organ Culture Techniques ; Ovary/physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Identification of a committed precursor for the mast cell lineage (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-09
    Description: Mast cells originate from hematopoietic stem cells, but the mast cell-committed precursor has not been identified. In the study presented here, a cell population in murine fetal blood that fulfills the criteria of progenitor mastocytes was identified. It is defined by the phenotype Thy-1loc-Kithi, contains cytoplasmic granules, and expresses RNAs encoding mast cell-associated proteases but lacks expression of the high-affinity immunoglobulin E receptor. Thy-1loc-Kithi cells generated functionally competent mast cells at high frequencies in vitro but lacked developmental potential for other hematopoietic lineages. When transferred intraperitoneally, this population reconstituted the peritoneal mast cell compartment of genetically mast cell-deficient W/Wv mice to wild-type levels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodewald, H R -- Dessing, M -- Dvorak, A M -- Galli, S J -- AI-33372/AI/NIAID NIH HHS/ -- AI/CA-23990/AI/NIAID NIH HHS/ -- CA/AI-72074/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 9;271(5250):818-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8629001" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Thy-1/analysis ; Base Sequence ; Cell Lineage ; Cell Transplantation ; Cells, Cultured ; Cytoplasmic Granules/ultrastructure ; Endopeptidases/genetics/metabolism ; Fetal Blood ; Hematopoietic Stem Cells/*cytology/physiology/ultrastructure ; Immunophenotyping ; Interleukin-3/pharmacology ; Mast Cells/*cytology/physiology/ultrastructure ; Mice ; Molecular Sequence Data ; Peritoneal Cavity/cytology ; Proto-Oncogene Proteins c-kit/analysis ; RNA, Messenger/genetics/metabolism ; Receptors, IgE/analysis/genetics ; Stem Cell Factor/pharmacology
    Print ISSN: 0036-8075
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  • 10
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    Cholesterol modification of hedgehog signaling proteins in animal development (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-11
    Description: Hedgehog (Hh) proteins comprise a family of secreted signaling molecules essential for patterning a variety of structures in animal embryogenesis. During biosynthesis, Hh undergoes an autocleavage reaction, mediated by its carboxyl-terminal domain, that produces a lipid-modified amino-terminal fragment responsible for all known Hh signaling activity. Here it is reported that cholesterol is the lipophilic moiety covalently attached to the amino-terminal signaling domain during autoprocessing and that the carboxyl-terminal domain acts as an intramolecular cholesterol transferase. This use of cholesterol to modify embryonic signaling proteins may account for some of the effects of perturbed cholesterol biosynthesis on animal development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Porter, J A -- Young, K E -- Beachy, P A -- New York, N.Y. -- Science. 1996 Oct 11;274(5285):255-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Biology and Genetics, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8824192" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cells, Cultured ; Cholesterol/*metabolism ; Dithiothreitol/pharmacology ; Drosophila ; *Drosophila Proteins ; *Embryonic Induction ; Embryonic and Fetal Development ; Hedgehog Proteins ; Humans ; Protein Processing, Post-Translational ; Proteins/genetics/*metabolism ; Signal Transduction ; *Trans-Activators
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  • 11
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    Lymphocyte apoptosis: mediation by increased type 3 inositol 1,4,5-trisphosphate receptor (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-26
    Description: B and T lymphocytes undergoing apoptosis in response to anti-immunoglobulin M antibodies and dexamethasone, respectively, were found to have increased amounts of messenger RNA for the inositol 1,4,5-trisphosphate receptor (IP3R) and increased amounts of IP3R protein. Immunohistochemical analysis revealed that the augmented receptor population was localized to the plasma membrane. Type 3 IP3R (IP3R3) was selectively increased during apoptosis, with no enhancement of type 1 IP3R (IP3R1). Expression of IP3R3 antisense constructs in S49 T cells blocked dexamethasone-induced apoptosis, whereas IP3R3 sense, IP3R1 sense, or IP3R1 antisense control constructs did not block cell death. Thus, the increases in IP3R3 may be causally related to apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Khan, A A -- Soloski, M J -- Sharp, A H -- Schilling, G -- Sabatini, D M -- Li, S H -- Ross, C A -- Snyder, S H -- AI-20922/AI/NIAID NIH HHS/ -- AI-37934/AI/NIAID NIH HHS/ -- MH43040/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Jul 26;273(5274):503-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662540" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Apoptosis ; B-Lymphocytes/*cytology/metabolism ; Base Sequence ; Calcium/metabolism ; Calcium Channels/genetics/immunology/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; DNA, Antisense ; Dexamethasone/pharmacology ; Immunoblotting ; Inositol 1,4,5-Trisphosphate/*metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; Mice ; Molecular Sequence Data ; Receptors, Cytoplasmic and Nuclear/genetics/immunology/*metabolism ; T-Lymphocytes/*cytology/metabolism ; Transfection ; Tumor Cells, Cultured
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  • 12
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    Correction of the mutation responsible for sickle cell anemia by an RNA-DNA oligonucleotide (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-09-06
    Description: A chimeric oligonucleotide composed of DNA and modified RNA residues was used to direct correction of the mutation in the hemoglobin betaS allele. After introduction of the chimeric molecule into lymphoblastoid cells homozygous for the betaS mutation, there was a detectable level of gene conversion of the mutant allele to the normal sequence. The efficient and specific conversion directed by chimeric molecules may hold promise as a therapeutic method for the treatment of genetic diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cole-Strauss, A -- Yoon, K -- Xiang, Y -- Byrne, B C -- Rice, M C -- Gryn, J -- Holloman, W K -- Kmiec, E B -- New York, N.Y. -- Science. 1996 Sep 6;273(5280):1386-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Kimmel Cancer Center, Thomas Jefferson University, 233 South 10th Street, Philadelphia, PA 19107, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8703073" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Anemia, Sickle Cell/*genetics/therapy ; Base Sequence ; Cells, Cultured ; *Gene Conversion ; Genetic Therapy ; Globins/genetics ; Hemoglobin, Sickle/*genetics ; Humans ; Lymphocytes ; Molecular Sequence Data ; Oligodeoxyribonucleotides/*genetics ; Oligoribonucleotides/*genetics ; Point Mutation ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; *Transfection
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  • 13
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    In vitro development of primitive and definitive erythrocytes from different precursors (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-03
    Description: During mouse embryogenesis the production of "primitive" erythrocytes (EryP) precedes the production of "definitive" erythrocytes (EryD) in parallel with the transition of the hematopoietic site from the yolk sac to the fetal liver. On a macrophage colony-stimulating factor-deficient stromal cell line OP9, mouse embryonic stem cells were shown to give rise to EryP and EryD sequentially with a time course similar to that seen in murine ontogeny. Studies of the different growth factor requirements and limiting dilution analysis of precursor frequencies indicate that most EryP and EryD probably developed from different precursors by way of distinct differentiation pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakano, T -- Kodama, H -- Honjo, T -- New York, N.Y. -- Science. 1996 May 3;272(5262):722-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Faculty of Medicine, Kyoto University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614833" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Line ; Cell Lineage ; Cell Separation ; Cells, Cultured ; Coculture Techniques ; Erythroid Precursor Cells/*cytology ; *Erythropoiesis ; Erythropoietin/pharmacology ; Kinetics ; Mice ; Signal Transduction ; Stem Cell Factor/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Induction of protective CTL responses in newborn mice by a murine retrovirus (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-22
    Description: The susceptibility of neonates to virus-induced disease is thought to reflect, in part, the immaturity of their immune systems. However, inoculation of newborn mice with low doses of Cas-Br-M murine leukemia virus induced a protective cytotoxic T lymphocyte (CTL) response. The inability of neonates to develop a CTL response to high doses of virus was not the result of immunological immaturity but correlated with the induction of a nonprotective type 2 cytokine response. Thus, the initial viral dose is critical in the development of protective immunity in newborns.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sarzotti, M -- Robbins, D S -- Hoffman, P M -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1726-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rsearch Service, Veterans Affairs Medical Center, Baltimore, MD 21201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596933" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn/*immunology ; Cells, Cultured ; Cytotoxicity, Immunologic ; Dose-Response Relationship, Immunologic ; Immunotherapy, Adoptive ; Interferon-gamma/biosynthesis ; Interleukin-4/biosynthesis ; Leukemia Virus, Murine/*immunology ; Mice ; Retroviridae Infections/*immunology ; T-Lymphocytes, Cytotoxic/*immunology ; Tumor Virus Infections/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    An essential role for NF-kappaB in preventing TNF-alpha-induced cell death (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-01
    Description: Studies on mice deficient in nuclear factor kappa B (NF-kappaB) subunits have shown that this transcription factor is important for lymphocyte responses to antigens and cytokine-inducible gene expression. In particular, the RelA (p65) subunit is required for induction of tumor necrosis factor-alpha (TNF-alpha)-dependent genes. Treatment of RelA-deficient (RelA-/-) mouse fibroblasts and macrophages with TNF-alpha resulted in a significant reduction in viability, whereas RelA+/+ cells were unaffected. Cytotoxicity to both cell types was mediated by TNF receptor 1. Reintroduction of RelA into RelA-/- fibroblasts resulted in enhanced survival, demonstrating that the presence of RelA is required for protection from TNF-alpha. These results have implications for the treatment of inflammatory and proliferative diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beg, A A -- Baltimore, D -- New York, N.Y. -- Science. 1996 Nov 1;274(5288):782-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8864118" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Antigens, CD/metabolism ; *Cell Death ; Cell Survival ; Cells, Cultured ; Gene Expression Regulation ; Humans ; Macrophages/cytology ; Mice ; NF-kappa B/genetics/*physiology ; Receptors, Tumor Necrosis Factor/metabolism ; Receptors, Tumor Necrosis Factor, Type I ; Signal Transduction ; Transcription Factor RelA ; Transfection ; Tumor Necrosis Factor-alpha/*pharmacology/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    How the brain gets rhythm (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schechter, B -- New York, N.Y. -- Science. 1996 Oct 18;274(5286):339-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8927989" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Brain/*physiology ; Cells, Cultured ; Computer Simulation ; Electric Stimulation ; Interneurons/*physiology ; Nerve Net/*physiology ; Neural Networks (Computer) ; Neural Pathways ; Perception ; Photic Stimulation ; Pyramidal Cells/*physiology ; Visual Cortex/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Antiviral effect and ex vivo CD4+ T cell proliferation in HIV-positive patients as a result of CD28 costimulation (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-28
    Description: Because stimulation of CD4+ lymphocytes leads to activation of human immunodeficiency virus-type 1 (HIV-1) replication, viral spread, and cell death, adoptive CD4+ T cell therapy has not been possible. When antigen and CD28 receptors on cultured T cells were stimulated by monoclonal antibodies (mAbs) to CD3 and CD28 that had been immobilized, there was an increase in the number of polyclonal CD4+ T cells from HIV-infected donors. Activated cells predominantly secreted cytokines associated with T helper cell type 1 function. The HIV-1 viral load declined in the absence of antiretroviral agents. Moreover, CD28 stimulation of CD4+ T cells from uninfected donors rendered these cells highly resistant to HIV-1 infection. Immobilization of CD28 mAb was crucial to the development of HIV resistance, as cells stimulated with soluble CD28 mAb were highly susceptible to HIV infection. The CD28-mediated antiviral effect occurred early in the viral life cycle, before HIV-1 DNA integration. These data may facilitate immune reconstitution and gene therapy approaches in persons with HIV infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levine, B L -- Mosca, J D -- Riley, J L -- Carroll, R G -- Vahey, M T -- Jagodzinski, L L -- Wagner, K F -- Mayers, D L -- Burke, D S -- Weislow, O S -- St Louis, D C -- June, C H -- AI29331/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Jun 28;272(5270):1939-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Naval Medical Research Institute, Bethesda, Maryland 20889, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658167" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal/immunology ; Antigens, CD28/*immunology ; Antigens, CD3/immunology ; CD4 Lymphocyte Count ; CD4-Positive T-Lymphocytes/cytology/*immunology/*virology ; Cell Division ; Cells, Cultured ; Chemokines/metabolism ; Cytokines/metabolism ; HIV Infections/immunology/*virology ; HIV-1/immunology/*physiology ; Humans ; Interleukin-2/pharmacology ; *Lymphocyte Activation ; Phytohemagglutinins/pharmacology ; Virus Integration ; Virus Replication
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  • 18
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    Reexpression of RAG-1 and RAG-2 genes in activated mature mouse B cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: Recombination activating genes (RAG-1 and RAG-2), involved in V(D)J rearrangement of immunoglobulin genes, have been thought to be expressed only in immature stages of B-cell development. However, RAG-1 and RAG-2 transcripts were found to be reexpressed in mature mouse B cells after culture with interleukin-4 in association with several different co-stimuli. Reexpression was also detected in draining lymph nodes from immunized mice. RAG-1 and RAG-2 proteins could be detected by immunofluorescence microscopy in the nuclei of B cells cultured in vitro and in the germinal centers of draining lymph nodes. These findings suggest that RAG gene products play a heretofore unsuspected role in mature B cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hikida, M -- Mori, M -- Takai, T -- Tomochika, K -- Hamatani, K -- Ohmori, H -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2092-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biotechnology, Faculty of Engineering, Okayama University, Tsushima-Naka, Okayama 700, Japan. hit2224@cc.okayama-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953042" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology/*metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; *DNA-Binding Proteins ; *Gene Expression ; *Genes, RAG-1 ; Germinal Center/metabolism ; *Homeodomain Proteins ; Immunoglobulin Class Switching ; Interleukin-4/pharmacology ; Interleukins/pharmacology ; Lipopolysaccharides/pharmacology ; Lymph Nodes/metabolism ; *Lymphocyte Activation ; Mice ; Mice, Inbred C3H ; Microscopy, Fluorescence ; Protein Biosynthesis ; Proteins/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    Plasma viral load, CD4+ cell counts, and HIV-1 production by cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levy, J A -- Ramachandran, B -- Barker, E -- Guthrie, J -- Elbeik, T -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):670-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571134" target="_blank"〉PubMed〈/a〉
    Keywords: Antiviral Agents/pharmacology/therapeutic use ; *CD4 Lymphocyte Count ; Cells, Cultured ; HIV Infections/drug therapy/immunology/*virology ; HIV-1/*physiology ; Humans ; Leukocytes, Mononuclear/*virology ; Lymphocyte Count ; T-Lymphocytes/*virology ; Tumor Cells, Cultured ; Viremia/virology ; Virus Replication ; Zidovudine/pharmacology/therapeutic use
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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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    Function of myosin-V in filopodial extension of neuronal growth cones (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-02
    Description: The molecular mechanisms underlying directed motility of growth cones have not been determined. The role of myosin-V, an unconventional myosin, in growth cone dynamics was examined by chromophore-assisted laser inactivation (CALI). CALI of purified chick brain myosin-V absorbed onto nitrocellulose-coated cover slips inhibited the ability of myosin-V to translocate actin filaments. CALI of myosin-V in growth cones of chick dorsal root ganglion neurons resulted in rapid filopodial retraction. The rate of filopodial extension was significantly decreased, whereas the rate of filopodial retraction was not affected, which suggests a specific role for myosin-V in filopodial extension.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, F S -- Wolenski, J S -- Cheney, R E -- Mooseker, M S -- Jay, D G -- NS-29007/NS/NINDS NIH HHS/ -- NS-34699/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 2;273(5275):660-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662560" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/pharmacology ; Animals ; Axons/*physiology/ultrastructure ; Calmodulin-Binding Proteins/antagonists & inhibitors/immunology/*physiology ; Cells, Cultured ; Chick Embryo ; Dendrites/*physiology/ultrastructure ; Fluorescent Antibody Technique, Indirect ; Ganglia, Spinal/cytology ; Lasers ; Microinjections ; Myosin Light Chains/antagonists & inhibitors/immunology/*physiology ; *Myosin Type V ; Nerve Tissue Proteins/antagonists & inhibitors/immunology/*physiology ; Pseudopodia/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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    Inhibition of HIV-1 replication in lymphocytes by mutants of the Rev cofactor eIF-5A (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-29
    Description: Eukaryotic initiation factor 5A(eIF-5A) is a cellular cofactor require d for the function of the human immunodeficiency virus type-1 (HIV-1) Rev trans-activator protein. The majority of a set of eIF-5A mutants did not support growth of yeast cells having an inactivated genomic copy of eIF-5A, indicating that the introduced mutation eliminated eIF-5A activity. Two nonfunctional mutants, eIF-5AM13 and eIF-5AM14, retained their binding capacity for the HIV-1 Rev response element:Rev complex. Both mutants were constitutively expressed in human T cells. When these T cells were infected with replication-competent HIV-1, virus replication was inhibited. The eIF-5AM13 and eIF5AM14 proteins blocked Rev trans-activation and Rev-mediated nuclear export.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bevec, D -- Jaksche, H -- Oft, M -- Wohl, T -- Himmelspach, M -- Pacher, A -- Schebesta, M -- Koettnitz, K -- Dobrovnik, M -- Csonga, R -- Lottspeich, F -- Hauber, J -- New York, N.Y. -- Science. 1996 Mar 29;271(5257):1858-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sandoz Research Institute, Department of Immunodermatology, Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596953" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Nucleus/metabolism ; Cells, Cultured ; Gene Products, rev/*metabolism ; Genes, env ; HIV-1/*physiology ; HeLa Cells ; Humans ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Peptide Initiation Factors/genetics/metabolism/*physiology ; *RNA-Binding Proteins ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/genetics/growth & development ; T-Lymphocytes/metabolism/*virology ; Transcriptional Activation ; Virus Replication ; rev Gene Products, Human Immunodeficiency Virus
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  • 22
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    Role of beta-chemokines in suppressing HIV replication (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mackewicz, C E -- Barker, E -- Levy, J A -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1393-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966605" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies/immunology ; Antiviral Agents/immunology/pharmacology/*physiology ; CD4-Positive T-Lymphocytes/*virology ; CD8-Positive T-Lymphocytes/*immunology ; Cells, Cultured ; Chemokine CCL4 ; Chemokine CCL5/immunology/pharmacology/physiology ; Chemokines/immunology/pharmacology/*physiology ; HIV Infections/virology ; HIV Long Terminal Repeat ; HIV-1/genetics/*physiology ; Humans ; Macrophage Inflammatory Proteins/immunology/pharmacology/physiology ; Neutralization Tests ; Virus Replication
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  • 23
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    Close-up of a killer (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1996 Oct 11;274(5285):176-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8927977" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Crystallography, X-Ray ; Drosophila melanogaster ; H-2 Antigens/*chemistry/immunology/metabolism ; Killer Cells, Natural/immunology ; *Major Histocompatibility Complex ; Models, Molecular ; Peptides/immunology/metabolism ; Protein Conformation ; Receptors, Antigen, T-Cell, alpha-beta/*chemistry/immunology/metabolism ; Recombinant Proteins/chemistry ; T-Lymphocytes, Cytotoxic/*immunology
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  • 24
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    Mutant enzyme provides new insights into the cause of ALS (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1996 Jan 26;271(5248):446-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8560253" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/*enzymology/genetics/pathology ; Animals ; Apoptosis ; Cells, Cultured ; Free Radicals ; Humans ; Lipid Peroxidation ; Mice ; Mutation ; Neurons/cytology ; Nitrates/metabolism ; Peroxidases/metabolism ; Selenium/administration & dosage ; Superoxide Dismutase/genetics/*metabolism ; Vitamin E/administration & dosage/metabolism
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  • 25
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    Somatic mutation of immunoglobulin V genes in vitro (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: The molecular mechanism behind affinity maturation is the introduction of point mutations in immunoglobulin (Ig) V genes, followed by the selective proliferation of B cells expressing mutants with increased affinity for antigen. An in vitro culture system was developed in which somatic hypermutation of Ig V genes was sustained in primed B cells. Cognate T cell help and cross-linking of the surface Ig were required, whereas the addition of lipopolysaccharide or a CD40 ligand to drive proliferation was insufficient. This system should facilitate understanding of the molecular and cellular mechanisms that regulate somatic mutation and B cell selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kallberg, E -- Jainandunsing, S -- Gray, D -- Leanderson, T -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1285-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Unit, Lund University, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638111" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD40 ; B-Lymphocytes/*immunology ; Base Sequence ; CD40 Ligand ; Cells, Cultured ; Coculture Techniques ; *Genes, Immunoglobulin ; Haptens/immunology ; Hybridomas ; Immunoglobulin Variable Region/*genetics ; Lipopolysaccharides/pharmacology ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; *Mutation ; Ovalbumin/immunology ; Oxazolone/analogs & derivatives/immunology ; Receptors, Antigen, B-Cell/immunology ; Th2 Cells/immunology ; Transfection
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  • 26
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    Genetic susceptibility to Leishmania: IL-12 responsiveness in TH1 cell development (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-16
    Description: The genetic background of T lymphocytes influences development of the T helper (TH) phenotype, resulting in either resistance or susceptibility of certain mouse strains to pathogens such as Leishmania major. With an in vitro model system, a difference in maintenance of responsiveness of T cells to interleukin-12 (IL-12) was detected between BALB/c and B10.D2 mice. Although naive T cells from both strains initially responded to IL-12, BALB/c T cells lost IL-12 responsiveness after stimulation with antigen in vitro, even when cocultured with B10.D2 T cells. Thus, susceptibility of BALB/c mice to infection with L. major may derive from the loss of the ability to generate IL-12-induced TH1 responses rather than from an IL-4-induced TH2 response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guler, M L -- Gorham, J D -- Hsieh, C S -- Mackey, A J -- Steen, R G -- Dietrich, W F -- Murphy, K M -- AI31238/AI/NIAID NIH HHS/ -- AI34580/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 16;271(5251):984-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8584935" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Coculture Techniques ; Genetic Predisposition to Disease ; Immunity, Innate/genetics ; Interferon-gamma/biosynthesis ; Interleukin-12/*pharmacology ; Interleukin-4/biosynthesis ; Leishmania major/*immunology ; Leishmaniasis, Cutaneous/*immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Phenotype ; Receptors, Interleukin-2/biosynthesis ; Signal Transduction ; Th1 Cells/*immunology ; Th2 Cells/immunology
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  • 27
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    Life-death balance within the cell (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1996 Nov 1;274(5288):724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966553" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cells, Cultured ; Humans ; Mice ; Mice, Knockout ; NF-kappa B/antagonists & inhibitors/metabolism/*physiology ; Neoplasms/metabolism/*pathology/therapy ; Proto-Oncogene Proteins/metabolism/pharmacology ; Transcription Factor RelB ; *Transcription Factors ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/pharmacology/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Preferential formation of benzo[a]pyrene adducts at lung cancer mutational hotspots in P53 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-18
    Description: Cigarette smoke carcinogens such as benzo[a]pyrene are implicated in the development of lung cancer. The distribution of benzo[a]pyrene diol epoxide (BPDE) adducts along exons of the P53 gene in BPDE-treated HeLa cells and bronchial epithelial cells was mapped at nucleotide resolution. Strong and selective adduct formation occurred at guanine positions in codons 157, 248, and 273. These same positions are the major mutational hotspots in human lung cancers. Thus, targeted adduct formation rather than phenotypic selection appears to shape the P53 mutational spectrum in lung cancer. These results provide a direct etiological link between a defined chemical carcinogen and human cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Denissenko, M F -- Pao, A -- Tang, M -- Pfeifer, G P -- CA65652/CA/NCI NIH HHS/ -- ES03124/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1996 Oct 18;274(5286):430-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Beckman Research Institute of the City of Hope, Duarte, CA 91010, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8832894" target="_blank"〉PubMed〈/a〉
    Keywords: 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide/metabolism/*toxicity ; Bronchi ; Carcinogens/metabolism/*toxicity ; Cells, Cultured ; Codon ; DNA Adducts/*metabolism ; Dinucleoside Phosphates/metabolism ; Exons ; Fibroblasts ; *Genes, p53 ; HeLa Cells ; Humans ; Lung Neoplasms/etiology/*genetics ; Mutagens/metabolism/toxicity ; *Mutation ; Plants, Toxic ; Smoke/adverse effects ; Tobacco
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  • 29
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    Regulation of a neuronal form of focal adhesion kinase by anandamide (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-09-20
    Description: Anandamide is an endogenous ligand for central cannabinoid receptors and is released after neuronal depolarization. Anandamide increased protein tyrosine phosphorylation in rat hippocampal slices and neurons in culture. The action of anandamide resulted from the inhibition of adenylyl cyclase and cyclic adenosine 3', 5'-monophosphate-dependent protein kinase. One of the proteins phosphorylated in response to anandamide was an isoform of pp125-focal adhesion kinase (FAK+) expressed preferentially in neurons. Focal adhesion kinase is a tyrosine kinase involved in the interactions between the integrins and actin-based cytoskeleton. Thus, anandamide may exert neurotrophic effects and play a role in synaptic plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Derkinderen, P -- Toutant, M -- Burgaya, F -- Le Bert, M -- Siciliano, J C -- de Franciscis, V -- Gelman, M -- Girault, J A -- New York, N.Y. -- Science. 1996 Sep 20;273(5282):1719-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U 114, Chaire de Neuropharmacologie, College de France, 11 place Marcelin Berthelot, 75231 Paris cedex 05, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8781236" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/metabolism ; Amino Acid Sequence ; Animals ; Arachidonic Acid/pharmacology ; Arachidonic Acids/*pharmacology ; Cell Adhesion Molecules/*metabolism ; Cell Line ; Cells, Cultured ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Endocannabinoids ; Focal Adhesion Kinase 1 ; Focal Adhesion Protein-Tyrosine Kinases ; Hippocampus/drug effects/*enzymology ; In Vitro Techniques ; Molecular Sequence Data ; Neuronal Plasticity/drug effects ; Neurons/drug effects/*enzymology ; Phosphorylation ; Phosphotyrosine/metabolism ; Polyunsaturated Alkamides ; Prosencephalon ; Protein-Tyrosine Kinases/*metabolism ; Rats ; Receptors, Cannabinoid ; Receptors, Drug/metabolism
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    Role of Rho in chemoattractant-activated leukocyte adhesion through integrins (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-02-16
    Description: Heterotrimeric guanine nucleotide binding protein (G protein)-linked receptors of the chemoattractant subfamily can trigger adhesion through leukocyte integrins, and in this role they are thought to regulate immune cell-cell interactions and trafficking. In lymphoid cells transfected with formyl peptide or interleukin-8 receptors, agonist stimulation activated nucleotide exchange on the small guanosine triphosphate-binding protein RhoA in seconds. Inactivation of Rho by C3 transferase exoenzyme blocked agonist-induced lymphocyte alpha4beta1 adhesion to vascular cell adhesion molecule-1 and neutrophil beta2 integrin adhesion to fibrinogen. These findings suggest that Rho participates in signaling from chemoattractant receptors to trigger rapid adhesion in leukocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laudanna, C -- Campbell, J J -- Butcher, E C -- 1F32 AI08930/AI/NIAID NIH HHS/ -- 5T32 CA09302/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 16;271(5251):981-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8584934" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD/genetics ; B-Lymphocytes/*physiology ; *Cell Adhesion ; Cells, Cultured ; Chemotactic Factors/*pharmacology ; GTP-Binding Proteins/metabolism/*physiology ; Guanosine 5'-O-(3-Thiotriphosphate)/metabolism ; Guanosine Diphosphate/metabolism ; Integrin alpha4beta1 ; Integrins/*physiology ; Interleukin-8/pharmacology ; Mice ; Molecular Sequence Data ; N-Formylmethionine Leucyl-Phenylalanine/pharmacology ; Receptors, Formyl Peptide ; Receptors, Immunologic/genetics ; Receptors, Interleukin/genetics ; Receptors, Interleukin-8A ; Receptors, Lymphocyte Homing/*physiology ; Receptors, Peptide/genetics ; Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; Transfection ; Vascular Cell Adhesion Molecule-1/*physiology ; rhoA GTP-Binding Protein
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    In vivo gene delivery and stable transduction of nondividing cells by a lentiviral vector (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-12
    Description: A retroviral vector system based on the human immunodeficiency virus (HIV) was developed that, in contrast to a murine leukemia virus-based counterpart, transduced heterologous sequences into HeLa cells and rat fibroblasts blocked in the cell cycle, as well as into human primary macrophages. Additionally, the HIV vector could mediate stable in vivo gene transfer into terminally differentiated neurons. The ability of HIV-based viral vectors to deliver genes in vivo into nondividing cells could increase the applicability of retroviral vectors in human gene therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Naldini, L -- Blomer, U -- Gallay, P -- Ory, D -- Mulligan, R -- Gage, F H -- Verma, I M -- Trono, D -- AG08514/AG/NIA NIH HHS/ -- AG10435/AG/NIA NIH HHS/ -- AI37510/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Apr 12;272(5259):263-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8602510" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/cytology/virology ; Cell Division ; Cells, Cultured ; Female ; *Gene Transfer Techniques ; Genetic Therapy ; *Genetic Vectors ; HIV/*genetics/physiology ; HeLa Cells ; Humans ; Macrophages/cytology/virology ; Molecular Sequence Data ; Neurons/cytology/virology ; Plasmids ; Rats ; Transfection ; Virus Integration
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    PKC-dependent stimulation of exocytosis by sulfonylureas in pancreatic beta cells (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-02-09
    Description: Hypoglycemic sulfonylureas represent a group of clinically useful antidiabetic compounds that stimulate insulin secretion from pancreatic beta cells. The molecular mechanisms involved are not fully understood but are believed to involve inhibition of potassium channels sensitive to adenosine triphosphate (KATP channels) in the beta cell membrane, causing membrane depolarization, calcium influx, and activation of the secretory machinery. In addition to these effects, sulfonylureas also promoted exocytosis by direct interaction with the secretory machinery not involving closure of the plasma membrane KATP channels. This effect was dependent on protein kinase C (PKC) and was observed at therapeutic concentrations of sulfonylureas, which suggests that it contributes to their hypoglycemic action in diabetics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eliasson, L -- Renstrom, E -- Ammala, C -- Berggren, P O -- Bertorello, A M -- Bokvist, K -- Chibalin, A -- Deeney, J T -- Flatt, P R -- Gabel, J -- Gromada, J -- Larsson, O -- Lindstrom, P -- Rhodes, C J -- Rorsman, P -- New York, N.Y. -- Science. 1996 Feb 9;271(5250):813-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Pharmacology, University of Goteborg, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8628999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Cells, Cultured ; Cytoplasmic Granules/metabolism ; Electric Conductivity ; Exocytosis/*drug effects ; Glipizide/pharmacology ; Glyburide/pharmacology ; Hypoglycemic Agents/*pharmacology ; Insulin/secretion ; Islets of Langerhans/drug effects/*physiology ; Membrane Potentials/drug effects ; Mice ; Patch-Clamp Techniques ; Protein Kinase C/*metabolism ; Sulfonylurea Compounds/*pharmacology ; Tolbutamide/*pharmacology
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    An alphabeta T cell receptor structure at 2.5 A and its orientation in the TCR-MHC complex (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-11
    Description: The central event in the cellular immune response to invading microorganisms is the specific recognition of foreign peptides bound to major histocompatibility complex (MHC) molecules by the alphabeta T cell receptor (TCR). The x-ray structure of the complete extracellular fragment of a glycosylated alphabeta TCR was determined at 2.5 angstroms, and its orientation bound to a class I MHC-peptide (pMHC) complex was elucidated from crystals of the TCR-pMHC complex. The TCR resembles an antibody in the variable Valpha and Vbeta domains but deviates in the constant Calpha domain and in the interdomain pairing of Calpha with Cbeta. Four of seven possible asparagine-linked glycosylation sites have ordered carbohydrate moieties, one of which lies in the Calpha-Cbeta interface. The TCR combining site is relatively flat except for a deep hydrophobic cavity between the hypervariable CDR3s (complementarity-determining regions) of the alpha and beta chains. The 2C TCR covers the class I MHC H-2Kb binding groove so that the Valpha CDRs 1 and 2 are positioned over the amino-terminal region of the bound dEV8 peptide, the Vbeta chain CDRs 1 and 2 are over the carboxyl-terminal region of the peptide, and the Valpha and Vbeta CDR3s straddle the peptide between the helices around the central position of the peptide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garcia, K C -- Degano, M -- Stanfield, R L -- Brunmark, A -- Jackson, M R -- Peterson, P A -- Teyton, L -- Wilson, I A -- R01 CA58896/CA/NCI NIH HHS/ -- T32-A107244/PHS HHS/ -- New York, N.Y. -- Science. 1996 Oct 11;274(5285):209-19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and the Skaggs Institute of Chemical Biology, Scripps Research Institute, 10550 N. Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8824178" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbohydrate Sequence ; Cells, Cultured ; Crystallization ; Crystallography, X-Ray ; Drosophila melanogaster ; Glycosylation ; H-2 Antigens/*chemistry/immunology/metabolism ; Hydrogen Bonding ; Major Histocompatibility Complex ; Mice ; Models, Molecular ; Molecular Sequence Data ; Peptides/*chemistry/immunology/metabolism ; *Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Receptors, Antigen, T-Cell, alpha-beta/*chemistry/immunology/metabolism ; Recombinant Proteins ; T-Lymphocytes, Cytotoxic/*immunology
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    Human foamy virus replication: a pathway distinct from that of retroviruses and hepadnaviruses (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-15
    Description: Human foamy virus (HFV) is the prototype of the Spumavirus genus of Retroviridae. In all other retroviruses, the pol gene products, including reverse transcriptase, are synthesized as Gag-Pol fusion proteins and are cleaved to functional enzymes during viral budding or release. In contrast, the Pol protein of HFV is translated from a spliced messenger RNA and lacks Gag domains. Infectious HFV particles contain double-stranded DNA similar in size to full-length provirus, suggesting that reverse transcription has taken place in viral particles before new rounds of infection, reminiscent of hepadnaviruses. These data suggest that foamy viruses possess a replication pathway containing features of both retroviruses and hepadnaviruses but distinct from both.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, S F -- Baldwin, D N -- Gwynn, S R -- Yendapalli, S -- Linial, M L -- CA18282/CA/NCI NIH HHS/ -- F32 CA60357/CA/NCI NIH HHS/ -- HL53762/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Mar 15;271(5255):1579-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8599113" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cells, Cultured ; Cricetinae ; Fusion Proteins, gag-pol/biosynthesis/genetics/metabolism ; Gene Products, gag/biosynthesis/genetics ; Gene Products, pol/*biosynthesis/genetics/metabolism ; Genes, gag ; Genes, pol ; Genome, Viral ; Hepatitis B virus/genetics/metabolism/physiology ; Humans ; Molecular Sequence Data ; RNA Splicing ; RNA, Viral/genetics ; RNA-Directed DNA Polymerase/metabolism ; Retroviridae/genetics/metabolism/physiology ; Spumavirus/genetics/metabolism/*physiology ; *Virus Replication
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    Immunologic NO synthase: elevation in severe AIDS dementia and induction by HIV-1 gp41 (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-12-13
    Description: Indirect mechanisms are implicated in the pathogenesis of the dementia associated with human immunodeficiency virus-type 1 (HIV-1) infection. Proinflammatory molecules such as tumor necrosis factor alpha and eicosanoids are elevated in the central nervous system of patients with HIV-1-related dementia. Nitric oxide (NO) is a potential mediator of neuronal injury, because cytokines may activate the immunologic (type II) isoform of NO synthase (iNOS). The levels of iNOS in severe HIV-1-associated dementia coincided with increased expression of the HIV-1 coat protein gp41. Furthermore, gp41 induced iNOS in primary cultures of mixed rat neuronal and glial cells and killed neurons through a NO-dependent mechanism. Thus, gp41-induced NO formation may contribute to the severe cognitive dysfunction associated with HIV-1 infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adamson, D C -- Wildemann, B -- Sasaki, M -- Glass, J D -- McArthur, J C -- Christov, V I -- Dawson, T M -- Dawson, V L -- AI35042/AI/NIAID NIH HHS/ -- NS07392/NS/NINDS NIH HHS/ -- NS22643/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Dec 13;274(5294):1917-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Pathology 2-210, Baltimore, MD 21287, USA. valina.dawson@qmail.bs.jhu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8943206" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Dementia Complex/*enzymology/metabolism ; Animals ; Brain/*enzymology/metabolism ; Cell Death ; Cells, Cultured ; Cerebral Cortex/enzymology/metabolism ; Enzyme Induction ; HIV Envelope Protein gp120/metabolism/pharmacology ; HIV Envelope Protein gp41/*metabolism/pharmacology ; *Hiv-1 ; Humans ; Neuroglia/cytology ; Neurons/cytology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/*biosynthesis/genetics ; Polymerase Chain Reaction ; Rats
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    Association of spindle assembly checkpoint component XMAD2 with unattached kinetochores (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-11
    Description: The spindle assembly checkpoint delays anaphase until all chromosomes are attached to a mitotic spindle. The mad (mitotic arrest-deficient) and bub (budding uninhibited by benzimidazole) mutants of budding yeast lack this checkpoint and fail to arrest the cell cycle when microtubules are depolymerized. A frog homolog of MAD2 (XMAD2) was isolated and found to play an essential role in the spindle assembly checkpoint in frog egg extracts. XMAD2 protein associated with unattached kinetochores in prometaphase and in nocodazole-treated cells and disappeared from kinetochores at metaphase in untreated cells, suggesting that XMAD2 plays a role in the activation of the checkpoint by unattached kinetochores. This study furthers understanding of the mechanism of cell cycle checkpoints in metazoa and provides a marker for studying the role of the spindle assembly checkpoint in the genetic instability of tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, R H -- Waters, J C -- Salmon, E D -- Murray, A W -- New York, N.Y. -- Science. 1996 Oct 11;274(5285):242-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of California, San Francisco, 94143, USA. Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8824188" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/analysis/chemistry/genetics/*metabolism ; Amino Acid Sequence ; Animals ; Calcium/pharmacology ; *Cell Cycle ; Cells, Cultured ; HeLa Cells ; Humans ; Interphase ; Kinetochores/*metabolism ; Lamins ; Microtubules/metabolism ; Mitosis ; Molecular Sequence Data ; Nuclear Envelope/chemistry ; Nuclear Proteins/metabolism ; Ovum ; P-Glycoprotein/analysis/chemistry/genetics/*metabolism ; *P-Glycoproteins ; Protamine Kinase/metabolism ; Spindle Apparatus/*physiology ; Xenopus
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    Leishmania susceptibility puzzle gets another twist (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-02-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1996 Feb 16;271(5251):912-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8584928" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Disease Susceptibility ; Immunity, Innate ; Interleukin-12/immunology ; Interleukin-4/genetics/*immunology ; Leishmania major/*immunology ; Leishmaniasis, Cutaneous/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Th1 Cells/immunology ; Th2 Cells/immunology
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  • 38
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    Complementary DNA for 12-kilodalton B cell growth factor: misassigned (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-10-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kovanen, P E -- Harju, L -- Timonen, T -- New York, N.Y. -- Science. 1996 Oct 25;274(5287):629-31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8928011" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Cloning, Molecular ; DNA Probes ; DNA, Complementary/*genetics ; Humans ; Interleukin-4/*genetics ; Leukocytes, Mononuclear/chemistry ; Lymphocyte Activation ; Lymphokines/*genetics ; Molecular Sequence Data ; RNA Probes ; RNA, Messenger/genetics ; Repetitive Sequences, Nucleic Acid
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  • 39
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    Neuroprotection by aspirin and sodium salicylate through blockade of NF-kappaB activation (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-11-22
    Description: Aspirin (acetylsalicylic acid) is a commonly prescribed drug with a wide pharmacological spectrum. At concentrations compatible with amounts in plasma during chronic anti-inflammatory therapy, acetylsalicylic acid and its metabolite sodium salicylate were found to be protective against neurotoxicity elicited by the excitatory amino acid glutamate in rat primary neuronal cultures and hippocampal slices. The site of action of the drugs appeared to be downstream of glutamate receptors and to involve specific inhibition of glutamate-mediated induction of nuclear factor kappa B. These results may contribute to the emerging theme of anti-inflammatory drugs and neurodegeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grilli, M -- Pizzi, M -- Memo, M -- Spano, P -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1383-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pharmacology, Department of Biomedical Sciences and Biotechnologies, University of Brescia Medical School, Brescia, I-25123 Italy. mpharm@master.cci.unibs.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8910280" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspirin/*pharmacology ; Calcium/metabolism ; Cell Survival/drug effects ; Cells, Cultured ; Cerebellum/cytology/drug effects/metabolism ; Dentate Gyrus/cytology/drug effects/metabolism ; Glutamic Acid/*pharmacology ; Hippocampus/cytology/*drug effects/metabolism ; In Vitro Techniques ; N-Methylaspartate/pharmacology ; NF-kappa B/*metabolism ; Neurons/cytology/*drug effects/metabolism ; Neuroprotective Agents/*pharmacology ; Pyramidal Cells/cytology/drug effects/metabolism ; Rats ; Rats, Sprague-Dawley ; Sodium Salicylate/*pharmacology ; Transcription Factor AP-1/metabolism ; Up-Regulation
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  • 40
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    Reduction of voltage-dependent Mg2+ blockade of NMDA current in mechanically injured neurons (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-13
    Description: Activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors is implicated in the pathophysiology of traumatic brain injury. Here, the effects of mechanical injury on the voltage-dependent magnesium (Mg2+) block of NMDA currents in cultured rat cortical neurons were examined. Stretch-induced injury was found to reduce the Mg2+ blockade, resulting in significantly larger ionic currents and increases in intracellular free calcium (Ca2+) concentration after NMDA stimulation of injured neurons. The Mg2+ blockade was partially restored by increased extracellular Mg2+ concentration or by pretreatment with the protein kinase C inhibitor calphostin C. These findings could account for the secondary pathological changes associated with traumatic brain injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, L -- Rzigalinski, B A -- Ellis, E F -- Satin, L S -- HL07537-14/HL/NHLBI NIH HHS/ -- NS 27214/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 13;274(5294):1921-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Post Office Box 980524, Richmond, VA 23298-0524, USA. lsatin@gems.vcu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8943207" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Injuries/metabolism ; Calcium/metabolism ; Cells, Cultured ; Cerebral Cortex/cytology/*metabolism ; Dizocilpine Maleate/pharmacology ; Enzyme Inhibitors/pharmacology ; Excitatory Amino Acid Antagonists/pharmacology ; Magnesium/*pharmacology ; Membrane Potentials ; N-Methylaspartate/*pharmacology ; Naphthalenes/pharmacology ; Neurons/cytology/*metabolism ; Patch-Clamp Techniques ; Protein Kinase C/antagonists & inhibitors/metabolism ; Rats ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/drug effects/*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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  • 41
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    Mechanism of suppression of cell-mediated immunity by measles virus (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-12
    Description: The mechanisms underlying the profound suppression of cell-mediated immunity (CMI) accompanying measles are unclear. Interleukin-12 (IL-12), derived principally from monocytes and macrophages, is critical for the generation of CMI. Measles virus (MV) infection of primary human monocytes specifically down-regulated IL-12 production. Cross-linking of CD46, a complement regulatory protein that is the cellular receptor for MV, with antibody or with the complement activation product C3b similarly inhibited monocyte IL-12 production, providing a plausible mechanism for MV-induced immunosuppression. CD46 provides a regulatory link between the complement system and cellular immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karp, C L -- Wysocka, M -- Wahl, L M -- Ahearn, J M -- Cuomo, P J -- Sherry, B -- Trinchieri, G -- Griffin, D E -- AI01223/AI/NIAID NIH HHS/ -- AI23047/AI/NIAID NIH HHS/ -- AI35149/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Jul 12;273(5272):228-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662504" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Antigens, CD/immunology/*physiology ; Antigens, CD46 ; Binding Sites ; Cells, Cultured ; Chemokines/biosynthesis ; Complement C3b/immunology/physiology ; Cytokines/biosynthesis ; Down-Regulation ; Humans ; *Immune Tolerance ; Interleukin-10/physiology ; Interleukin-12/*biosynthesis ; Measles virus/*immunology/metabolism ; Membrane Glycoproteins/immunology/*physiology ; Monocytes/*immunology/*virology ; Receptors, Virus/immunology/*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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  • 42
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    Suppression of TNF-alpha-induced apoptosis by NF-kappaB (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-01
    Description: Tumor necrosis factor alpha (TNF-alpha) signaling gives rise to a number of events, including activation of transcription factor NF-kappaB and programmed cell death (apoptosis). Previous studies of TNF-alpha signaling have suggested that these two events occur independently. The sensitivity and kinetics of TNF-alpha-induced apoptosis are shown to be enhanced in a number of cell types expressing a dominant-negative IkappaBalpha (IkappaBalphaM). These findings suggest that a negative feedback mechanism results from TNF-alpha signaling in which NF-kappaB activation suppresses the signals for cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van Antwerp, D J -- Martin, S J -- Kafri, T -- Green, D R -- Verma, I M -- GM52735/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Nov 1;274(5288):787-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, Salk Institute, La Jolla, CA 92037, USA. Jolla Institute for Allergy and Immu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8864120" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Annexin A5/metabolism ; *Apoptosis ; Cells, Cultured ; DNA-Binding Proteins/genetics/physiology ; Feedback ; Humans ; *I-kappa B Proteins ; Jurkat Cells ; Mice ; NF-kappa B/*antagonists & inhibitors/*physiology ; Phosphatidylserines/metabolism ; *Signal Transduction ; Transcription Factor RelA ; Tumor Necrosis Factor-alpha/*pharmacology
    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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  • 43
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    Requirement for invariant chain in B cell maturation and function (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-04
    Description: Previously the role of invariant chain (Ii) had been described only as a chaperone that facilitates folding and transport of major histocompatability complex class II molecules; here it is shown that Ii is required for B cell development. B cells from mice lacking Ii were found to have a low response to T-independent type II antigen and could not proliferate after the mice were injected with antigen. Study of cell surface markers revealed a developmental arrest that prevented immature virgin B cells from becoming mature B cells in the periphery. This block was independent of major histocompatability complex class II expression and was an intrinsic feature of B cells that correlated with the amount of Ii. Thus, Ii participates by an unknown mechanism in B cell maturation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shachar, I -- Flavell, R A -- New York, N.Y. -- Science. 1996 Oct 4;274(5284):106-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8810244" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; Antigens, Differentiation, B-Lymphocyte/*physiology ; B-Lymphocytes/*immunology/physiology ; Bone Marrow Cells ; Cells, Cultured ; Histocompatibility Antigens Class II/*physiology ; Immunization ; Immunoglobulin D/analysis ; Immunoglobulin M/analysis ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Mice, Transgenic ; Receptors, IgE/analysis
    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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