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  • Articles  (108)
  • Mice  (108)
  • 1985-1989  (108)
  • 1950-1954
  • 1986  (108)
Collection
  • Articles  (108)
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  • 1985-1989  (108)
  • 1950-1954
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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Theoretical and applied genetics 73 (1986), S. 148-157 
    ISSN: 1432-2242
    Keywords: Mice ; Correlated responses ; Organ growth ; Degree of maturity ; Allometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Correlated responses to selection for increased 3–6 week postweaning gain in male mice were estimated for seven internal organs (testes, spleen, liver, kidneys, heart, small intestine (S intest) and stomach) weighed at specific degrees of maturity in body weight (37.5, 50.0, 62.5, 75.0, 87.5 and 100%). Correlated responses in organ weights were generally large, but the magnitude and direction of response depended upon whether 1) comparisons were made at the same age, degree of maturity or body weight and 2) absolute or proportional organ weights were used. The selected line (M16) weighed more and had larger organ weights than controls (ICR) when compared at either the same degree of maturity or the same age, indicating positive genetic correlations between body weight and the respective organ weights. Positive correlated responses were found in spleen weight/body weight at all degrees of maturity and in liver and S intest weights as a proportion of body weight at some degrees of maturity. Testes, kidneys, heart and stomach weights as a proportion of body weight had negative correlated responses, though this was consistent only for kidneys across all degrees of maturity. Correlated responses in organ weights adjusted for body weight by covariance analysis were positive for spleen, S intest and stomach and negative for testes and kidneys. Based on the constrained quadratic model, degree of maturity in organ weight relative to degree of maturity in body weight responded positively for testes, kidneys and S intest and negatively for spleen and liver. Selection for increased growth caused negative correlated responses in allometric growth of testes, kidneys, S intest and stomach.
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Lasers in medical science 1 (1986), S. 125-130 
    ISSN: 1435-604X
    Keywords: Wound contraction ; Fibroblasts ; Infrared laser ; Helium-neon laser ; Mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine , Physics , Technology
    Notes: Abstract The effect was investigated of combined pulsed infrared and continuous wave heliumneon mid-laser therapy on wound contraction and wound bed cellularity, and the effects were compared of variation in the infrared pulsing frequency. The laser used was the Space Mix-5 Mid-Laser and the wounds studied were full-thickness excised skin lesions made in the flank skin of CD1 adult female mice, which were maintained under general anaesthesia during both excision and irradiation. Treatment at 700 Hz increased wound contraction in comparison with treatment at 1200 Hz, when all other controllable parameters were kept constant. By 11 days after injury the cellularity of the wound bed was greater in the wounds treated with 700 Hz than in those treated with 1200 Hz, with the greatest difference being found in the number of fibroblasts, the cells primarily responsible for wound contraction.
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 243 (1986), S. 65-68 
    ISSN: 1432-0878
    Keywords: Epithelial differentiation ; Stomach ; Duodenum ; Mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The response of adult epithelium in contact with heterologous mesenchymes/stromas was studied in three digestive organs (forestomach, glandular stomach, and duodenum). After various tissues were implanted beneath the epithelial layer of adult mice, the epithelial differentiation was examined after sacrifice of animals at intervals up to 24 weeks. In the forestomach and duodenum, the epithelial differentiation was not affected at all by the tissue implantation. In the glandular stomach, in contrast, epithelial cells exhibited altered differentiation in which chief and parietal cells disappeared and were replaced by columnar epithelial cells with PAS-positive granules. These epithelial cells often formed immature villi. Such differentiation-altered columnar epithelium (DACE) was induced by implanting any type of tissue and even by sham operation, indicating that it was induced by disorganization of the tissue-implanted stroma. The size of DACE was significantly influenced by the stage of implanted tissue; 14.5-day fetal mesenchyme induced the largest DACE, and was followed by 16.5-day fetal mesenchyme, adult stroma, and sham operation. These results suggest the importance of stromal organization in maintaining epithelial differentiation in the glandular stomach.
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 245 (1986), S. 183-188 
    ISSN: 1432-0878
    Keywords: Spleen ; Lymph nodes ; Mice ; Cyclophosphamide ; Levan ; Light microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Morphological changes in spleen and lymph nodes of C57B1 mice induced by the cytotoxic agent cyclophosphamide and the polysaccharide levan, separately and in combination were studied. In the spleen, an early decrease (phase 1) and a late increase (phase 2) in weight were found to result from all drug administrations. The hypocellularity of phase 1 was due to a depletion in the white pulp affecting mainly the B-region. Splenic weight decrease was parallel to B-cell depletion and most marked in animals exposed to cyclophosphamide with levan. The splenomegaly observed during phase 2 with all treatments was due to extramedullary hematopoiesis in the red pulp. In the lymph nodes, administration of cyclophosphamide and levan produced opposite effects on the B-cell region: cyclophosphamide eliminated the germinal centers for 8 days, but levan seemed to enhance B-cell activity. In animals given both cyclophosphamide and levan, inhibition of B-cell activity began earlier than with cyclophosphamide alone. Levan does not antagonize the suppressive effect of cyclophosphamide on the B-cell component at the early phase when the drugs are given together.
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 246 (1986), S. 549-556 
    ISSN: 1432-0878
    Keywords: Submandibular gland ; Adrenal X zone ; Ovariectomy ; Morphometrical analysis ; Mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Morphological changes in submandibular glands of female mice following ovariectomy were studied morphometrically by light microscopy and ultrastructurally by electron microscopy. The X zone of the adrenal gland was examined in order to assess possible changes that might be expected to occur after ovariectomy. In submandibular glands, 1 to 4 weeks after ovariectomy, no changes were observed in percentages of the acinar, intercalated duct, and granular convoluted tubular areas occupying photomicrographs. However, an increase in the granular content of both intercalated duct and granular convoluted tubular cells was recognized. By contrast, the glandular picture 4 months after ovariectomy changed remarkably, resembling that of the male mouse both morphometrically and in terms of fine structure. In the adrenal cortex of control female mice, the X zone became thinner with aging. As compared with this, the X zone of ovariectomized mice at any time after the operation was thicker than that of controls. These observations suggest that the absence of ovarian hormones in the ovariectomized mouse may lead to prolonged functioning of X zone cells, which in turn may cause masculinization of the submandibular gland.
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  • 6
    Publication Date: 1986-04-04
    Description: A lectin in Giardia lamblia was activated by secretions from the human duodenum, the environment where the parasite lives. Incubation of the secretions with trypsin inhibitors prevented the appearance of lectin activity, implicating proteases as the activating agent. Accordingly, lectin activation was also produced by crystalline trypsin and Pronase; other proteases tested were ineffective. When activated, the lectin agglutinated intestinal cells to which the parasite adheres in vivo. The lectin was most specific to mannose-6-phosphate and apparently was bound to the plasma membrane. Activation of a parasite lectin by a host protease represents a novel mechanism of host-parasite interaction and may contribute to the affinity of Giardia lamblia to the infection site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lev, B -- Ward, H -- Keusch, G T -- Pereira, M E -- P-1-P30-AM 39428-01/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):71-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3513312" target="_blank"〉PubMed〈/a〉
    Keywords: Agglutination ; Animals ; Duodenum/enzymology/parasitology ; Giardia/*metabolism ; *Host-Parasite Interactions ; Humans ; Intestine, Small/enzymology/*parasitology ; Lectins/*metabolism ; Mice ; Peptide Hydrolases/*metabolism ; Sheep ; Species Specificity ; Trypsin/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 1986-01-31
    Description: p-Chloromercuriphenylsulfonic acid (PCMS), a sulfhydryl inhibitor, prevented the mycelial-to-yeast transition of the dimorphic fungal pathogen, Histoplasma capsulatum. The effect of PCMS was specific for the mycelial-to-yeast transformation; it had no effect on growth of either the yeast or mycelial forms or on the yeast-to-mycelial transition. The failure of PCMS-treated mycelia to transform to yeast was permanent and irreversible. PCMS-treated mycelia could not infect mice but could stimulate resistance to infection by a pathogenic strain of Histoplasma capsulatum. These results suggest a new general strategy for vaccine development in diseases caused by dimorphic pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Medoff, G -- Sacco, M -- Maresca, B -- Schlessinger, D -- Painter, A -- Kobayashi, G S -- Carratu, L -- AI 07015/AI/NIAID NIH HHS/ -- AI 07172/AI/NIAID NIH HHS/ -- AI 16228/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 31;231(4737):476-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3001938" target="_blank"〉PubMed〈/a〉
    Keywords: 4-Chloromercuribenzenesulfonate/pharmacology ; Animals ; Cytochromes/metabolism ; Energy Metabolism/drug effects ; Fungal Proteins/biosynthesis ; Histoplasma/drug effects/pathogenicity/*physiology ; Histoplasmosis/etiology ; Kinetics ; Mice ; Oxidative Phosphorylation/drug effects ; Oxygen Consumption/drug effects
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  • 8
    Publication Date: 1986-11-07
    Description: Binding of antibodies to effector cells by way of receptors to their constant regions (Fc receptors) is central to the pathway that leads to clearance of antigens by the immune system. The structure and function of this important class of receptors on immune cells is addressed through the molecular characterization of Fc receptors (FcR) specific for the murine immunoglobulin G isotype. Structural diversity is encoded by two genes that by alternative splicing result in expression of molecules with highly conserved extracellular domains and different transmembrane and intracytoplasmic domains. The proteins encoded by these genes are members of the immunoglobulin supergene family, most homologous to the major histocompatibility complex molecule E beta. Functional reconstitution of ligand binding by transfection of individual FcR genes demonstrates that the requirements for ligand binding are encoded in a single gene. These studies demonstrate the molecular basis for the functional heterogeneity of FcR's, accounting for the possible transduction of different signals in response to a single ligand.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ravetch, J V -- Luster, A D -- Weinshank, R -- Kochan, J -- Pavlovec, A -- Portnoy, D A -- Hulmes, J -- Pan, Y C -- Unkeless, J C -- AI 24322/AI/NIAID NIH HHS/ -- GM 36306/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):718-25.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2946078" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA/genetics ; Gene Expression Regulation ; Histocompatibility Antigens Class II/genetics ; Immunoglobulin G ; Lymphocytes/*physiology ; Macrophages/*physiology ; Membrane Proteins ; Mice ; Protein Conformation ; *Receptors, Fc/genetics ; Receptors, IgG ; Transcription, Genetic ; Transfection
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  • 9
    Publication Date: 1986-02-28
    Description: Transgenic mice expressing a metallothionein-somatostatin fusion gene contain high concentrations of somatostatin in the anterior pituitary gland, a tissue that does not normally produce somatostatin. Immunoreactive somatostatin within the anterior pituitaries was found exclusively within gonadotrophs. Similarly, a metallothionein-human growth-hormone fusion gene was also expressed selectively in gonadotrophs. It is proposed that sequences common to the two fusion genes are responsible for the gonadotroph-specific expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Low, M J -- Lechan, R M -- Hammer, R E -- Brinster, R L -- Habener, J F -- Mandel, G -- Goodman, R H -- AM 01313/AM/NIADDK NIH HHS/ -- AM 30457/AM/NIADDK NIH HHS/ -- AM 31400/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Feb 28;231(4741):1002-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2868526" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Recombinant/metabolism ; Genes ; Genetic Engineering ; Humans ; Immunoenzyme Techniques ; Luteinizing Hormone/metabolism ; Metallothionein/*genetics ; Mice ; Pituitary Gland, Anterior/*metabolism ; Rats ; Somatostatin/*genetics/metabolism
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  • 10
    Publication Date: 1986-02-21
    Description: Partial amino acid sequence analysis of a purified lymphocyte homing receptor demonstrates the presence of two amino termini, one of which corresponds precisely to the amino terminus of ubiquitin. This observation extends the province of this conserved polypeptide to the cell surface and leads to a proposed model of the receptor complex as a core polypeptide modified by glycosylation and ubiquitination. Independent antibodies to ubiquitin serve to identify additional cell surface species, an indication that ubiquitination of cell surface proteins may be more general. It is proposed that functional binding of lymphocytes to lymph node high endothelial venules might involve the ubiquitinated region of the receptor; if true, cell surface ubiquitin could play a more general role in cell-cell interaction and adhesion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Siegelman, M -- Bond, M W -- Gallatin, W M -- St John, T -- Smith, H T -- Fried, V A -- Weissman, I L -- AI 19512/AI/NIAID NIH HHS/ -- CA 09151/CA/NCI NIH HHS/ -- GM 31461/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Feb 21;231(4740):823-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3003913" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal ; Cell Movement ; Endothelium/metabolism ; Glycoproteins/metabolism/*physiology ; Glycoside Hydrolases/metabolism ; High Mobility Group Proteins/*metabolism ; Lymphocytes/*physiology ; Mannosyl-Glycoprotein Endo-beta-N-Acetylglucosaminidase ; Membrane Proteins/metabolism/*physiology ; Mice ; Molecular Weight ; Protein Processing, Post-Translational ; Receptors, Cell Surface/metabolism/*physiology ; Ubiquitins/immunology/*metabolism
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  • 11
    Publication Date: 1986-04-04
    Description: Experiments were conducted to isolate and characterize the gene and gene product of a human hematopoietic colony-stimulating factor with pluripotent biological activities. This factor has the ability to induce differentiation of a murine myelomonocytic leukemia cell line WEHI-3B(D+) and cells from patients with newly diagnosed acute nonlymphocytic leukemia (ANLL). A complementary DNA copy of the gene encoding a pluripotent human granulocyte colony-stimulating factor (hG-CSF) was cloned and expressed in Escherichia coli. The recombinant form of hG-CSF is capable of supporting neutrophil proliferation in a CFU-GM assay. In addition, recombinant hG-CSF can support early erythroid colonies and mixed colony formation. Competitive binding studies done with 125I-labeled hG-CSF and cell samples from two patients with newly diagnosed human leukemias as well as WEHI-3B(D+) cells showed that one of the human leukemias (ANLL, classified as M4) and the WEHI-3B(D+) cells have receptors for hG-CSF. Furthermore, the murine WEHI-3B(D+) cells and human leukemic cells classified as M2, M3, and M4 were induced by recombinant hG-CSF to undergo terminal differentiation to macrophages and granulocytes. The secreted form of the protein produced by the bladder carcinoma cell line 5637 was found to be O-glycosylated and to have a molecular weight of 19,600.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Souza, L M -- Boone, T C -- Gabrilove, J -- Lai, P H -- Zsebo, K M -- Murdock, D C -- Chazin, V R -- Bruszewski, J -- Lu, H -- Chen, K K -- CA00966/CA/NCI NIH HHS/ -- CA20194/CA/NCI NIH HHS/ -- CA32516/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):61-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2420009" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects ; Cell Line ; Colony-Forming Units Assay ; Colony-Stimulating Factors/genetics/*pharmacology ; DNA/metabolism ; Escherichia coli/genetics ; Genes ; Granulocyte Colony-Stimulating Factor ; Granulocytes/*physiology ; Humans ; Leukemia/*pathology ; Leukemia, Myeloid/pathology ; Mice ; Plasmids ; Recombinant Proteins/*pharmacology
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  • 12
    Publication Date: 1986-02-07
    Description: Comparison of HTLV-III, the putative AIDS virus, with other related viruses, may help to reveal more about the origin of AIDS in humans. In this study, the nucleotide sequence of the gag and pol genes of an equine infectious anemia virus (EIAV) proviral DNA clone was determined. The sequence was compared with that of HTLV-III and of visna, a pathogenic lentivirus of sheep. The results show that these viruses constitute a family clearly distinct from that of the type C viruses or the BLV-HTLV-I and -II group. Within the family, EIAV, HTLV-III, and visna appear to be equally divergent from a common evolutionary ancestor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stephens, R M -- Casey, J W -- Rice, N R -- N0I-C-23909/PHS HHS/ -- New York, N.Y. -- Science. 1986 Feb 7;231(4738):589-94.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3003905" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Codon ; DNA, Viral/genetics ; Deltaretrovirus/*genetics ; *Genes, Viral ; Horses ; Humans ; Infectious Anemia Virus, Equine/*genetics ; Mice ; Visna-maedi virus/*genetics
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  • 13
    Publication Date: 1986-05-23
    Description: Infection of the central nervous system by mouse hepatitis virus strain A59, a murine neurotropic coronavirus, induces class I major histocompatibility complex antigens on mouse oligodendrocytes and astrocytes, cells that do not normally express these antigens on their surfaces. This induction, which occurs through soluble factors elaborated by infected glial cells, potentially allows immunocytes to interact with the glial cells and may play a critical role in the pathogenesis of virus-induced, immune-mediated demyelination in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzumura, A -- Lavi, E -- Weiss, S R -- Silberberg, D H -- NS11037/NS/NINDS NIH HHS/ -- NS21954/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 May 23;232(4753):991-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3010460" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*immunology ; Cells, Cultured ; Fluorescent Antibody Technique ; H-2 Antigens/*immunology ; Hepatitis, Viral, Animal/*immunology ; Macrophages/immunology ; Mice ; Murine hepatitis virus/immunology ; Neuroglia/*immunology ; Oligodendroglia/*immunology
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  • 14
    Publication Date: 1986-08-15
    Description: The genetic and molecular mechanisms that determine the capacity of a virus to utilize distinct pathways of spread in an infected host were examined by using reoviruses. Both reovirus type 1 and reovirus type 3 spread to the spinal cord following inoculation into the hindlimb or forelimb footpad of newborn mice. For type 3 this spread is through nerves and occurs via the microtubule-associated system of fast axonal transport. By contrast, type 1 spreads to the spinal cord through the bloodstream. With the use of reassortant viruses containing various combinations of double-stranded RNA segments (genes) derived from type 1 and type 3, the viral S1 double-stranded RNA segment was shown to be responsible for determining the capacity of reoviruses to spread to the central nervous system through these distinct pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tyler, K L -- McPhee, D A -- Fields, B N -- 2 P01 NS16998/NS/NINDS NIH HHS/ -- 5 R01 AI13178/AI/NIAID NIH HHS/ -- K11-AI00610/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 15;233(4765):770-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3016895" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Forelimb ; *Genes, Viral ; Hindlimb ; Mammalian orthoreovirus 3/*genetics/pathogenicity ; Mice ; Reoviridae/*genetics/pathogenicity ; Reoviridae Infections/microbiology ; Sciatic Nerve/physiology ; Species Specificity ; Spinal Cord/*microbiology
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  • 15
    Publication Date: 1986-05-09
    Description: Antigenic or mitogenic stimulation of T cells induces the secretion of an array of protein hormones that regulate immune responses. Molecular cloning has contributed strongly to our present understanding of the nature of this regulation. A complementary DNA (cDNA) library prepared from a cloned concanavalin A-activated mouse T-helper cell line was screened for abundant and induction-specific cDNA's. One such randomly chosen cDNA was found to encode mouse preproenkephalin messenger RNA (mRNA). Preproenkephalin mRNA represented about 0.4 percent of the mRNA in the activated cell line but was absent in resting cells of this line. Other induced T-helper cell lines have 0.1 to 0.5 percent of their mRNA as preproenkephalin mRNA. Induced T-helper cell culture supernatants have [Met]enkephalin-immunoreactive material. The production by activated T cells of a peptide neurotransmitter identifies a signal that can potentially permit T cells to modulate the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zurawski, G -- Benedik, M -- Kamb, B J -- Abrams, J S -- Zurawski, S M -- Lee, F D -- New York, N.Y. -- Science. 1986 May 9;232(4751):772-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2938259" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cattle ; Cell Line ; Cloning, Molecular ; DNA/genetics ; Enkephalins/*biosynthesis/genetics ; Humans ; *Lymphocyte Activation ; Mice ; Protein Precursors/*biosynthesis/genetics ; RNA, Messenger/*biosynthesis ; Rats ; T-Lymphocytes, Helper-Inducer/drug effects/metabolism/*physiology
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  • 16
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-01-24
    Description: The dynamics of the attachment of lymphocytes to the endothelium of high endothelial venules in murine Peyer's patches were studied in vivo. Lymphocytes adhered readily to the endothelium lining these vessels, but most of the adhering cells detached within a few seconds. Many lymphocytes, however, experienced multiple collisions with the high endothelial venules, and this substantially increased the efficiency of lymphocyte collection by these vessels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bjerknes, M -- Cheng, H -- Ottaway, C A -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):402-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3941903" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Endothelium/physiology ; Female ; In Vitro Techniques ; Lymphocytes/*physiology ; Mice ; Mice, Inbred BALB C ; Microscopy, Fluorescence ; Peyer's Patches/*physiology
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  • 17
    Publication Date: 1986-08-08
    Description: The production and action of immunoregulatory cytokines, including interleukin-1 (IL-1), are inhibited by glucocorticoid hormones in vivo and in vitro. Conversely, glucocorticoid blood levels were increased by factors released by human leukocytes exposed to Newcastle disease virus preparations. This activity was neutralized by an antibody to IL-1. Therefore the capacity of IL-1 to stimulate the pituitary-adrenal axis was tested. Administration of subpyrogenic doses of homogeneous human monocyte-derived IL-1 or the pI 7 form of human recombinant IL-1 to mice and rats increased blood levels of adrenocorticotropic hormone (ACTH) and glucocorticoids. Another monokine, tumor necrosis factor, and the lymphokines IL-2 and gamma-interferon had no such effects when administered in doses equivalent to or higher than those of IL-1. The stimulatory effect of IL-1 on the pituitary-adrenal axis seemed not to be mediated by the secondary release of products from mature T lymphocytes since IL-1 was endocrinologically active when injected into athymic nude mice. These results strongly support the existence of an immunoregulatory feedback circuit in which IL-1 acts as an afferent and glucocorticoid as an efferent hormonal signal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Besedovsky, H -- del Rey, A -- Sorkin, E -- Dinarello, C A -- AI15614/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 8;233(4764):652-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3014662" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/blood/physiology ; Animals ; Corticosterone/blood/physiology ; Female ; Glucocorticoids/blood/immunology/*physiology ; Humans ; Interleukin-1/immunology/pharmacology/*physiology ; Leukocytes/drug effects/physiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Nude ; Newcastle disease virus/immunology ; Rats ; Rats, Inbred Strains
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  • 18
    Publication Date: 1986-01-17
    Description: T lymphocytes recognize foreign antigen together with allele-specific determinants on membrane-bound class I and class II (Ia) gene products of the major histocompatibility complex. To identify amino acids of class II molecules critical to this recognition process, the genes encoding the beta chains of the I-Ak molecule were cloned from a wild-type B-cell hybridoma and from an immunoselected variant subline showing distinct serological and T-cell stimulatory properties. Nucleotide sequencing and DNA-mediated gene transfer established that a single base transition (G----A) encoding a change from glutamic acid to lysine at position 67 in the I-Ak beta molecule accounted for all the observed phenotypic changes of the variant cells. These results confirm the importance of residues 62 to 78 in the amino terminal domain of I-A beta for class II-restricted T-cell recognition of antigen and demonstrate the ability of a single substitution in this region to alter this recognition event.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, M A -- Glimcher, L A -- Nielsen, E A -- Paul, W E -- Germain, R N -- New York, N.Y. -- Science. 1986 Jan 17;231(4735):255-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3484558" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/genetics/immunology ; Base Sequence ; Cloning, Molecular ; Histocompatibility Antigens Class II/*immunology ; Humans ; Hybridomas/immunology ; Major Histocompatibility Complex ; Mice ; Mice, Inbred BALB C ; T-Lymphocytes/*immunology
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  • 19
    Publication Date: 1986-04-25
    Description: Nerve growth factor (NGF) and its receptor are important in the development of cells derived from the neural crest. Mouse L cell transformants have been generated that stably express the human NGF receptor gene transfer with total human DNA. Affinity cross-linking, metabolic labeling and immunoprecipitation, and equilibrium binding with 125I-labeled NGF revealed that this NGF receptor had the same size and binding characteristics as the receptor from human melanoma cells and rat PC12 cells. The sequences encoding the NGF receptor were molecularly cloned using the human Alu repetitive sequence as a probe. A cosmid clone that contained the human NGF receptor gene allowed efficient transfection and expression of the receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chao, M V -- Bothwell, M A -- Ross, A H -- Koprowski, H -- Lanahan, A A -- Buck, C R -- Sehgal, A -- NS-17551/NS/NINDS NIH HHS/ -- NS-23343-01/NS/NINDS NIH HHS/ -- NS21072/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Apr 25;232(4749):518-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3008331" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Transformation, Neoplastic/drug effects ; *Cloning, Molecular ; DNA, Recombinant ; Genes ; Humans ; Melanoma/metabolism ; Mice ; Oncogenes ; Rats ; Receptors, Cell Surface/*genetics ; Receptors, Nerve Growth Factor ; Repetitive Sequences, Nucleic Acid ; Tunicamycin/pharmacology
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  • 20
    Publication Date: 1986-03-14
    Description: Approximately 80 percent of all human sera that react with antigens of HTLV-III, the etiologic agent of the acquired immune deficiency syndrome (AIDS), recognize protein bands at 66 and 51 kilodaltons. A mouse hybridoma was produced that was specific to these proteins. Repeated cloning of the hybridoma did not separate the two reactivities. The p66/p51 was purified from HTLV-III lysates by immunoaffinity chromatography and subjected to NH2-terminal Edman degradation. Single amino acid residues were obtained in 17 successive degradation cycles. The sequence determined was a perfect translation of the nucleotide sequence of a portion of the HTLV-III pol gene. The purified p66/51 had reverse transcriptase activity and the monoclonal immunoglobulin G specifically removed the enzyme activity from crude viral extract as well as purified enzyme.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉di Marzo Veronese, F -- Copeland, T D -- DeVico, A L -- Rahman, R -- Oroszlan, S -- Gallo, R C -- Sarngadharan, M G -- New York, N.Y. -- Science. 1986 Mar 14;231(4743):1289-91.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2418504" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; Animals ; Antibodies, Monoclonal ; Antigens, Viral/genetics/immunology/isolation & purification ; Base Sequence ; Chromatography, Affinity ; Deltaretrovirus/*enzymology/genetics/immunology ; Electrophoresis, Polyacrylamide Gel ; Genes, Viral ; Humans ; Hybridomas/immunology ; Mice ; Mice, Inbred BALB C ; RNA-Directed DNA Polymerase/genetics/*immunology/isolation & purification
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  • 21
    Publication Date: 1986-07-25
    Description: The hepatitis B virus (HBV) envelope protein carrying the surface antigen (HBsAg) is assembled with cellular lipids in mammalian cells into empty viral envelopes. In a study to evaluate the capacity of such particles to present foreign peptide sequences in a biologically active form, in-phase insertions were created in the S gene encoding the major envelope protein. One of the sequences inserted was a synthetic DNA fragment encoding a poliovirus neutralization epitope. Mammalian cells expressing the modified gene secreted hybrid particles closely resembling authentic 22-nanometer HBsAg particles. These particles reacted with a poliovirus-specific monoclonal antibody and induced neutralizing antibodies against poliovirus. The results indicate that empty viral envelopes of HBV may provide a means for the presentation of peptide sequences and for their export from mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delpeyroux, F -- Chenciner, N -- Lim, A -- Malpiece, Y -- Blondel, B -- Crainic, R -- van der Werf, S -- Streeck, R E -- New York, N.Y. -- Science. 1986 Jul 25;233(4762):472-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2425433" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Viral/genetics/*immunology ; Epitopes/genetics/*immunology ; Genetic Engineering ; Hepatitis B Surface Antigens/genetics/*immunology ; Mice ; Neutralization Tests ; Poliovirus/*immunology ; Viral Envelope Proteins/genetics/immunology
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  • 22
    Publication Date: 1986-06-20
    Description: The hormone 17 beta-estradiol acts through its receptor system to induce MCF-7 human breast cancer cells to form tumors in athymic mice. In vitro studies have identified the production of estrogen-induced growth factors from MCF-7 cells that may have a role in growth control. These induced growth factors were sufficient to stimulate MCF-7 tumor growth in ovariectomized athymic mice, thus partially replacing estradiol. Growth factors may act as estrogen-induced "second messengers" in estrogen-responsive growth of human breast cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dickson, R B -- McManaway, M E -- Lippman, M E -- New York, N.Y. -- Science. 1986 Jun 20;232(4757):1540-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3715461" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*pathology ; Cell Division ; Cell Line ; Culture Media ; Estradiol/*physiology ; Female ; Humans ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Ovariectomy ; Receptors, Estradiol/*physiology ; Receptors, Estrogen/*physiology ; Transplantation, Heterologous
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  • 23
    Publication Date: 1986-07-25
    Description: The H-2 histocompatibility complex of the mouse is a multigene family, some members of which are essential for the immune response to foreign antigens. The structure and organization of these genes have been established by molecular cloning, and their regulation and function is being defined by expression of the cloned genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flavell, R A -- Allen, H -- Burkly, L C -- Sherman, D H -- Waneck, G L -- Widera, G -- New York, N.Y. -- Science. 1986 Jul 25;233(4762):437-43.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; H-2 Antigens/*genetics ; *Major Histocompatibility Complex ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Polymorphism, Genetic
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  • 24
    Publication Date: 1986-05-16
    Description: Two human T-cell leukemias carrying a t(8;14)(q24;q11) chromosome translocation were studied for rearrangements and expression of the c-myc oncogene. For one leukemia, rearrangement was detected in a region immediately distal (3') to the c-myc locus; no rearrangements of c-myc were observed in the second case (DeF). However, studies with hybrids between human and mouse leukemic T cells indicated that in the leukemic cells of DeF, the breakpoint in chromosome 14 occurred between genes for the variable (V alpha) and the constant (C alpha) regions for the alpha chain of the T-cell receptor. The C alpha locus had translocated to a region more than 38 kilobases 3' to the involved c-myc oncogene. Since human c-myc transcripts were expressed only in hybrids carrying the 8q+ chromosome but not in hybrids containing the normal chromosome 8, it is concluded that the translocation of the C alpha locus 3' to the c-myc oncogene can result in its transcriptional deregulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Erikson, J -- Finger, L -- Sun, L -- ar-Rushdi, A -- Nishikura, K -- Minowada, J -- Finan, J -- Emanuel, B S -- Nowell, P C -- Croce, C M -- CA10815/CA/NCI NIH HHS/ -- CA25875/CA/NCI NIH HHS/ -- CA39860/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 May 16;232(4752):884-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3486470" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Burkitt Lymphoma/genetics ; Chromosomes, Human, 13-15 ; Chromosomes, Human, 6-12 and X ; Humans ; Hybrid Cells ; Karyotyping ; Leukemia/*genetics ; Male ; Mice ; Middle Aged ; Nucleic Acid Hybridization ; *Oncogenes ; Receptors, Antigen, T-Cell/*genetics ; *T-Lymphocytes ; *Translocation, Genetic
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  • 25
    Publication Date: 1986-05-16
    Description: A specific DNA probe was used to study the effect of recombinant rat, mouse, and human gamma-interferon (gamma-IFN) on the course of sporozoite-induced malaria infections. In mice and rats infected with sporozoites of Plasmodium berghei, mouse and rat gamma-IFN's strongly inhibited the development of the exoerythrocytic forms in the liver liver cells of the hosts, but not the development of the erythrocytic stages. The degree of inhibition of the exoerythrocytic forms was proportional to the dose of gamma-IFN administered, but was independent of the number of sporozoites used for challenge. A 30 percent reduction in the development of exoerythrocytic forms in rat liver was achieved when 150 units (about 15 nanograms of protein) of rat gamma-IFN were injected a few hours before sporozoite challenge; the reduction was 90 percent or more with higher doses of gamma-IFN. The effect was less pronounced if the gamma-IFN was administered 18 hours before or a few hours after challenge. Human gamma-IFN also diminished the parasitemia in chimpanzees infected with sporozoites of the human malaria parasite Plasmodium vivax. The target of gamma-IFN activity may be the infected hepatocytes themselves, as shown by in vitro experiments in which small doses of the human lymphokine inhibited the development of exoerythrocytic forms of Plasmodium berghei in a human hepatoma cell line. These results suggest that immunologically induced interferon may be involved in controlling malaria infection under natural conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferreira, A -- Schofield, L -- Enea, V -- Schellekens, H -- van der Meide, P -- Collins, W E -- Nussenzweig, R S -- Nussenzweig, V -- New York, N.Y. -- Science. 1986 May 16;232(4752):881-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3085218" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Humans ; Interferon-gamma/pharmacology/*therapeutic use ; Liver/cytology ; Malaria/*drug therapy ; Mice ; Pan troglodytes ; Plasmodium berghei/drug effects ; Plasmodium vivax/drug effects ; Toxoplasma/drug effects
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  • 26
    Publication Date: 1986-12-05
    Description: Clonal cell lines derived from specific types of central neurons can be used to identify and characterize properties specific to those neurons. With somatic cell fusion techniques, nine clonal hybrid cell lines have been developed from the septal region of the mouse basal forebrain. Two lines express characteristics typical of cholinergic neurons--choline acetyltransferase activity and immunoreactivity, neurite formation with neurofilament protein immunoreactivity, and aggregation in rotation-mediated cell culture. These cell lines may be useful for studying the trophic interactions that support the development and maintenance of central cholinergic connections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hammond, D N -- Wainer, B H -- Tonsgard, J H -- Heller, A -- HD04583/HD/NICHD NIH HHS/ -- NS07195/NS/NINDS NIH HHS/ -- NS17661/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Dec 5;234(4781):1237-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3775382" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology ; Cell Line ; Choline O-Acetyltransferase/metabolism ; Cholinergic Fibers/*physiology ; Clone Cells ; Hybrid Cells ; Mice ; Mice, Inbred C57BL ; Neuroblastoma/metabolism ; Neurons/*physiology
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  • 27
    Publication Date: 1986-05-30
    Description: Primary Sjogren's syndrome is an autoimmune disorder characterized by dryness of the mouth and eyes. The human leukocyte antigen (HLA) locus DQ is related to the primary Sjogren's syndrome autoantibodies that bind the RNA proteins Ro/SSA and La/SSB. Both DQ1 and DQ2 alleles are associated with high concentrations of these autoantibodies. An analysis of all possible combinations at DQ has shown that the entire effect was due to heterozygotes expressing the DQ1 and DQ2 alleles. These data suggest that gene interaction between DQ1 and DQ2 (or alleles at associated loci), possibly from gene complementation of trans-associated surface molecules, influences the autoimmune response in primary Sjogren's syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harley, J B -- Reichlin, M -- Arnett, F C -- Alexander, E L -- Bias, W B -- Provost, T T -- AM 31133/AM/NIADDK NIH HHS/ -- AM 34159/AM/NIADDK NIH HHS/ -- HL 30748/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 May 30;232(4754):1145-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3458307" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Autoantibodies/*biosynthesis/genetics ; HLA-DQ Antigens ; HLA-DR Antigens ; Histocompatibility Antigens Class II/*genetics/immunology ; Mice ; Sjogren's Syndrome/*genetics/immunology
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  • 28
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-05-16
    Description: A new serine protease was encoded by a clone isolated from a murine cytotoxic T-lymphocyte complementary DNA library by an RNA-hybridization competition protocol. Complementary transcripts were detected in cytotoxic T lymphocytes, spleen cells from nude mice, a rat natural killer cell leukemia, and in two of eight T-helper clones (both cytotoxic), but not in normal mouse kidney, liver, spleen, or thymus, nor in several tested T- and B-cell tumors. T-cell activation with concanavalin A plus interleukin-2 induced spleen cells to express this gene with kinetics correlating with the acquisition of cytolytic capacity. The nucleotide sequence of this gene encoded an amino acid sequence of approximately 25,700 daltons, with 25 to 35 percent identity to members of the serine protease family. The active site "charge-relay" residues (His57, Asp102, and Ser195 of the chymotrypsin numbering system) are conserved, as well as the trypsin-specific Asp (position 189 in trypsin). A Southern blot analysis indicated that this gene is conserved in humans, mouse, and chicken. This serine protease may have a role in lymphocyte lysis and a "lytic cascade."〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gershenfeld, H K -- Weissman, I L -- AI 19512/AI/NIAID NIH HHS/ -- CA09032/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 May 16;232(4752):854-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2422755" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cloning, Molecular ; Concanavalin A/pharmacology ; DNA/genetics ; Endopeptidases/*genetics ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Nude ; Nucleic Acid Hybridization ; RNA/genetics ; Serine Endopeptidases ; T-Lymphocytes, Cytotoxic/drug effects/*metabolism
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  • 29
    Publication Date: 1986-02-14
    Description: Examination of the histocompatibility region of the nonobese diabetic (NOD) mouse with antibodies against class II glycoproteins (products of immune response genes of the major histocompatibility complex I-A and I-E), hybrid T-cell clones, and mixed-lymphocyte cultures and analysis of restriction fragment length polymorphisms indicate that the NOD mouse has a unique class II major histocompatibility complex with no expression of surface I-E, no messenger RNA for I-E alpha, and an I-A not recognized by any monoclonal antibodies or hybrid T-cell clones studied. In crosses of NOD mice with control C3H mice, the development of diabetes was dependent on homozygosity for the NOD mouse's unique major histocompatibility region.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hattori, M -- Buse, J B -- Jackson, R A -- Glimcher, L -- Dorf, M E -- Minami, M -- Makino, S -- Moriwaki, K -- Kuzuya, H -- Imura, H -- AM07009-01/AM/NIADDK NIH HHS/ -- AM32083-03/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Feb 14;231(4739):733-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3003909" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; DNA Restriction Enzymes/metabolism ; Diabetes Mellitus, Type 1/*genetics ; Genes, Recessive ; Genetic Linkage ; Genotype ; H-2 Antigens/genetics ; Histocompatibility Antigens Class II/*genetics ; Interleukin-2/biosynthesis ; *Major Histocompatibility Complex ; Mice ; Mice, Mutant Strains/*genetics ; Spleen/physiology
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  • 30
    Publication Date: 1986-11-14
    Description: The chromosomal localization of the genes encoding the four subunits of muscle nicotinic receptor was determined by analyzing restriction fragment length polymorphisms between two mouse species Mus musculus domesticus (DBA/2) and Mus spretus (SPE). Analysis of the progeny of the interspecies mouse backcross (DBA/2 X SPE) X DBA/2 showed that the alpha-subunit gene cosegregates with the alpha-cardiac actin gene on chromosome 17, that the beta-subunit gene is located on chromosome 11, and that the gamma- and delta-subunit genes cosegregate and are located on chromosome 1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heidmann, O -- Buonanno, A -- Geoffroy, B -- Robert, B -- Guenet, J L -- Merlie, J P -- Changeux, J P -- New York, N.Y. -- Science. 1986 Nov 14;234(4778):866-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3022377" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/genetics ; Animals ; *Chromosome Mapping ; Crosses, Genetic ; DNA/genetics ; DNA Restriction Enzymes ; Mice ; Mice, Inbred DBA ; Muridae ; Muscles/*analysis ; Nucleic Acid Hybridization ; Polymorphism, Genetic ; Receptors, Nicotinic/*genetics ; Species Specificity
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  • 31
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-12-12
    Description: Transformation of C3H10T1/2 cells by exposure to ultraviolet (UV) irradiation followed by tetradecanoyl phorbol acetate (TPA) has been used as a model of two-stage carcinogenesis. However, cells cloned from UV-TPA-induced foci (UV-TDTx cells) had a unique phenotype. Cloned UV-TDTx cells appeared transformed in pure culture but were unable to form foci when cocultured with C3H10T1/2 cells. However, in the presence of TPA, UV-TDTx cells form foci in mixed culture with C3H10T1/2 cells. This phenotype was the only one observed for UV-TPA transformants. These data suggest that communal suppression of cell division is a discrete phenomenon that must be overcome as one step in the multistage process of transformation, and this protocol permits the routine isolation of transformed cells responsive to density-dependent growth suppression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herschman, H R -- Brankow, D W -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1385-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3787250" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Line ; *Cell Transformation, Neoplastic/drug effects/radiation effects ; Clone Cells ; Mice ; Mice, Inbred C3H ; Phenotype ; Tetradecanoylphorbol Acetate/pharmacology ; *Ultraviolet Rays
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  • 32
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-04-04
    Description: Goat antibodies to idiotypes (anti-idiotypic antibodies; Ab2) that recognize an idiotype associated with the combining site of a BALB/c mouse IgG2a monoclonal antibody (Ab1) to human gastric carcinoma were used to immunize BALB/c mice and rabbits. A monoclonal anti-anti-idiotypic antibody (Ab3) of IgG1 isotype was obtained after immunization of mice. The Ab3 and the Ab1 showed identical binding specificities and bound with similar avidities to the same tumor antigen. The induction of Ab1-like Ab3 by Ab2 was not restricted to mice, since Ab3 could also be induced in rabbits. Both the mouse- and the rabbit-derived Ab3 bound the same gastrointestinal cancer-associated antigen as Ab1. These findings indicate that Ab2 induced the formation of antigen-specific Ab3, probably because it bears the internal image of the tumor-associated antigen. This Ab2 may therefore have potential for modulating the immune response of cancer patients to their tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herlyn, D -- Ross, A H -- Koprowski, H -- CA-10815/CA/NCI NIH HHS/ -- CA-21124/CA/NCI NIH HHS/ -- CA-33490/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):100-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3952496" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibodies ; Antibodies, Monoclonal ; Antigen-Antibody Complex ; Antigens, Neoplasm/*immunology ; Female ; Goats/immunology ; Humans ; Immunoglobulin Idiotypes/*immunology ; Mice ; Mice, Inbred BALB C/immunology ; Neoplasms/immunology ; Rabbits/immunology
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  • 33
    Publication Date: 1986-05-30
    Description: Glutamate decarboxylase (GAD; E.C. 4.1.1.15) converts glutamate to gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the vertebrate central nervous system. This report describes the isolation of a GAD complementary DNA clone by immunological screening of a lambda gt-11 brain complementary DNA expression library. The fusion protein produced by this clone catalyzes the conversion of glutamate to GABA and carbon dioxide, confirming its identity as GAD. Antibodies to beta-galactosidase remove GAD enzymatic activity from solution, showing that this activity is associated with the fusion protein. In immunoblotting experiments all three available antisera to GAD reacted with the fusion polypeptide and with two major polypeptides (molecular size, 60,000 and 66,000 daltons) in brain extracts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaufman, D L -- McGinnis, J F -- Krieger, N R -- Tobin, A J -- HD05615/HD/NICHD NIH HHS/ -- NS20356/NS/NINDS NIH HHS/ -- NS22256/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 May 30;232(4754):1138-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3518061" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*enzymology ; Cloning, Molecular ; DNA/genetics ; Escherichia coli/metabolism ; Glutamate Decarboxylase/biosynthesis/genetics/*metabolism ; Humans ; Mice ; Rats ; Recombinant Proteins/biosynthesis/metabolism ; gamma-Aminobutyric Acid/*biosynthesis
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  • 34
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-09-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kohler, G -- New York, N.Y. -- Science. 1986 Sep 19;233(4770):1281-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3092353" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*biosynthesis/genetics/immunology ; *Antibody Diversity ; Antibody Specificity ; Cell Fusion ; Hybridomas ; Immunoglobulin Heavy Chains/immunology ; Immunoglobulin Light Chains/immunology ; Immunoglobulin Variable Region/immunology ; Immunoglobulin kappa-Chains/immunology ; Immunoglobulin mu-Chains/immunology ; Mice ; Mice, Inbred BALB C ; Mutation
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  • 35
    Publication Date: 1986-04-25
    Description: Anterior pituitaries from the dwarf mouse strain "little" did not release growth hormone or accumulate adenosine 3',5'-monophosphate (cyclic AMP) in response to human and rat growth hormone-releasing factor (GRF). Dibutyryl cyclic AMP, as well as the adenylate cyclase stimulators forskolin and cholera toxin, markedly stimulated growth hormone (GH) release. The basis of the GH deficiency in the little mouse may therefore be a defect in an early stage of GRF-stimulated GH release related either to receptor binding or to the function of the hormone-receptor complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jansson, J O -- Downs, T R -- Beamer, W G -- Frohman, L A -- AM 17947/AM/NIADDK NIH HHS/ -- AM 30667/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 25;232(4749):511-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3008329" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Colforsin/pharmacology ; Cyclic AMP/analysis ; Dwarfism, Pituitary/*physiopathology ; Female ; Growth Hormone-Releasing Hormone/metabolism/pharmacology/physiology/secretion ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains/*physiology ; Pituitary Gland, Anterior/analysis/drug effects/physiopathology/secretion ; Receptors, Cell Surface/metabolism/*physiology ; *Receptors, Neuropeptide ; *Receptors, Pituitary Hormone-Regulating Hormone
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  • 36
    Publication Date: 1986-10-03
    Description: The cyclosporines are a family of cyclic endecapeptides that cause a profound suppression of primary immune stimulation both in vitro and in vivo. Recently, the regulatory protein calmodulin (CaM) has been implicated as a target for cyclosporin A (CsA) binding. This study utilized two less-active isomers of CsA to evaluate the specificity and biological significance of CaM binding. The three cyclosporines exhibited equivalent in vitro binding to CaM, regardless of immunosuppressive activity. Furthermore, CaM-dependent enzyme systems were inhibited equally by active and inactive cyclosporines, but only at concentrations 100 times those necessary to block lymphocyte activation. Thus the exquisite immunosuppressive stereospecificity displayed by cyclosporine isomers is not reflected in the binding to and inhibition of CaM, suggesting that inhibition of CaM-dependent processes is not sufficient to explain the immunosuppressive activity of CsA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LeGrue, S J -- Turner, R -- Weisbrodt, N -- Dedman, J R -- GM29323/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 3;234(4772):68-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3749892" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calmodulin/antagonists & inhibitors/metabolism/*physiology ; *Cyclosporine ; Cyclosporins/metabolism/*pharmacology ; Immune Tolerance/*drug effects ; Lymphocyte Activation/drug effects ; Mice ; Muscle Contraction/drug effects ; Muscle, Smooth/drug effects ; Stereoisomerism ; Sulfonamides/pharmacology ; Trifluoperazine/pharmacology
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  • 37
    Publication Date: 1986-07-18
    Description: Addition of mouse interferon-alpha/beta (IFN) to confluent, quiescent BALB/c 3T3 (clone A31) mouse fibroblasts resulted in a block or delay in serum-induced activation of the cell cycle. It was necessary to add IFN within 6 hours after serum stimulation to inhibit nuclear labeling with [3H]thymidine. This is consistent with the time required for platelet-derived growth factor (PDGF) to induce cells to become competent to respond to additional growth factors present in platelet-poor plasma. Simultaneous addition of IFN with PDGF inhibited the PDGF-induced synthesis of a 29-kilodalton and a 35-kilodalton protein that normally occurs within 1 hour after PDGF addition. IFN also suppressed the general increase in protein synthesis that occurs by the fifth hour after PDGF addition. These results show that IFN antagonizes the action of PDGF, thereby interfering with the activation of Go cells for G1 traverse and S-phase entry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, S L -- Kikuchi, T -- Pledger, W J -- Tamm, I -- CA 18213/CA/NCI NIH HHS/ -- CA 18608/CA/NCI NIH HHS/ -- CA 42713/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Jul 18;233(4761):356-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726533" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood ; Cell Cycle/*drug effects ; Electrophoresis, Polyacrylamide Gel ; Interferon Type I/*pharmacology ; Interphase ; Mice ; Mice, Inbred BALB C ; Molecular Weight ; Platelet-Derived Growth Factor/pharmacology ; Protein Biosynthesis ; Time Factors
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  • 38
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-10-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1986 Oct 31;234(4776):543-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3532323" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Epidermal Growth Factor ; History, 20th Century ; Italy ; Mice ; *Nerve Growth Factors ; *Nobel Prize ; United States
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  • 39
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-05-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1986 May 16;232(4752):824-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3085217" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/deficiency/genetics ; Animals ; Bone Marrow ; Genetic Diseases, Inborn/genetics/*therapy ; *Genetic Engineering ; Genetic Vectors ; Haplorhini ; Humans ; Mice
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  • 40
    Publication Date: 1986-12-12
    Description: The hypogonadal (hpg) mouse lacks a complete gonadotropin-releasing hormone (GnRH) gene and consequently cannot reproduce. Introduction of an intact GnRH gene into the genome of these mutant mice resulted in complete reversal of the hypogonadal phenotype. Transgenic hpg/hpg homozygotes of both sexes were capable of mating and producing offspring. Pituitary and serum concentrations of luteinizing hormone, follicle-stimulating hormone, and prolactin were restored to those of normal animals. Immunocytochemistry and in situ hybridization showed that GnRH expression was restored in the appropriate hypothalamic neurons of the transgenic hpg animals, an indication of neural-specific expression of the introduced gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mason, A J -- Pitts, S L -- Nikolics, K -- Szonyi, E -- Wilcox, J N -- Seeburg, P H -- Stewart, T A -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1372-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3097822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Follicle Stimulating Hormone/blood ; Gene Expression Regulation ; *Genetic Engineering ; Gonadotropin-Releasing Hormone/genetics ; Histocytochemistry ; Hypogonadism/*genetics ; Hypothalamus/analysis/cytology ; Infertility/genetics/*therapy ; Luteinizing Hormone/blood ; Male ; Mice ; Mutation ; Neurons/analysis ; Phenotype ; Prolactin/blood ; Tissue Distribution
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  • 41
    Publication Date: 1986-12-12
    Description: One characteristic of the immune response during hepatitis B virus (HBV) infection in humans is the vigorous production and subsequent persistence of antibodies of immunoglobulin (Ig) classes M and G to the nucleocapsid antigen (HBcAg). In this study HBcAg was shown to be similarly immunogenic in mice. When injected into athymic (nude) B10.BR and athymic BALB/c mice, HBcAg induced IgM and IgG class antibodies to HBc in spite of the absence of T cells in nude mice. In euthymic mice, HBcAg efficiently stimulated T-cell proliferation in vitro and helper T-cell function in vivo. The dual functions of HBcAg as a T-cell-independent and a T-cell-dependent antigen may explain its enhanced immunogenicity. Denaturation of HBcAg yields a nonparticulate antigen designated HBeAg; when HBeAg was used as the immunogen, antibody production required helper T-cell function. Although HBcAg and HBeAg are serologically distinct, they are structurally related, and in these experiments were highly cross-reactive at the T-cell level. These results suggest that the elevated levels of IgM antibodies to HBc and the enhanced immunogenicity of HBcAg during HBV infection in humans reflect the ability of HBcAg to directly activate B cells to produce antibodies to HBc in the presence or absence of HBcAg- or HBeAg-sensitized T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Milich, D R -- McLachlan, A -- AI00585/AI/NIAID NIH HHS/ -- AI20720/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1398-401.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3491425" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Capsid/*immunology ; Cross Reactions ; Hepatitis B Core Antigens/analysis ; Hepatitis B e Antigens/analysis ; Hepatitis B virus/*immunology ; Immunization ; Mice ; Mice, Inbred BALB C ; T-Lymphocytes/*immunology ; Viral Core Proteins/*immunology
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  • 42
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-08-01
    Description: Plasmacytoma (PCT) cell lines dependent for proliferation and survival on a factor elaborated by the murine macrophage cell line, P388D1, were established in vitro. Adherent peritoneal cells induced by pristane produced 50-fold greater amounts of this activity in vitro than did resident cells. The molecules responsible for plasmacytoma growth were distinct from a number of characterized factors including interleukin-1, -2, and -3, macrophage colony-stimulating factor, B-cell stimulatory factor-1, B-cell growth factor II, epidermal growth factor, transforming growth factor-beta, and gamma- and beta-interferon, none of which were able to support the growth of the factor-dependent PCT cell lines. These results suggest that PCT growth factor may be a novel factor that has not been previously characterized and, further, that its production is associated with the pristane-induced, chronic peritoneal inflammatory response that precedes plasmacytoma formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nordan, R P -- Potter, M -- New York, N.Y. -- Science. 1986 Aug 1;233(4763):566-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726549" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Division/drug effects ; Cell Line ; *Cell Survival/drug effects ; Growth Substances/*isolation & purification/pharmacology/physiology ; Humans ; In Vitro Techniques ; Macrophages/*physiology ; Mice ; Plasmacytoma/*physiopathology
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  • 43
    Publication Date: 1986-03-28
    Description: Transgenic mice were generated with pRSV-CAT, a chimeric gene construct containing the long terminal repeat of Rous sarcoma virus (RSV) linked to the bacterial gene encoding chloramphenicol acetyltransferase (CAT). CAT expression, detected in adult animals of five independent strains, was preferentially directed to organs rich in tendon, bone, and muscle. This pattern reflects the disease specificity of the intact virus and suggests that the tissue tropism of RSV is determined at least in part by the presence of endogenous tissue-specific factors that can promote expression of genetic information linked to the long terminal repeat. In two of the mouse strains, insertion of the pRSV-CAT DNA resulted in developmental abnormalities. One of these strains was characterized by a dominant trait of embryonic lethality, the other by a recessive trait of fused toes in all four feet.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Overbeek, P A -- Lai, S P -- Van Quill, K R -- Westphal, H -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1574-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006249" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Age Factors ; Animals ; Avian Sarcoma Viruses/*genetics ; Chloramphenicol O-Acetyltransferase ; DNA, Viral/*genetics ; Gene Expression Regulation ; Genes, Regulator ; Limb Deformities, Congenital ; Mice ; Repetitive Sequences, Nucleic Acid ; Tissue Distribution ; Transcription, Genetic ; Transfection
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  • 44
    Publication Date: 1986-07-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paul, S M -- Schwartz, R D -- Creveling, C R -- Hollingsworth, E B -- Daly, J W -- Skolnick, P -- New York, N.Y. -- Science. 1986 Jul 11;233(4760):228-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3014649" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Brain/*metabolism ; Cell Membrane/metabolism/*physiology ; Chick Embryo ; Chlorides/*metabolism ; Guinea Pigs ; Mice ; Rats ; Receptors, GABA-A/metabolism/*physiology ; Synaptosomes/metabolism
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  • 45
    Publication Date: 1986-05-16
    Description: Interleukin-1 (IL-1) is a product of mononuclear phagocytes that mediates changes characteristic of the response to inflammation or tissue injury (the acute-phase response). One of two structurally and functionally homologous major histocompatibility complex (MHC) class III genes encodes a positive acute-phase protein, complement factor B. The closely linked complement C2 gene is not affected during the acute-phase response. Purified human IL-1, pH 7.0, and recombinant-generated murine IL-1, pH 5.0, increased the expression of factor B and other positive acute-phase proteins in human hepatoma cells but decreased the expression of albumin, a negative acute-phase reactant. Furthermore, in a murine fibroblast L-cell line transfected with cosmid DNA bearing the human C2 and factor B genes, IL-1 mediated a reversible dose- and time-dependent increase in factor B expression in the transfected cells. Expression of the C2 gene was not affected by IL-1. The effect of IL-1 on factor B expression involves a mechanism acting at a pre-translational level as demonstrated by an increase in specific messenger RNA content and a corresponding increase in biosynthesis and secretion of factor B. The structural basis and mechanism for selective and independent regulation of these genes provides insight into the molecular control of the inflammatory response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perlmutter, D H -- Goldberger, G -- Dinarello, C A -- Mizel, S B -- Colten, H R -- AI20032/AI/NIAID NIH HHS/ -- GM33293/GM/NIGMS NIH HHS/ -- HD17461/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 May 16;232(4752):850-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3010455" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Hepatocellular/metabolism ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts/metabolism ; Gene Expression Regulation/drug effects ; Humans ; Interleukin-1/*pharmacology ; Liver Neoplasms/metabolism ; Major Histocompatibility Complex/*drug effects ; Mice
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  • 46
    Publication Date: 1986-10-10
    Description: Biological and serological assays have been used to define four subregions for the I region of the major histocompatibility complex (MHC) in the order I-A, I-B, I-J, and I-E. The I-J subregion presumably encodes the I-J polypeptide of the elusive T-cell suppressor factors. Restriction enzyme site polymorphisms and DNA sequence analyses of the I region from four recombinant mouse strains were used to localize the putative I-B and I-J subregions to a 1.0-kilobase (kb) region within the E beta gene. Sequencing this region from E beta clones derived from the two mouse strains: B10.A(3R), I-Jb and B10.A(5R), I-Jk initially used to define the I-J subregion revealed that these regions are identical, hence the distinct I-Jb and I-Jk molecules cannot be encoded by this DNA. In addition, the DNA sequence data also refute the earlier mapping of the I-B subregion. Analysis of the DNA sequences of three parental and four I region recombinants reveals that the recombinant events in three of the recombinant strains occurred within a 1-kb region of DNA, supporting the proposition that a hotspot for recombination exists in the I region. The only striking feature of this hotspot is a tetramer repeat (AGGC)n that shows 80 percent homology to the minisatellite sequence which may facilitate recombination in human chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kobori, J A -- Strauss, E -- Minard, K -- Hood, L -- New York, N.Y. -- Science. 1986 Oct 10;234(4773):173-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3018929" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA Restriction Enzymes ; Genes, MHC Class II ; *Major Histocompatibility Complex ; Mice ; *Recombination, Genetic ; Repetitive Sequences, Nucleic Acid ; Suppressor Factors, Immunologic/genetics
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  • 47
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-11-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kolata, G -- New York, N.Y. -- Science. 1986 Nov 28;234(4780):1076-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3775376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; H-Y Antigen/genetics ; Humans ; Lizards ; Male ; Mice ; *Sex Determination Analysis ; *Y Chromosome
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  • 48
    Publication Date: 1986-01-10
    Description: Antibodies were raised in mice immunized with several recombinant and synthetic peptides of the circumsporozoite protein of Plasmodium falciparum. The antibodies were evaluated for protective activity in a human hepatocyte culture system. They exerted their protective effect against the parasite at three points: sporozoite attachment to the hepatocyte surface, entry, and subsequent intracellular development. Inhibition of attachment and entry were found to be related to the antibody titer against the authentic circumsporozoite protein on the sporozoite surface, especially when peptides were administered with alum or complete Freund's adjuvant. Even when invasion was not totally inhibited, the presence of abnormal trophozoites and a frequent inhibition of schizont development in long-term cultures suggested continued activity of antibodies at the intracellular level after sporozoite penetration had been completed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mazier, D -- Mellouk, S -- Beaudoin, R L -- Texier, B -- Druilhe, P -- Hockmeyer, W -- Trosper, J -- Paul, C -- Charoenvit, Y -- Young, J -- New York, N.Y. -- Science. 1986 Jan 10;231(4734):156-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3510455" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/*immunology ; Antigens, Protozoan/*immunology ; Fluorescent Antibody Technique ; Humans ; In Vitro Techniques ; Liver/cytology/parasitology ; Mice ; Peptides/immunology ; Plasmodium falciparum/*immunology ; Recombinant Proteins/immunology
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  • 49
    Publication Date: 1986-11-28
    Description: The bombesin-like peptides are potent mitogens for Swiss 3T3 fibroblasts, human bronchial epithelial cells, and cells isolated from small cell carcinoma of the lung. The mechanism of signal transduction in the proliferative response to bombesin was investigated by studying the effect of Bordetella pertussis toxin on bombesin-stimulated mitogenesis. At nanomolar concentrations, bombesin increased levels of c-myc messenger RNA and stimulated DNA synthesis in Swiss 3T3 cells. Treatment of the cells with pertussis toxin (5 nanograms per milliliter) completely blocked bombesin-enhanced c-myc expression and eliminated bombesin-stimulated DNA synthesis. This treatment had essentially no effect on the mitogenic responses to either platelet-derived growth factor or phorbol 12,13-dibutyrate. These results suggest that the mitogenic actions of bombesin-like growth factors are mediated through a pertussis toxin-sensitive guanine nucleotide-binding protein. Furthermore they indicate that bombesin-like growth factors act through pathways that are different from those activated by platelet-derived growth factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Letterio, J J -- Coughlin, S R -- Williams, L T -- R01 HL 32898/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 28;234(4780):1117-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3465038" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bombesin/*pharmacology ; Cells, Cultured ; DNA, Neoplasm/*biosynthesis ; Humans ; Mice ; Oncogenes/*drug effects ; *Pertussis Toxin ; Phorbol 12,13-Dibutyrate ; Phorbol Esters/pharmacology ; Platelet-Derived Growth Factor/pharmacology ; Virulence Factors, Bordetella/*pharmacology
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  • 50
    Publication Date: 1986-03-14
    Description: Human malignant melanoma cells express specific chondroitin sulfate proteoglycans (mel-CSPG) on the surface, both in vivo and in vitro. Melanocytes in normal skin show no detectable mel-CSPG but can be induced to express the antigen when cultured in the presence of cholera toxin and the tumor promoter 12-O-tetradecanoylphorbol-13-acetate. Most other cell types do not express mel-CSPG either in vivo or in vitro. A study was designed to examine regulatory signals controlling mel-CSPG expression. The gene encoding mel-CSPG was mapped to human chromosome 15, and this chromosome was introduced into rodent cells derived from distinct differentiation lineages. Three types of mel-CSPG--expressing hybrids were found: (i) hybrids derived from human melanomas; (ii) hybrids derived from human cells that do not express mel-CSPG; and (iii) hybrids derived from human cells expressing mel-CSPG that are antigen-negative but that are induced to express mel-CSPG when cultured on extracellular matrix instead of plastic surfaces. Thus, mel-CSPG expression can be controlled both through intrinsic signals, provided by the differentiation program of the rodent fusion partner, and through extrinsic signals, provided by specific cell-matrix interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rettig, W J -- Real, F X -- Spengler, B A -- Biedler, J L -- Old, L J -- CA-08748/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Mar 14;231(4743):1281-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3633135" target="_blank"〉PubMed〈/a〉
    Keywords: Aggrecans ; Animals ; Antibodies, Monoclonal ; Cell Line ; Cholera Toxin/pharmacology ; Chromosome Mapping ; Chromosomes, Human, 13-15 ; Cricetinae ; Cricetulus ; *Extracellular Matrix Proteins ; Gene Expression Regulation/drug effects ; Glycoproteins/*biosynthesis/genetics ; Humans ; Hybrid Cells/drug effects/*metabolism ; Lectins, C-Type ; Lymphocytes/metabolism ; Melanocytes/drug effects/metabolism ; Melanoma/*metabolism ; Mice ; Neoplasm Proteins/*biosynthesis/genetics ; Neuroblastoma/metabolism ; *Proteoglycans ; Rats ; Tetradecanoylphorbol Acetate/pharmacology
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  • 51
    Publication Date: 1986-07-25
    Description: Bovine papillomavirus (BPV-1) contains two independent transforming genes that have been mapped to the E5 and E6 open reading frames (ORF's). The E5 transforming protein was identified by means of an antiserum against a synthetic peptide corresponding to the 20 COOH-terminal amino acids of the E5 ORF. The E5 polypeptide is the smallest viral transforming protein yet characterized; it had an apparent size of 7 kilodaltons. The transforming polypeptide is encoded entirely within the second half of the E5 ORF and its predicted amino acid composition is very unusual; 68% of the amino acids are strongly hydrophobic and 34% are leucine. Cell fractionation studies localized this polypeptide predominantly to cellular membranes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schlegel, R -- Wade-Glass, M -- Rabson, M S -- Yang, Y C -- New York, N.Y. -- Science. 1986 Jul 25;233(4762):464-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3014660" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bovine papillomavirus 1/*genetics ; Cell Line ; Cell Transformation, Viral ; *Genes, Viral ; Mice ; Oncogene Proteins, Viral/*genetics ; Papillomaviridae/*genetics
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  • 52
    Publication Date: 1986-06-13
    Description: Almost all B cells in autoimmune mice with the viable motheaten (mev) mutation express the Ly-1 cell surface antigen, which marks a minor population of B cells constituting a separate lineage in normal mice. Immunoglobulins primarily of the M and G3 classes, which in both normal and mev mice contain high levels of lambda light chain, are produced in excess in mev mice. These and other observations suggest that the development of B cells that express Ly-1 is regulated independently from the development of B cells that do not express Ly-1. B cells bearing the Ly-1 surface antigen may play specialized roles in the normal immune system and in autoimmunity by regulating other B cells via lymphokines, by producing antibodies to self and certain foreign antigens, and by preferentially secreting immunoglobulin M and immunoglobulin G3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sidman, C L -- Shultz, L D -- Hardy, R R -- Hayakawa, K -- Herzenberg, L A -- AI-20232/AI/NIAID NIH HHS/ -- CA-20408/CA/NCI NIH HHS/ -- CA-35845/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Jun 13;232(4756):1423-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3487115" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Ly/*immunology ; Autoimmune Diseases/genetics/*immunology ; B-Lymphocytes/classification/*immunology ; Flow Cytometry ; Immunoglobulin D/metabolism ; Immunoglobulin G/metabolism ; Immunoglobulin M/metabolism ; Immunoglobulins/analysis ; Lymph Nodes/cytology ; Mice ; Mice, Mutant Strains/*immunology ; Peritoneal Cavity/cytology ; Spleen/cytology
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  • 53
    Publication Date: 1986-02-14
    Description: While assessing a potential role of adrenal glands in the production of the hitherto unidentified puberty-delaying pheromone of female mice, the urinary volatile profiles of normal and adrenalectomized animals were quantitatively compared. Six components, whose concentrations were depressed after adrenalectomy, were identified: 2-heptanone, trans-5-hepten-2-one, trans-4-hepten-2-one, n-pentyl acetate, cis-2-penten-1-yl acetate, and 2,5-dimethylpyrazine. When these laboratory-synthesized chemicals were added (in their natural concentrations) to either previously inactive urine from adrenalectomized females or plain water, the biological activity was fully restored.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Novotny, M -- Jemiolo, B -- Harvey, S -- Wiesler, D -- Marchlewska-Koj, A -- New York, N.Y. -- Science. 1986 Feb 14;231(4739):722-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3945805" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/*physiology ; Animals ; Female ; Ketones/urine ; Mice ; Ovary/physiology ; Pentanols/urine ; Pheromones/physiology/urine ; Pyrazines/urine ; *Sexual Maturation
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  • 54
    Publication Date: 1986-08-08
    Description: The MH-3 gene, which contains a homeo box that is expressed specifically in the adult testis, was identified and mapped to mouse chromosome 6. By means of in situ hybridization with adult testis sections and Northern blot hybridization with testis RNA from prepuberal mice and from Sl/Sld mutant mice, it was demonstrated that this gene is expressed in male germ cells during late meiosis. In the embryo, MH-3 transcripts were present at day 11.5 post coitum, a stage in mouse development when gonadal differentiation has not yet occurred. The MH-3 gene may have functions in spermatogenesis and embryogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rubin, M R -- Toth, L E -- Patel, M D -- D'Eustachio, P -- Nguyen-Huu, M C -- New York, N.Y. -- Science. 1986 Aug 8;233(4764):663-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726554" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA/genetics ; Drosophila ; Embryo, Mammalian/*metabolism ; *Embryo, Nonmammalian ; *Genes ; Male ; Mice ; Morphogenesis ; Mutation ; Nucleic Acid Hybridization ; Sequence Homology, Nucleic Acid ; Spermatocytes/*metabolism ; Spermatogenesis
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  • 55
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-06-27
    Description: Recent studies of animals with complex nervous systems, including humans and other primates, have improved our understanding of how the brain accomplishes learning and memory. Major themes of recent work include the locus of memory storage, the taxonomy of memory, the distinction between declarative and procedural knowledge, and the question of how memory changes with time, that is, the concepts of forgetting and consolidation. An important recent advance is the development of an animal model of human amnesia in the monkey. The animal model, together with newly available neuropathological information from a well-studied human patient, has permitted the identification of brain structures and connections involved in memory functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Squire, L R -- MH24600/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1986 Jun 27;232(4758):1612-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3086978" target="_blank"〉PubMed〈/a〉
    Keywords: Alcohol Amnestic Disorder/physiopathology ; Amnesia/physiopathology ; Amnesia, Retrograde/physiopathology ; Amygdala/physiology ; Animals ; Brain/physiology/physiopathology ; Electroconvulsive Therapy ; Haplorhini ; Hippocampus/physiology ; Humans ; Learning/physiology ; Memory/*physiology ; Memory Disorders/physiopathology ; Memory, Short-Term/physiology ; Mice ; Models, Neurological ; Retention (Psychology)/physiology
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  • 56
    Publication Date: 1986-04-11
    Description: Second-passage rat embryo cells were transfected with a neomycin resistance gene and the activated form of the c-Ha-ras I gene, or with these two genes plus the adenovirus type 2 E1a gene. Foci of morphologically transformed cells were observed in both cases; however, the frequency of transformation was at least ten times higher with two oncogenes than with the ras gene alone. All the transformed cell lines gave rise to rapidly growing tumors when injected subcutaneously into nude mice. All but one of the cell lines transformed by the ras oncogene alone formed metastatic nodules in the lungs of animals that had been injected subcutaneously with transformed cells. When transformed cells were injected intravenously, all the ras single-gene transformants gave rise to many metastatic lung nodules. In contrast, cell lines transformed with ras and E1a did not generate metastases after subcutaneous injection and gave rise to very few metastatic lung nodules after intravenous injection. These data demonstrate that a fully malignant cell with metastatic potential, as measured in an immunodeficient animal, can be obtained from early passage embryo cells by the transfection of the ras oncogene alone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pozzatti, R -- Muschel, R -- Williams, J -- Padmanabhan, R -- Howard, B -- Liotta, L -- Khoury, G -- 3F32CA07245-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 11;232(4747):223-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3456644" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma/genetics ; Cell Line ; Cell Transformation, Neoplastic/*metabolism ; Cricetinae ; Genetic Engineering ; Mice ; Mice, Nude ; *Oncogenes ; Plasmids ; Rats/embryology ; Rats, Inbred Strains/embryology ; Transfection ; Urinary Bladder Neoplasms/genetics
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  • 57
    Publication Date: 1986-06-27
    Description: The posttranslational maturation of a complex precursor polyprotein, human proenkephalin, was assessed by infection of a wide spectrum of cell types with a recombinant vaccinia virus that expressed human proenkephalin. The infected cells rapidly produced both cellular and secreted Met-enkephalin immunoreactivity. Although each cell line could secrete intact proenkephalin, only a mouse pituitary line was capable of processing proenkephalin to mature enkephalin peptides. The quantity of intact proenkephalin secreted from BSC-40 cells (derived from African Green monkey kidney) was sufficient to establish the value of vaccinia virus as a mammalian cell expression vector.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomas, G -- Herbert, E -- Hruby, D E -- 7 RO1 DA04154-01/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1986 Jun 27;232(4758):1641-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3754979" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cercopithecus aethiops ; Enkephalin, Methionine/biosynthesis ; Enkephalins/*biosynthesis/genetics ; Genetic Vectors ; Humans ; Mice ; Protein Precursors/*biosynthesis/genetics ; Rats ; Recombinant Proteins/*biosynthesis ; Vaccinia virus/*genetics
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  • 58
    Publication Date: 1986-10-31
    Description: T lymphocytes express on their surface not only a specific receptor for antigen and major histocompatibility complex proteins, but also a number of additional glycoproteins that are thought to play accessory roles in the processes of recognition and signal transduction. L3T4 is one such T-cell surface protein that is expressed on most mouse thymocytes and on mature mouse T cells that recognize class II (Ia) major histocompatibility complex proteins. Such cells are predominantly of the helper/inducer phenotype. In this study, complementary DNA clones encoding L3T4 were isolated and sequenced. The predicted protein sequence shows that L3T4 is a member of the immunoglobulin gene superfamily. It is encoded by a single gene that does not require rearrangement prior to expression. Although the protein has not previously been demonstrated on nonhematopoietic cells, two messenger RNA species specific for L3T4 are found in brain. The minor species comigrates with the L3T4 transcript in T cells, whereas the major species is 1 kilobase smaller.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tourvieille, B -- Gorman, S D -- Field, E H -- Hunkapiller, T -- Parnes, J R -- 1 F32 CA07877-01/CA/NCI NIH HHS/ -- AI11313/AI/NIAID NIH HHS/ -- GM34991/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 31;234(4776):610-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3094146" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, Differentiation, T-Lymphocyte ; Antigens, Surface/genetics/*isolation & purification ; Base Sequence ; Brain/*metabolism ; Cloning, Molecular ; DNA/genetics/isolation & purification ; Humans ; Mice ; Mice, Inbred C57BL ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Sequence Homology, Nucleic Acid ; T-Lymphocytes/*immunology/metabolism
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  • 59
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-10-17
    Description: Human interferon stimulates a transient two- to threefold increase in the concentration of diacylglycerol and inositol tris-phosphate within 15 to 30 seconds of cell exposure to interferon. Antibodies to interferon inhibit this effect. The stimulation was measurable in isolated cell membranes exposed to interferon. Human alpha and beta, but not gamma, interferon stimulate this increase in cells containing the appropriate interferon receptor. The effect was proportional to the number of interferon receptors. Both the diacylglycerol increase and antiviral effects induced by interferon could be correlated in terms of dose dependence. Thus, a transient diacylglycerol increase is an early event in the interferon-induced transmembrane signaling process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yap, W H -- Teo, T S -- Tan, Y H -- New York, N.Y. -- Science. 1986 Oct 17;234(4774):355-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2429366" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication ; Cell Membrane/drug effects ; Diglycerides/analysis ; Dose-Response Relationship, Drug ; Fibroblasts/analysis/drug effects ; Humans ; Inositol 1,4,5-Trisphosphate ; Inositol Phosphates/analysis ; Interferon Type I/pharmacology ; Interferon-gamma/pharmacology ; Interferons/*pharmacology/physiology ; Mice ; Receptors, Immunologic/metabolism ; Receptors, Interferon
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  • 60
    Publication Date: 1986-04-11
    Description: Serum amyloid A protein (SAA) is a precursor for a major component of amyloid fibrils, which, upon deposition, cause secondary amyloidosis in diseases such as rheumatoid arthritis. In mice, SAA is encoded by at least three genes, which show diverse expression during inflammation. Furthermore, in amyloidosis-resistant SJL mice, the gene expression for one SAA isotype, SAA2, is defective, although SAA2 gene expression is normal in amyloidosis-susceptible BALB/c mice. Because only SAA2-derived products deposit in mouse amyloid tissues, the resistance of SJL mice to amyloidosis seems to be due to defective SAA2 gene expression. Thus, the study emphasizes the importance of SAA gene structure in determining susceptibility to amyloidosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamamoto, K -- Shiroo, M -- Migita, S -- New York, N.Y. -- Science. 1986 Apr 11;232(4747):227-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3456645" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid/*genetics ; Amyloidosis/*genetics ; Animals ; DNA/genetics/metabolism ; Genetic Engineering ; Humans ; Mice ; Mice, Inbred BALB C ; Nucleic Acid Hybridization ; Serum Amyloid A Protein/*genetics
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  • 61
    Publication Date: 1986-07-11
    Description: The ninth component of complement (C9) and the pore-forming protein (PFP or perforin) from cytotoxic T lymphocytes polymerize to tubular lesions having an internal diameter of 100 A and 160 A, respectively, when bound to lipid bilayers. Polymerized C9, assembled by slow spontaneous or rapid Zn2+-induced polymerization, and polyperforin, which is assembled only in the presence of Ca2+, constitute large aqueous pores that are stable, nonselective for solutes, and insensitive to changes of membrane potential. Monospecific polyclonal antibodies to purified C9 and PFP show cross-reactivity, suggesting structural homology between the two molecules. The structural and functional homologies between these two killer molecules imply an active role for pore formation during cell lysis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, J D -- Cohn, Z A -- Podack, E R -- AI070127/AI/NIAID NIH HHS/ -- AI18525/AI/NIAID NIH HHS/ -- CA3019/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Jul 11;233(4760):184-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2425429" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Centrifugation, Isopycnic ; Complement C9/*immunology/physiology ; Cross Reactions ; Humans ; Ion Channels/physiology ; *Membrane Glycoproteins ; Membrane Proteins/*immunology/physiology ; Mice ; Molecular Weight ; Perforin ; Pore Forming Cytotoxic Proteins ; T-Lymphocytes, Cytotoxic/*physiology ; Zinc/physiology
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  • 62
    Publication Date: 1986-05-16
    Description: Genes that are expressed exclusively in cytotoxic T cells should encode proteins that are essential for target cell lysis in cell-mediated immune responses. The sequences of two cytotoxic T lymphocyte-specific complementary DNA's (cDNA's) suggest that the two genes encode serine proteases. A full-length cDNA corresponding to one of the genes was isolated and sequenced. The predicted protein resembles serine proteases in that it includes all the residues that form the catalytic triad of the active site of serine proteases. Moreover, it has sequence characteristics thought to occur only in rat mast cell protease type II. These results are in accord with the view that a protease cascade plays a key role in cytotoxic T-cell activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lobe, C G -- Finlay, B B -- Paranchych, W -- Paetkau, V H -- Bleackley, R C -- New York, N.Y. -- Science. 1986 May 16;232(4752):858-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3518058" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Endopeptidases/*genetics ; Genes ; Mice ; Serine Endopeptidases ; T-Lymphocytes, Cytotoxic/*metabolism
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  • 63
    Publication Date: 1986-11-14
    Description: Interleukin-2 (IL-2) binds to both high- and low-affinity classes of IL-2 receptors on activated T lymphocytes. Only the high-affinity receptors are involved in receptor-mediated endocytosis and normally transduce the mitogenic signals of IL-2; however, the structural features distinguishing the high- and low-affinity receptors are unknown. When 125I-labeled IL-2 was chemically cross-linked to activated human T lymphocytes, two major bands were identified. First, as predicted, a 68- to 72-kilodalton band, consisting of IL-2 (15.5 kilodaltons) cross-linked to the IL-2 receptor (55 kilodaltons), was observed. Second, an unpredicted 85- to 92-kilodalton moiety was detected. This band was not present when IL-2 was cross-linked to transfected C127 cells, which exclusively express low-affinity receptors. The data presented are most consistent with the existence of a 70- to 77-kilodalton glycoprotein subunit (p70) which, upon associating with the 55-kilodalton low-affinity receptor (p55), transforms it into a high-affinity site. It is proposed that p55 and p70 be referred to as the alpha and beta subunits, respectively, of the high-affinity IL-2 receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharon, M -- Klausner, R D -- Cullen, B R -- Chizzonite, R -- Leonard, W J -- New York, N.Y. -- Science. 1986 Nov 14;234(4778):859-63.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3095922" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cross-Linking Reagents ; Humans ; Immunosorbent Techniques ; Interleukin-2/metabolism ; Leukemia, Lymphoid/metabolism ; Lymphocyte Activation ; Mice ; Molecular Weight ; Receptors, Immunologic/*metabolism ; Receptors, Interleukin-2 ; Succinimides ; T-Lymphocytes/metabolism
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  • 64
    Publication Date: 1986-01-24
    Description: Parathyroid hormone-like factors have been found in extracts of tumors associated with humoral hypercalcemia of malignancy, many of which are of squamous epithelial origin. Cultured, nonmalignant human keratinocytes were examined for the production of similar factors. Keratinocyte-conditioned medium from ten cultures stimulated the production of cyclic adenosine monophosphate in clonally derived rat osteosarcoma cells sensitive to parathyroid hormone. Bovine [Nle8,18, Tyr34]PTH-(3-34)NH2, a competitive inhibitor of parathyroid hormone, stopped the adenylate cyclase production stimulated by keratinocyte-conditioned medium, but antisera to parathyroid hormone had no effect on such adenylate cyclase activity. The active component of keratinocyte-conditioned medium has a molecular weight exceeding that of native parathyroid hormone. These characteristics are shared by the parathyroid hormone receptor agonists associated with humoral hypercalcemia of malignancy, which suggests that normal human keratinocytes may produce a factor related to that produced by malignant tumors associated with humoral hypercalcemia of malignancy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merendino, J J Jr -- Insogna, K L -- Milstone, L M -- Broadus, A E -- Stewart, A F -- AM 30102/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):388-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2417317" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Animals ; Cattle ; Cells, Cultured ; Cyclic AMP/metabolism ; Epidermis/*cytology/metabolism/physiology ; Humans ; Isoproterenol/pharmacology ; Keratins/*metabolism ; Mice ; Osteosarcoma/metabolism ; Parathyroid Hormone/pharmacology/*physiology ; Peptide Fragments/pharmacology ; Rats ; Teriparatide
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  • 65
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-05-02
    Description: A novel procedure for saturation mutagenesis of cloned DNA was used to obtain more than 100 single base substitutions within the promoter of the mouse beta-major globin gene. The effects of these promoter substitutions on transcription were determined by transfecting the cloned mutant genes into HeLa cells on plasmids containing an SV40 transcription enhancer, and measuring the levels of correctly initiated beta-globin transcripts after 2 days. Mutations in three regions of the promoter resulted in a significant decrease in the level of transcription: (i) the CACCC box, located between -87 and -95, (ii) the CCAAT box, located between -72 and -77, and (iii) the TATA box, located between -26 and -30 relative to the start site of transcription. In contrast, two different mutations in nucleotides immediately upstream from the CCAAT box resulted in a 3- to 3.5-fold increase in transcription. With two minor exceptions, single base substitutions in all other regions of the promoter had no effect on transcription. These results precisely delineate the cis-acting sequences required for accurate and efficient initiation of beta-globin transcription, and they establish a general approach for the fine structure genetic analysis of eukaryotic regulatory sequences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myers, R M -- Tilly, K -- Maniatis, T -- New York, N.Y. -- Science. 1986 May 2;232(4750):613-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3457470" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Genes ; Genetic Engineering ; Globins/biosynthesis/*genetics ; HeLa Cells ; Humans ; Mice ; Mutation ; *Promoter Regions, Genetic ; Transcription, Genetic
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  • 66
    Publication Date: 1986-04-11
    Description: The hypothesis that red-green "color blindness" is caused by alterations in the genes encoding red and green visual pigments has been tested and shown to be correct. Genomic DNA's from 25 males with various red-green color vision deficiencies were analyzed by Southern blot hybridization with the cloned red and green pigment genes as probes. The observed genotypes appear to result from unequal recombination or gene conversion (or both). Together with chromosome mapping experiments, these data identify each of the cloned human visual pigment genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nathans, J -- Piantanida, T P -- Eddy, R L -- Shows, T B -- Hogness, D S -- New York, N.Y. -- Science. 1986 Apr 11;232(4747):203-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3485310" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Chromosomes, Human ; Color ; *Color Perception/physiology ; Color Vision Defects/genetics ; DNA/genetics/metabolism ; Gene Frequency ; *Genes ; Genetic Variation ; Genotype ; Humans ; Mice ; Nucleic Acid Hybridization ; Retinal Pigments/genetics ; X Chromosome
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 67
    Publication Date: 1986-08-29
    Description: Insulin action may involve the intracellular generation of low molecular weight substances that modulate certain key enzymes. The production of two substances that regulate the activity of adenosine 3',5'-monophosphate phosphodiesterase was evaluated in cultured myocytes by incorporation of radiolabeled precursors. Insulin caused the rapid hydrolysis of a chemically undefined membrane glycolipid, resulting in the production of two related complex carbohydrates as well as diacylglycerol. Both the glycolipid precursor and the aqueous products were monitored by labeling with radioactive inositol and glucosamine. Depletion of the labeled precursor and the appearance of labeled water-soluble products and diacylglycerol occurred within 30 seconds after hormone treatment and was followed by rapid resynthesis of the precursor. The aqueous products that were radioactively labeled appeared chromatographically and electrophoretically identical to phosphodiesterase modulating activities produced by insulin from the same cells. The purified radiolabeled and bioactive substances had similar chemical properties. Hydrolysis of the glycolipid precursor and subsequent generation of products could be reproduced by incubation of extracted lipids with a phosphatidylinositol-specific phospholipase C. These studies suggest that insulin stimulates an endogenous, selective phospholipase C activity that hydrolyzes a novel glycolipid, resulting in the generation of a complex carbohydrate-phosphate substance containing inositol and glucosamine that may mediate some of the actions of the hormone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saltiel, A R -- Fox, J A -- Sherline, P -- Cuatrecasas, P -- AM33804/AM/NIADDK NIH HHS/ -- F32 AI07185/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 29;233(4767):967-72.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3016898" target="_blank"〉PubMed〈/a〉
    Keywords: 3',5'-Cyclic-AMP Phosphodiesterases/*metabolism ; Animals ; Cell Line ; Glucosamine/metabolism ; Glycolipids/*metabolism ; Hydrolysis ; Inositol/metabolism ; Insulin/*pharmacology ; Liver/metabolism ; Mice ; Phosphatidylinositol Diacylglycerol-Lyase ; Phosphoinositide Phospholipase C ; Phosphoric Diester Hydrolases/metabolism ; Staphylococcus aureus/enzymology
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  • 68
    Publication Date: 1986-02-21
    Description: The lymphocyte cell surface receptor for the high endothelial venules (HEV's) of peripheral lymph nodes is specifically recognized by the monoclonal antibody MEL-14. Three independent complementary DNA (cDNA) clones, each of which encodes the protein ubiquitin, were detected by virtue of the expression of the MEL-14 antigenic determinant on cDNA-beta-galactosidase bacterial fusion proteins. The antigenic determinant defined by MEL-14 resides in the carboxyl terminal 13-amino-acid proteolytic peptide of ubiquitin, but is undetected in intact undenatured ubiquitin and other cellular ubiquitinated proteins. Antisera and monoclonal antibodies to ubiquitin determinants bind to the surface of both HEV-receptor positive and negative cell lines. The MEL-14-identified cDNA clones hydridize to RNA transcripts that encode tandemly repeated ubiquitins. Sequence analysis of these polyubiquitin cDNA's does not identify a leader sequence for export to the cell surface. The expression of the MEL-14 epitope of ubiquitin depends upon its local environment. The steady-state levels of expression of the ubiquitin messenger RNA's do not correlate with either the tissue derivation of the RNA or the expression of the lymphocyte HEV receptor. Regulation of the expression of the HEV receptor is not likely to reflect the transcriptional control of ubiquitin genes, but rather to reflect control of the expression of the HEV core polypeptide or its level or form of ubiquitination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉St John, T -- Gallatin, W M -- Siegelman, M -- Smith, H T -- Fried, V A -- Weissman, I L -- AI19512/AI/NIAID NIH HHS/ -- CA 09151/CA/NCI NIH HHS/ -- GM 31461/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Feb 21;231(4740):845-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3003914" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/*immunology ; Antibody Specificity ; Base Sequence ; Cloning, Molecular ; Endothelium/metabolism ; Gene Expression Regulation ; High Mobility Group Proteins/*genetics ; Lymphatic System/metabolism ; Lymphocytes/*physiology ; Mice ; Receptors, Cell Surface/*genetics/immunology/metabolism ; Ubiquitins/*genetics/immunology/metabolism
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  • 69
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-07-11
    Description: In studies to determine the biochemical mechanisms responsible for cell proliferation, synchronized T cells were used as a model for cellular growth control. By metabolic and morphologic criteria, it was found that activation of the T-cell antigen receptor rendered the cells responsive to interleukin-2 (IL-2), but did not move them through the cell cycle. Instead, IL-2 stimulated G1 progression to S phase, or lymphocyte "blastic transformation." During IL-2-promoted G1 progression, expression of the cellular proto-oncogene c-myb was induced transiently at six to seven times basal levels, maximal levels occurring at the midpoint of G1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stern, J B -- Smith, K A -- CA 09367/CA/NCI NIH HHS/ -- CA-17643/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Jul 11;233(4760):203-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3523754" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/drug effects ; Cell Division/*drug effects ; Gene Expression Regulation/drug effects ; Humans ; Interleukin-2/*pharmacology ; Mice ; Proto-Oncogene Proteins/biosynthesis ; *Proto-Oncogenes/drug effects ; Receptors, Antigen, T-Cell/drug effects ; T-Lymphocytes/drug effects/*growth & development
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  • 70
    Publication Date: 1986-10-31
    Description: The mechanism by which Trypanosoma cruzi, the protozoan parasite that causes Chagas' disease, becomes attached to mammalian cells is not well understood. Fibronectin is thought to participate in the attachment, and in this study the region of fibronectin that interacts with the surface receptors of T. cruzi trypomastigotes was investigated by testing the binding of the amino acid sequence Arg-Gly-Asp-Ser, corresponding to the cell attachment site of fibronectin to T. cruzi trypomastigotes. Peptides with the sequence Arg-Gly-Asp-Ser, but not Arg-Phe-Asp-Ser, Arg-Phe-Asp-Ser-Ala-Ala-Arg-Phe-Asp, Ser-Lys-Pro, Glu-Ser-Gly, or Ala-Lys-Thr-Lys-Pro, bound to the parasite surface and inhibited cell invasion by the pathogen. Monoclonal antibodies to the cell attachment domain of fibronectin also inhibited cell infection by the parasite. The immunization of BALB/c mice with tetanus toxoid-conjugated peptide induced a significant protection against T. cruzi. The data support the notion that the sequence Arg-Gly-Asp-Ser of cell surface fibronectin acts as a recognition site for attachment of the parasites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ouaissi, M A -- Cornette, J -- Afchain, D -- Capron, A -- Gras-Masse, H -- Tartar, A -- New York, N.Y. -- Science. 1986 Oct 31;234(4776):603-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3094145" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/immunology ; Chagas Disease/parasitology/*prevention & control ; Fibronectins/immunology/*physiology ; Mice ; Mice, Inbred BALB C ; Peptides/*therapeutic use ; Trypanocidal Agents/*therapeutic use ; Trypanosoma cruzi/drug effects
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  • 71
    Publication Date: 1986-01-17
    Description: The human T-cell gamma chain genes have been characterized in an attempt to better understand their role in immune response. These immunoglobulin-like genes are encoded in the genome in variable, joining, and constant segments. The human gamma genes include at least six variable region genes, two joining segments, and two constant-region genes in germline DNA. Variable and joining segments recombine during the development of T cells to form rearranged genes. The diversity of human gamma genes produced by this recombinational mechanism is greater than that produced by the murine genome but is more limited than that of other immunoglobulin-like genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Quertermous, T -- Murre, C -- Dialynas, D -- Duby, A D -- Strominger, J L -- Waldman, T A -- Seidman, J G -- AI-15669/AI/NIAID NIH HHS/ -- AM-30241/AM/NIADDK NIH HHS/ -- T32-HL-07208/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Jan 17;231(4735):252-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3079918" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA/genetics ; *Genes, MHC Class II ; Humans ; Immunoglobulin J-Chains/genetics ; Immunoglobulin Variable Region/genetics ; Immunoglobulin gamma-Chains/genetics ; Mice ; Nucleic Acid Hybridization ; T-Lymphocytes/*physiology
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  • 72
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-08-29
    Description: Epidermal growth factor (EGF) stimulates the proliferation of various mammalian cells in culture, but its physiological role is not well defined. In mature male mice, large amounts of EGF are produced in the submandibular gland; it is present in the circulation at approximately 5 nanograms of EGF per milliliter of plasma. Sialoadenectomy (removal of the submandibular glands) decreased the amount of circulating EGF to an undetectable level but did not affect the circulating levels of testosterone or follicle-stimulating hormone. The number of mature sperm in the epididymis decreased by as much as 55 percent; the number of spermatids in the testis decreased by 40 to 50 percent; and the number of spermatocytes increased by about 20 percent. Administration of EGF to sialoadenectomized mice restored both the sperm content of the epididymis and the number of spermatids in the testis to normal. Thus, EGF may play a role in male reproductive function by stimulating the meiotic phase of spermatogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsutsumi, O -- Kurachi, H -- Oka, T -- New York, N.Y. -- Science. 1986 Aug 29;233(4767):975-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3090686" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dose-Response Relationship, Drug ; Epidermal Growth Factor/pharmacology/*physiology ; Epididymis/drug effects/physiology ; Follicle Stimulating Hormone/physiology ; Genitalia, Male/*physiology ; Luteinizing Hormone/physiology ; Male ; Mice ; Sexual Maturation ; Sperm Count/drug effects ; Spermatogenesis/drug effects ; Spermatozoa/physiology ; Submandibular Gland/physiology ; Testis/drug effects
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  • 73
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-06-06
    Description: A bovine rhodopsin complementary DNA probe was used to detect homologous visual pigment genes in a variety of species. Under stringent DNA hybridization conditions, genomic DNA from most vertebrate species carried a single homologous fragment. Additional homologies were detected in some vertebrates by reducing the hybridization stringency. Homologous fragments were also detected in DNA isolated from invertebrate species, a unicellular alga, and an archaebacterium; many of these fragments were homologous to a Drosophila opsin probe. These results suggest that photosensory pigments in a wide variety of species arose from a common precursor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, R L -- Wood, C -- Baehr, W -- Applebury, M L -- EY04801/EY/NEI NIH HHS/ -- EY07008/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1986 Jun 6;232(4755):1266-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3010467" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Base Sequence ; Cattle ; Chickens ; Dna ; DNA Restriction Enzymes ; Drosophila ; Eye Proteins/*genetics ; Mice ; Nucleic Acid Hybridization ; Plants ; Retinal Pigments/*genetics ; Rhodopsin/genetics ; Rod Opsins ; *Sequence Homology, Nucleic Acid ; Sheep
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  • 74
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-05-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1986 May 30;232(4754):1093-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3458306" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Division/drug effects ; Cricetinae ; Glycoproteins/pharmacology ; Growth Inhibitors/pharmacology ; Growth Substances/pharmacology ; Humans ; Mesocricetus ; Mice ; Mice, Nude ; Neoplasms, Experimental/metabolism ; Peptides/pharmacology ; Platelet-Derived Growth Factor/pharmacology ; Transforming Growth Factors ; Tumor Necrosis Factor-alpha
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  • 75
    Publication Date: 1986-12-12
    Description: Hereditary hypogonadism in the hypogonadal (hpg) mouse is caused by a deletional mutation of at least 33.5 kilobases encompassing the distal half of the gene for the common biosynthetic precursor of gonadotropin-releasing hormone (GnRH) and GnRH-associated peptide (GAP). The partially deleted gene is transcriptionally active as revealed by in situ hybridization histochemistry of hpg hypothalamic tissue sections, but immunocytochemical analysis failed to show the presence of antigen corresponding to any part of the precursor protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mason, A J -- Hayflick, J S -- Zoeller, R T -- Young, W S 3rd -- Phillips, H S -- Nikolics, K -- Seeburg, P H -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1366-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3024317" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Brain Chemistry ; Chromosome Deletion ; Chromosome Mapping ; DNA Restriction Enzymes/metabolism ; Gonadotropin-Releasing Hormone/*genetics ; Histocytochemistry ; Hypogonadism/*genetics ; Mice ; Nucleic Acid Hybridization ; Protein Precursors/*genetics ; Transcription, Genetic
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  • 76
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-07-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1986 Jul 11;233(4760):160.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3460175" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Genetic Engineering ; Humans ; Mice ; Transfection
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  • 77
    Publication Date: 1986-04-18
    Description: Efforts to investigate the progression of events that lead human cells of epithelial origin to become neoplastic in response to carcinogenic agents have been aided by the development of tissue culture systems for propagation of epithelial cells. In the present study, nontumorigenic human epidermal keratinocytes immortalized by adenovirus 12 and simian virus 40 (Ad 12-SV40) were transformed by treatment with the chemical carcinogens N-methyl-N'-nitro-N-nitrosoguanidine or 4-nitroquinoline-1-oxide. Such transformants showed morphological alterations and induced carcinomas when transplanted into nude mice, whereas primary human epidermal keratinocytes treated with these chemical carcinogens failed to show any evidence of transformation. This in vitro system may be useful in assessing environmental carcinogens for human epithelial cells and in detecting new human oncogenes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rhim, J S -- Fujita, J -- Arnstein, P -- Aaronson, S A -- New York, N.Y. -- Science. 1986 Apr 18;232(4748):385-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2421406" target="_blank"〉PubMed〈/a〉
    Keywords: 4-Nitroquinoline-1-oxide/*pharmacology ; Adenoviruses, Human/*metabolism ; Animals ; Cell Line ; Cell Transformation, Neoplastic/*chemically induced/metabolism ; Cell Transformation, Viral ; Epidermis/*cytology ; Humans ; *Keratins ; Methylnitronitrosoguanidine/*pharmacology ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Nitroquinolines/*pharmacology ; Oncogenes ; Simian virus 40/*metabolism ; Skin Neoplasms/chemically induced/*etiology/microbiology
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  • 78
    Publication Date: 1986-06-06
    Description: Transforming growth factor-alpha (TGF-alpha) and epidermal growth factor (EGF) are structurally related peptides. Purified human TGF-alpha produced in Escherichia coli and pure natural mouse EGF were compared for their ability to bind to target cells in vitro and to promote angiogenesis in the hamster cheek pouch bioassay. Both polypeptides were found to bind in vitro to several target cells, including endothelial cells, and to stimulate their DNA synthesis in an equipotent fashion. In vivo, however, TGF-alpha was more potent than EGF in promoting angiogenesis and, because TGF-alpha is known to be secreted by a variety of human tumors, it is suggested that this growth factor may contribute to tumor-induced angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schreiber, A B -- Winkler, M E -- Derynck, R -- New York, N.Y. -- Science. 1986 Jun 6;232(4755):1250-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2422759" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Assay ; Epidermal Growth Factor/pharmacology ; Humans ; Mice ; *Neovascularization, Pathologic ; Peptides/metabolism/*pharmacology ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/metabolism ; Transforming Growth Factors
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  • 79
    Publication Date: 1986-05-09
    Description: In multidrug resistance, which is observed clinically and in tissue culture, cells that are challenged with certain cytotoxic drugs develop resistance not only to the selective agent but also to other, seemingly unrelated, agents. The multidrug-resistant phenotype is associated with DNA sequence amplification and with the overproduction of a number of cytosolic and membrane glycoproteins. The differential amplification and altered expression of at least two related genes, termed multidrug-resistant associated genes has been shown in multidrug-resistant Chinese hamster cells. In multidrug-resistant mouse and human cells, genes homologous to those in Chinese hamster cells are also amplified. The level of expression of these genes varied and did not correlate with their copy number. Furthermore, in Chinese hamster cells, the development of resistance to a single drug and multidrug resistance were closely related, but uncoupled, events. The overexpression of the multidrug-resistant genes was better correlated with the degree of resistance to the selective agent than it was with the extent of multidrug resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scotto, K W -- Biedler, J L -- Melera, P W -- CA-08748/CA/NCI NIH HHS/ -- CA-09207/CA/NCI NIH HHS/ -- CA-28595/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 May 9;232(4751):751-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2421411" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cloning, Molecular ; Colchicine/pharmacology ; Cricetinae ; Cricetulus ; DNA/genetics ; Dactinomycin/pharmacology ; Daunorubicin/pharmacology ; *Drug Resistance ; Gene Amplification/*drug effects ; Gene Expression Regulation/*drug effects ; Humans ; Lung/cytology/drug effects ; Mice ; Nucleic Acid Hybridization ; RNA/genetics ; Vincristine/pharmacology
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  • 80
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-06-13
    Description: Genetic diseases can be treated by transplantation of either normal allogeneic bone marrow or, potentially, autologous bone marrow into which the normal gene has been inserted in vitro (gene therapy). Histocompatible allogeneic bone marrow transplantation is used for the treatment of genetic diseases whose clinical expression is restricted to lymphoid or hematopoietic cells. The therapeutic role of bone marrow transplantation in the treatment of generalized genetic diseases, especially those affecting the central nervous system, is under investigation. The response of a generalized genetic disease to allogeneic bone marrow transplantation may be predicted by experiments in vitro. Gene therapy can be used only when the gene responsible for the disease has been characterized. Success of gene therapy for a specific genetic disease may be predicted by its clinical response to allogeneic bone marrow transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parkman, R -- New York, N.Y. -- Science. 1986 Jun 13;232(4756):1373-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3520819" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Marrow Transplantation ; Enzymes/deficiency/genetics ; Genetic Diseases, Inborn/*therapy ; Genetic Engineering ; Humans ; Mice ; Transfection
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  • 81
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-03-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Milstein, C -- New York, N.Y. -- Science. 1986 Mar 14;231(4743):1261-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3080810" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology/*physiology ; Antibodies, Monoclonal/genetics ; *Antibody Diversity ; *Antibody Formation ; DNA, Recombinant/metabolism ; Genes, MHC Class II ; Genetic Engineering ; Humans ; Hybridomas/metabolism ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin Light Chains/genetics ; Immunoglobulins/physiology ; Mice ; Multiple Myeloma/genetics ; Mutation ; Myeloma Proteins/genetics ; RNA, Messenger/genetics
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  • 82
    Publication Date: 1986-09-19
    Description: The adoptive transfer of tumor-infiltrating lymphocytes (TIL) expanded in interleukin-2 (IL-2) to mice bearing micrometastases from various types of tumors showed that TIL are 50 to 100 times more effective in their therapeutic potency than are lymphokine-activated killer (LAK) cells. Therefore the use of TIL was explored for the treatment of mice with large pulmonary and hepatic metastatic tumors that do not respond to LAK cell therapy. Although treatment of animals with TIL alone or cyclophosphamide alone had little impact, these two modalities together mediated the elimination of large metastatic cancer deposits in the liver and lung. The combination of TIL and cyclophosphamide was further potentiated by the simultaneous administration of IL-2. With the combination of cyclophosphamide, TIL, and IL-2, 100% of mice (n = 12) bearing the MC-38 colon adenocarcinoma were cured of advanced hepatic metastases, and up to 50% of mice were cured of advanced pulmonary metastases. Techniques have been developed to isolate TIL from human tumors. These experiments provide a rationale for the use of TIL in the treatment of humans with advanced cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenberg, S A -- Spiess, P -- Lafreniere, R -- New York, N.Y. -- Science. 1986 Sep 19;233(4770):1318-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3489291" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/secondary/therapy ; Animals ; Colonic Neoplasms/therapy ; Combined Modality Therapy ; Cyclophosphamide/therapeutic use ; Humans ; *Immunotherapy ; Interleukin-2/pharmacology ; Liver Neoplasms/secondary ; Lung Neoplasms/secondary ; Lymphocyte Activation/drug effects ; Lymphocytes/immunology/*physiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neoplasms, Experimental/*therapy ; Sarcoma, Experimental/secondary/therapy
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  • 83
    Publication Date: 1986-01-24
    Description: A semisterile male translocation heterozygote [t(2; 14) 1Gso] that exhibited neurological symptoms and an inability to swim (diver) was found among the offspring of male mice treated with triethylenemelamine. All breeding and cytogenetic data showed a complete concordance between translocation heterozygosity and the neurological disorders. Homozygosity for the translocation seemed to be lethal at an early embryonic stage. Despite the distinctive neurologic symptoms, no anatomic or histological defects in either the ear or in the central nervous system were observed. Thus, a balanced chromosomal translocation can produce disease with an inheritance pattern that mimics a single dominant gene defect.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rutledge, J C -- Cain, K T -- Cacheiro, N L -- Cornett, C V -- Wright, C G -- Generoso, W M -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):395-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3941902" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Female ; Heterozygote ; Humans ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Neurologic Mutants/*genetics ; Muscular Dystrophies/genetics ; *Translocation, Genetic ; Triethylenemelamine/pharmacology
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  • 84
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-01-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, M -- New York, N.Y. -- Science. 1986 Jan 31;231(4737):448.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3941909" target="_blank"〉PubMed〈/a〉
    Keywords: Air Pollutants, Occupational/*toxicity ; Animals ; Ethylene Oxide/*toxicity ; Female ; Humans ; Male ; Mice ; Pregnancy ; Risk ; *Teratogens ; United States ; United States Occupational Safety and Health Administration
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  • 85
    Publication Date: 1986-09-12
    Description: The observation that voltage-dependent K+ channels are required for activation of human T lymphocytes suggests that pathological conditions involving abnormal mitogen responses might be reflected in ion channel abnormalities. Gigaohm seal techniques were used to study T cells from MRL/MpJ-lpr/lpr mice; these mice develop generalized lymphoproliferation of functionally and phenotypically abnormal T cells and a disease resembling human systemic lupus erythematosus. The number and predominant type of K+ channels in T cells from these mice differ dramatically from those in T cells from control strains and a congenic strain lacking the lpr gene locus. Thus an abnormal pattern of ion channel expression has now been associated with a genetic defect in cells of the immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandy, K G -- DeCoursey, T E -- Fischbach, M -- Talal, N -- Cahalan, M D -- Gupta, S -- AI-20717/AI/NIAID NIH HHS/ -- AI-21808/AI/NIAID NIH HHS/ -- NS-14609/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Sep 12;233(4769):1197-200.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2426784" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila ; Humans ; Ion Channels/*metabolism/physiology ; Lymphocyte Activation ; Membrane Potentials ; Mice ; Mice, Inbred Strains ; Mice, Mutant Strains ; *Mutation ; Potassium/*metabolism ; T-Lymphocytes/abnormalities/*metabolism/physiology
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  • 86
    Publication Date: 1986-11-07
    Description: The current prevalence of the acquired immune deficiency syndrome in humans has provoked renewed interest in methods of protective immunization against retrovirus-induced diseases. In this study, a vaccinia-retrovirus recombinant vector was constructed to study mechanisms of immune protection against Friend virus leukemia in mice. The envelope (env) gene from Friend murine leukemia virus (F-MuLV) was inserted into the genome of a vaccinia virus expression vector. Infected cells synthesized gp85, the glycosylated primary product of the env gene. Processing to gp70 and p15E, and cell surface localization, were similar to that occurring in cells infected with F-MuLV. Mice inoculated with live recombinant vaccinia virus had an envelope-specific T-cell proliferative response and, after challenge with Friend virus complex, developed neutralizing antibody and cytotoxic T cells (CTL) and were protected against leukemia. In contrast, unimmunized and control groups developed a delayed neutralizing antibody response, but no detectable CTL, and succumbed to leukemia. Genes of the major histocompatibility complex influenced protection induced by the vaccinia recombinant but not that induced by attenuated N-tropic Friend virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Earl, P L -- Moss, B -- Morrison, R P -- Wehrly, K -- Nishio, J -- Chesebro, B -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):728-31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3490689" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/immunology ; Antigens/*immunology ; DNA, Recombinant ; Female ; Friend murine leukemia virus/genetics/immunology ; *Genes, Viral ; Leukemia, Erythroblastic, Acute/prevention & control ; Leukemia, Experimental/*prevention & control ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred Strains ; Sex Factors ; Spleen/microbiology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/immunology ; Vaccines, Synthetic/*immunology ; Vaccinia virus/genetics/immunology ; Viral Envelope Proteins/genetics/*immunology ; Viral Vaccines/*immunology
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  • 87
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-01-31
    Description: Pineal melatonin may play an important role in regulation of vertebrate circadian rhythms and in human affective disorders. In some mammals, such as hamsters and sheep, melatonin is involved in photoperiodic time measurement and in control of reproduction. Although wild mice (Mus domesticus) and some wild-derived inbred strains of mice have melatonin in their pineal glands, several inbred strains of laboratory mice (for example, C57BL/6J) were found not to have detectable melatonin in their pineal glands. Genetic analysis suggests that melatonin deficiency in C57BL/6J mice results from mutations in two independently segregating, autosomal recessive genes. Synthesis of melatonin from serotonin in the pineal gland requires the enzymes N-acetyltransferase (NAT) and hydroxyindole-O-methyltransferase (HIOMT). Pineal glands from C57BL/6J mice have neither NAT nor HIOMT activity. These results suggest that the two genes involved in melatonin deficiency are responsible for the absence of normal NAT and HIOMT enzyme activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ebihara, S -- Marks, T -- Hudson, D J -- Menaker, M -- 13162/PHS HHS/ -- FO5TW03377/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 31;231(4737):491-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3941912" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatography, High Pressure Liquid ; Female ; Kinetics ; Male ; Melatonin/biosynthesis/deficiency/*genetics ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Pineal Gland/*metabolism ; Reference Values ; Species Specificity
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  • 88
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-04-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, C -- New York, N.Y. -- Science. 1986 Apr 11;232(4747):147-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3952503" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Care Committees ; *Animal Experimentation ; Animal Testing Alternatives ; *Animal Welfare ; Animals ; *Animals, Laboratory ; Aplysia ; Birds ; Chick Embryo ; Decapodiformes ; Federal Government ; Government Regulation ; Horseshoe Crabs ; Macaca ; Mice ; National Institutes of Health (U.S.) ; Rabbits ; Rats ; United States ; are discussed. The enactment of amendments to the Animal Welfare Act of 1966 and ; revisions to the Public Health Service's animal care guidelines are described as ; major federal moves to tighten standards and to locate responsibility for proper ; animal care at the institutional level. These regulatory changes will have a ; significant economic impact on the cost of doing research, but are generally ; accepted by the scientific community as necessary. Although moderate animal ; welfare groups see signs of progress, there is a growing number of activists who ; see recent policy developments as only a step toward the real goal of total ; elimination of the use of animals in research. It is apparent that the ; combination of political pressure, financial stringency, and better experimental ; methodologies will result in a continued reduction in laboratory animal use.
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  • 89
    Publication Date: 1986-07-25
    Description: Adhesive interactions between cells and the extracellular matrix occur at several stages of metastasis. Such interactions might be inhibited by synthetic peptide probes derived from the cell-binding regions of matrix molecules. Gly-Arg-Gly-Asp-Ser (GRGDS) is a pentapeptide sequence that appears to be critical for cell interaction with fibronectin. Coinjection of GRGDS with B16-F10 murine melanoma cells dramatically inhibited the formation of lung colonies in C57BL/6 mice. Two closely related control peptides, in which specific amino acids within the GRGDS sequence were transposed or substituted, displayed little or no activity. Inhibition by GRGDS was dose-dependent, noncytotoxic, and did not result from an impairment of cellular tumorigenicity. GRGDS may function by inhibiting tumor cell retention in the lung since radiolabeled B16-F10 tumor cells injected with the peptide were lost at a substantially greater rate than control cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Humphries, M J -- Olden, K -- Yamada, K M -- CA-34918/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Jul 25;233(4762):467-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726541" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Fibronectins ; Lung Neoplasms/drug therapy/*secondary ; Melanoma/drug therapy/pathology/*secondary ; Mice ; Mice, Inbred C57BL ; *Neoplasm Metastasis ; Neoplasm Transplantation ; Oligopeptides/*therapeutic use
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  • 90
    Publication Date: 1986-12-12
    Description: While much information exists about the structure and function of the clonally distributed T cell receptor (TCR) alpha beta heterodimer, little is known about the gamma protein, the product of a third rearranging TCR gene. An antiserum to a carboxyl-terminal peptide common to several of the murine gamma chain constant regions and a monoclonal antibody to the murine T3 complex were used to identify products of this TCR gene family in a subpopulation of Lyt2-, L3T4- thymocytes. This subpopulation does not express TCR alpha or full-length TCR beta messenger RNA. The gamma chain is a 35-kilodalton (kD) protein that is disulfide-bonded to a 45-kD partner and is associated with the T3 complex. Analysis of the glycosylation pattern of this thymic gamma chain revealed that the major variable region gamma (V gamma) gene transcribed in activated peripheral T cells is absent from this subpopulation. The cells that bear this second T cell receptor may therefore represent a distinct lineage differentiating within the thymus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lew, A M -- Pardoll, D M -- Maloy, W L -- Fowlkes, B J -- Kruisbeek, A -- Cheng, S F -- Germain, R N -- Bluestone, J A -- Schwartz, R H -- Coligan, J E -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1401-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3787252" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Disulfides/analysis ; Electrophoresis, Polyacrylamide Gel ; Glycosylation ; Macromolecular Substances ; Mice ; Molecular Weight ; RNA, Messenger/metabolism ; Receptors, Antigen, T-Cell/*biosynthesis/genetics ; Structure-Activity Relationship ; Thymus Gland/*metabolism
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  • 91
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-03-21
    Description: The mutation rates of DNA sequences during evolution can be estimated from interspecies DNA sequence differences by assaying changes that have little or no effect on the phenotype (neutral mutations). Examination of available measurements shows that rates of DNA change of different phylogenetic groups differ by a factor of 5. The slowest rates are observed for higher primates and some bird lineages, while faster rates are seen in rodents, sea urchins, and drosophila. The rate of DNA sequence change has decreased markedly during primate evolution. The contrast in rates of DNA sequence change is probably due to evolutionary variation and selection of biochemical mechanisms such as DNA replication or repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Britten, R J -- GM34031/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Mar 21;231(4744):1393-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3082006" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Base Sequence ; *Biological Evolution ; Cricetinae ; DNA/*genetics ; DNA Repair ; DNA Replication ; Drosophila ; Gene Frequency ; Genes ; Genetics, Population ; Gorilla gorilla ; Haplorhini ; Humans ; Hylobates ; Mice ; Nucleic Acid Hybridization ; Pan troglodytes ; Phenotype ; Rabbits ; Rats ; Species Specificity
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  • 92
    Publication Date: 1986-08-01
    Description: The specific inhibitor of glutathione biosynthesis, L-buthionine sulfoximine (L-BSO), although relatively nontoxic in adult mice, induces severe glutathione depletion and age-specific pathological changes when repeatedly administered to male suckling mice. Dense cataracts developed when mice aged 9 to 12 days were given a series of injections of L-BSO, despite excellent survival and the absence of other significant long-term effects. By contrast, similar treatment of mice aged 14 to 17 days, although slightly less effective in reducing glutathione levels, resulted frequently in death, hind-leg paralysis, or impaired spermatogenesis, but did not produce cataracts. Administration of L-BSO to preweanling mice provides a novel model system for the induction of cataracts by depletion of lens glutathione and may enable the study of critical functions of glutathione in the lens and other growing tissues during early postnatal development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Calvin, H I -- Medvedovsky, C -- Worgul, B V -- EY-02648/EY/NEI NIH HHS/ -- HD-17932/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 1;233(4763):553-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726547" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Animals ; Buthionine Sulfoximine ; Cataract/*chemically induced ; Disease Models, Animal ; Glutathione/analysis/*metabolism ; Humans ; Kidney/analysis ; Lens, Crystalline/analysis ; Liver/analysis ; Male ; Methionine Sulfoximine/*analogs & derivatives/pharmacology ; Mice ; Testis/analysis
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  • 93
    Publication Date: 1986-01-10
    Description: Interleukin-3 (IL-3), a protein of 140 amino acids, was chemically synthesized by means of an automated peptide synthesizer and was shown to have the biological activities attributed to native IL-3. Assays of synthetic analogues established that an amino terminal fragment has detectable IL-3 activity, but that the stable tertiary structure of the complete molecule was required for full activity. The results demonstrate that automated peptide synthesis can be applied to the study of the structure and function of proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clark-Lewis, I -- Aebersold, R -- Ziltener, H -- Schrader, J W -- Hood, L E -- Kent, S B -- R01-CA38684-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 10;231(4734):134-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3079915" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Chromatography, High Pressure Liquid ; Electrophoresis, Polyacrylamide Gel ; Interleukin-3 ; Lymphokines/*chemical synthesis/pharmacology ; Mast Cells/drug effects ; Megakaryocytes/drug effects ; Mice ; Protein Conformation ; Structure-Activity Relationship
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  • 94
    Publication Date: 1986-10-31
    Description: Neuroleukin is a lymphokine product of lectin-stimulated T cells that induces immunoglobulin secretion by cultured human peripheral blood mononuclear cells. Neuroleukin acts early in the in vitro response that leads to formation of antibody-secreting cells, but continued production of immunoglobulin by differentiated antibody-secreting cells is neuroleukin-independent. Although the factor is not directly mitogenic, cellular proliferation is a late component of the response to neuroleukin. Neuroleukin does not have B-cell growth factor (BCGF) or B-cell differentiation factor (BCDF) activity in defined assays. Neuroleukin-evoked induction of immunoglobulin secretion is both monocyte- and T-cell-dependent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gurney, M E -- Apatoff, B R -- Spear, G T -- Baumel, M J -- Antel, J P -- Bania, M B -- Reder, A T -- 5PO1 NS24412/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 31;234(4776):574-81.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3020690" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/drug effects/physiology ; Bone Marrow/metabolism ; Cell Line ; Cells, Cultured ; Deltaretrovirus/genetics ; Glucose-6-Phosphate Isomerase ; Growth Substances/genetics/pharmacology/*physiology ; Humans ; Immunity, Cellular/drug effects ; Immunoglobulins/biosynthesis ; Lectins/pharmacology ; Leukemia/metabolism ; Lymphokines/genetics/pharmacology/*physiology ; Lymphoma/metabolism ; Mice ; Pokeweed Mitogens/pharmacology ; Sequence Homology, Nucleic Acid ; T-Lymphocytes/drug effects/*physiology
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  • 95
    Publication Date: 1986-10-31
    Description: A novel 56,000-dalton growth factor found in mouse salivary gland was purified, molecularly cloned, and expressed in monkey COS cells. The protein is a neurotrophic factor and also, surprisingly, a lymphokine product of lectin-stimulated T cells. The factor was therefore named neuroleukin. Neuroleukin promotes the survival in culture of a subpopulation of embryonic spinal neurons that probably includes skeletal motor neurons. Neuroleukin also supports the survival of cultured sensory neurons that are insensitive to nerve growth factor, but has no effect on sympathetic or parasympathetic neurons. The amino acid sequence of neuroleukin is partly homologous to a highly conserved region of the external envelope protein of HTLV-III/LAV, the retrovirus that causes acquired immune deficiency syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gurney, M E -- Heinrich, S P -- Lee, M R -- Yin, H S -- 5PO1 NS-21442/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 31;234(4776):566-74.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3764429" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Chick Embryo ; Cloning, Molecular ; DNA/genetics ; Glucose-6-Phosphate Isomerase ; Growth Substances/genetics/*physiology ; Lymphokines/genetics/*physiology ; Male ; Mice ; Mice, Inbred BALB C ; Motor Neurons/drug effects ; Muscles/innervation ; Nerve Growth Factors/genetics/isolation & purification/*physiology ; Neurons/drug effects ; Neurons, Afferent/drug effects ; Salivary Glands/metabolism ; Spinal Cord/cytology
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  • 96
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-06-27
    Description: Two reovirus isolates (type 1 Lang and type 3 Dearing) differ in their transmissibility between littermates of newborn mice. They also differ in the amounts of virus excreted by the gastrointestinal tract. With the use of reassortant viruses, these properties were mapped to the L2 gene. Thus environmental spread of reovirus is a genetic property.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keroack, M -- Fields, B N -- 5R01 AI13178/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 Jun 27;232(4758):1635-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3012780" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn/microbiology ; Digestive System/microbiology ; *Genes, Viral ; Mammalian orthoreovirus 3/physiology ; Mice ; Reoviridae/physiology ; Reoviridae Infections/microbiology/*transmission
    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
    Publication Date: 1986-04-11
    Description: Anti-idiotypic antibodies (anti-Id) that contain an internal image component that mimics the surface antigen of hepatitis B virus (HBsAg) were used to immunize chimpanzees. Four injections of the rabbit anti-Id preparation elicited an antibody response to HBsAg (anti-HBs). The antibody specificity appeared to be against the anti-Id, since the anti-Id immunogen was shown to bind the chimpanzee anti-HBs. Two chimpanzees immunized with the anti-Id, along with two control animals that were either untreated or received a nonimmune rabbit immunoglobulin G preparation, were challenged with infectious hepatitis B virus. Both control chimpanzees developed clinical and serological characteristics consistent with an active hepatitis B virus infection, whereas the two anti-Id treated chimpanzees were protected from infection. Since chimpanzees provide a relevant model of a human response to hepatitis B virus immunization and infection, these results indicate that anti-Id preparations such as that described here might be candidates for vaccines against human diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kennedy, R C -- Eichberg, J W -- Lanford, R E -- Dreesman, G R -- 1 P01 AI-22380-01-MID/AI/NIAID NIH HHS/ -- 1 R23 AI-22307-01/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 11;232(4747):220-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3952505" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine Transaminase/metabolism ; Animals ; Antibody Formation ; Dose-Response Relationship, Immunologic ; Hepatitis B/immunology/*prevention & control ; Hepatitis B Antibodies/*immunology ; Humans ; Immunoglobulin Idiotypes/*immunology ; Immunotherapy ; Infant, Newborn ; Mice ; Pan troglodytes ; Rabbits/immunology ; Rats ; Schistosoma mansoni/immunology ; Trypanosoma/immunology ; *Vaccines
    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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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-06-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kolata, G -- New York, N.Y. -- Science. 1986 Jun 6;232(4755):1197.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3704645" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Diseases/*etiology ; Cricetinae ; Gene Expression Regulation ; *Genes ; Humans ; Mice ; Prions/*genetics
    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
    Publication Date: 1986-08-01
    Description: Lymphocytes are essential mediators of normal tissue inflammatory reactions and of pathologic tissue damage in, for example, rheumatoid arthritis and other autoimmune diseases. In a study of the mechanisms controlling lymphocyte entry into sites of inflammation from the blood, the function and specificity of lymphocyte-endothelial interactions were examined in inflamed joint tissue (synovium) from patients with rheumatoid arthritis. Synovial high endothelial venules (HEV) supported the binding of normal peripheral blood lymphocytes in vitro. The characteristics of this binding, which were similar to those of lymphocyte-HEV interactions controlling lymphocyte migration into organized lymphoid tissues, included a requirement for calcium ions, a dependence on metabolic activity, and a preferential adherence of circulating lymphocytes as opposed to immature thymocytes. However, the binding of lymphocytes to synovial HEV was not inhibited by a monoclonal antibody to lymphocyte receptors for lymph node HEV, and synovial HEV failed to bind either lymph node HEV-specific or mucosal HEV-specific B lymphoblastoid cells. The results suggest that a lymphocyte-endothelial cell recognition system that is distinct from such systems in organized lymphoid tissues directs the extravasation of normal lymphocytes as well as pathologically important effector cells into inflamed synovium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jalkanen, S -- Steere, A C -- Fox, R I -- Butcher, E C -- AI19957/AI/NIAID NIH HHS/ -- AM-20358/AM/NIADDK NIH HHS/ -- RR-00125/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 1;233(4763):556-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis, Rheumatoid/immunology ; Endothelium/immunology ; Humans ; Immunity, Cellular ; Lymph Nodes/cytology ; Lymphocytes/immunology/*physiology ; Mice ; Synovial Membrane/immunology ; Synovitis/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-05-23
    Description: A monoclonal antibody bound to a protein antigen decreases the rate of proteolytic cleavage of the antigen, having the greatest effect on those regions involved in antibody contact. Thus, an epitope can be identified by the ability of the antibody to protect one region of the antigen more than others from proteolysis. By means of this approach, two distinct epitopes, both conformationally well-ordered, were characterized on horse cytochrome c.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jemmerson, R -- Paterson, Y -- AI 19499/AI/NIAID NIH HHS/ -- AI21486/AI/NIAID NIH HHS/ -- GM 31841/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 May 23;232(4753):1001-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2422757" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; *Antigen-Antibody Complex ; Cytochrome c Group/*immunology ; *Epitopes ; Mice ; Oligopeptides/immunology ; Protein Conformation ; Trypsin
    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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