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  • Mice  (103)
  • Base Sequence  (62)
  • In Vitro Techniques  (22)
  • American Association for the Advancement of Science (AAAS)  (168)
  • Periodicals Archive Online (PAO)
  • Wiley
  • 2020-2022
  • 2005-2009
  • 1985-1989  (168)
  • 1965-1969
  • 1935-1939
  • 1986  (168)
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Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (168)
  • Periodicals Archive Online (PAO)
  • Wiley
  • Springer  (5)
Years
  • 2020-2022
  • 2005-2009
  • 1985-1989  (168)
  • 1965-1969
  • 1935-1939
Year
  • 11
    Publication Date: 1986-05-09
    Description: The human N-myc gene is related to the c-myc proto-oncogene, and has been shown to have transforming potential in vitro. Many studies have reported amplification of N-myc in human neuroblastoma and retinoblastoma cell lines. In primary tumors, amplification of the gene was found to correlate directly with behavior of the tumor. Specific restriction fragments of a partial complementary DNA clone of N-myc from LA-N-5 human neuroblastoma cells were placed into a bacterial expression vector for the purpose of producing antigens representative of the N-myc protein. Rabbits immunized with these antigens produced antisera that recognized a protein of 62-64 kilodaltons in neuroblastoma cells. By several criteria, this protein appears to be part of the same proto-oncogene family as the c-myc protein. Moreover, the antisera to fragments of this protein were capable of histochemically identifying malignant cells in clinical specimens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slamon, D J -- Boone, T C -- Seeger, R C -- Keith, D E -- Chazin, V -- Lee, H C -- Souza, L M -- CA 16042/CA/NCI NIH HHS/ -- CA 36827/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 May 9;232(4751):768-72.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3008339" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Carcinoma, Small Cell/metabolism ; Immune Sera/immunology ; Immunoenzyme Techniques ; Leukemia, Myeloid, Acute/metabolism ; Lung Neoplasms/metabolism ; Neoplasm Proteins/genetics/*isolation & purification/physiology ; Neuroblastoma/metabolism ; *Oncogenes ; Proto-Oncogene Proteins/genetics/*isolation & purification/physiology ; Proto-Oncogene Proteins c-myc ; Proto-Oncogenes ; Rabbits/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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  • 12
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
    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
    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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  • 14
    Publication Date: 1986-08-01
    Description: In Trypanosomatidae the messenger RNA's (mRNA's) that code for the variant surface glycoproteins (VSG's), tubulins, calmodulin, and at least a subset of other proteins contain a common 35-nucleotide leader sequence at their 5' ends. Hybrid-arrested in vitro translation has been used to show that all mRNA's in both African and South American trypanosomes contain this 35-nucleotide sequence. Oligonucleotides complementary to this sequence blocked translation of all trypanosome mRNA's in a rabbit reticulocyte lysate system, but did not inhibit translation of mRNA's from other organisms lacking this sequence. An oligonucleotide complementary to the VSG mRNA downstream from the spliced leader sequence arrested only VSG synthesis. Thus, the 35-nucleotide leader sequence is a general feature of all trypanosome mRNA's. The high specificity of oligonucleotides complementary to the spliced leader for their target sequence suggests that analogues permeable to the cell membrane may be useful in the treatment of trypanosomal infections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walder, J A -- Eder, P S -- Engman, D M -- Brentano, S T -- Walder, R Y -- Knutzon, D S -- Dorfman, D M -- Donelson, J E -- AI-18954/AI/NIAID NIH HHS/ -- AM-25295/AM/NIADDK NIH HHS/ -- HL-33555/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Aug 1;233(4763):569-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3523758" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Protein Biosynthesis ; Protein Sorting Signals/*genetics ; RNA, Messenger/*genetics ; Trypanosoma/*genetics ; Trypanosoma brucei brucei/genetics ; Trypanosoma cruzi/genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
    Publication Date: 1986-06-06
    Description: The Watanabe heritable hyperlipidemic (WHHL) rabbit, an animal with familial hypercholesterolemia, produces a mutant receptor for plasma low-density lipoprotein (LDL) that is not transported to the cell surface at a normal rate. Cloning and sequencing of complementary DNA's from normal and WHHL rabbits, shows that this defect arises from an in-frame deletion of 12 nucleotides that eliminates four amino acids from the cysteine-rich ligand binding domain of the LDL receptor. A similar mutation, detected by S1 nuclease mapping of LDL receptor messenger RNA, occurred in a patient with familial hypercholesterolemia whose receptor also fails to be transported to the cell surface. These findings suggest that animal cells may have fail-safe mechanisms that prevent the surface expression of improperly folded proteins with unpaired or improperly bonded cysteine residues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4451858/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4451858/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamamoto, T -- Bishop, R W -- Brown, M S -- Goldstein, J L -- Russell, D W -- HL 01287/HL/NHLBI NIH HHS/ -- HL 20948/HL/NHLBI NIH HHS/ -- HL 31346/HL/NHLBI NIH HHS/ -- P01 HL020948/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Jun 6;232(4755):1230-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3010466" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Biological Transport ; *Chromosome Deletion ; Cloning, Molecular ; Cysteine/genetics ; Dna ; DNA Restriction Enzymes ; Genes ; Humans ; Hyperlipoproteinemia Type II/*genetics ; Mutation ; RNA, Messenger ; Rabbits ; Receptors, LDL/*genetics
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  • 16
    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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  • 17
    Publication Date: 1986-08-15
    Description: The 2.8 A resolution three-dimensional structure of a complex between an antigen (lysozyme) and the Fab fragment from a monoclonal antibody against lysozyme has been determined and refined by x-ray crystallographic techniques. No conformational changes can be observed in the tertiary structure of lysozyme compared with that determined in native crystalline forms. The quaternary structure of Fab is that of an extended conformation. The antibody combining site is a rather flat surface with protuberances and depressions formed by its amino acid side chains. The antigen-antibody interface is tightly packed, with 16 lysozyme and 17 antibody residues making close contacts. The antigen contacting residues belong to two stretches of the lysozyme polypeptide chain: residues 18 to 27 and 116 to 129. All the complementarity-determining regions and two residues outside hypervariable positions of the antibody make contact with the antigen. Most of these contacts (10 residues out of 17) are made by the heavy chain, and in particular by its third complementarity-determining region. Antigen variability and antibody specificity and affinity are discussed on the basis of the determined structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amit, A G -- Mariuzza, R A -- Phillips, S E -- Poljak, R J -- New York, N.Y. -- Science. 1986 Aug 15;233(4765):747-53.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2426778" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibodies, Monoclonal ; *Antigen-Antibody Complex ; Chickens ; Egg White ; Epitopes ; *Immunoglobulin Fab Fragments ; Immunoglobulin Heavy Chains ; Immunoglobulin Light Chains ; In Vitro Techniques ; Kinetics ; Models, Molecular ; Muramidase/*immunology ; Protein Conformation ; X-Ray Diffraction
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  • 18
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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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  • 19
    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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  • 20
    Publication Date: 1986-03-28
    Description: In human right atria obtained from 21 patients during open-heart surgery, beta-adrenoceptor density [assessed by iodine-125-labeled (-)-cyanopindolol binding] and responsiveness (positive inotropic responses to isoprenaline) were linearly related to the beta-adrenoceptor density in the corresponding circulating lymphocytes. This direct relation of human myocardial and lymphocyte beta-adrenoceptor alterations, therefore, makes it possible to monitor drug- or disease-induced beta-adrenoceptor changes in tissues not easily accessible in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brodde, O E -- Kretsch, R -- Ikezono, K -- Zerkowski, H R -- Reidemeister, J C -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1584-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006250" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Heart Atria ; Humans ; In Vitro Techniques ; Isoproterenol/pharmacology ; Lymphocytes/*metabolism ; Male ; Middle Aged ; Myocardial Contraction/drug effects ; Myocardium/*metabolism ; Receptors, Adrenergic, beta/*metabolism
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