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  • Cell Line  (22)
  • American Association for the Advancement of Science (AAAS)  (22)
  • American Chemical Society
  • Elsevier
  • 1980-1984  (22)
  • 1940-1944
  • 1984  (22)
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (22)
  • American Chemical Society
  • Elsevier
Years
  • 1980-1984  (22)
  • 1940-1944
Year
  • 1
    Publication Date: 1984-02-10
    Description: Macaque monkeys with the recently described acquired immunodeficiency syndrome show a marked defect in T-lymphocyte function and die with opportunistic infections and lymphoproliferative abnormalities. In the study described here a new type D retrovirus was isolated from two Macaca cyclopis with this syndrome. This virus is related to, but distinct from, Mason-Pfizer monkey virus, a type D retrovirus previously isolated from a mammary tumor of a rhesus monkey (Macaca mulatta).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daniel, M D -- King, N W -- Letvin, N L -- Hunt, R D -- Sehgal, P K -- Desrosiers, R C -- R01-A1 20729/PHS HHS/ -- RR00168/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Feb 10;223(4636):602-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695172" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Burkitt Lymphoma ; Cell Line ; Humans ; Immunologic Deficiency Syndromes/*microbiology ; Macaca ; Nucleic Acid Hybridization ; Retroviridae/genetics/immunology/*isolation & purification
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 1984-10-05
    Description: The human T-cell leukemia viruses HTLV-I and HTLV-II are unique among the transforming retroviruses of vertebrates in their ability to transform human T cells in vitro and in their close association with human malignancies (T-cell lymphomas and leukemia). Their genomes are relatively simple, containing the genes gag, pol, env, and a 3' region termed "X." This 3' region may be responsible for the transforming potential of the viruses. The existence of proteins encoded by the 3' region has been postulated on the basis of multiple open reading frames. In the present study this region is shown to contain a gene encoding a protein of 40 kilodaltons in HTLV-I and 37 kilodaltons in HTLV-II. It is proposed that these proteins be called, respectively, p40xI and p37xII.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slamon, D J -- Shimotohno, K -- Cline, M J -- Golde, D W -- Chen, I S -- CA 16042/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- RR 00865/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Oct 5;226(4670):61-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6089351" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; B-Lymphocytes/microbiology ; Cell Line ; *Cell Transformation, Viral ; Deltaretrovirus/analysis/*genetics/physiology ; *Genes, Viral ; Humans ; Immune Sera ; Molecular Weight ; T-Lymphocytes/*microbiology ; Trans-Activators ; Viral Proteins/genetics/immunology/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 1984-06-29
    Description: The gene encoding human interleukin-2 (IL-2) has been cloned from human spleen cells, peripheral blood lymphocytes, and the Jurkat cell line. Nucleotide sequence analysis of the gene revealed that the encoded IL-2 protein has three cysteines located at amino acid residues 58, 105, and 125 of the mature protein. Site-specific mutagenesis procedures were used to modify the IL-2 gene by changing each of the cysteine codons individually to serine codons. Substitution of serine for cysteine residues at either position 58 or 105 of the IL-2 protein substantially reduced biological activity, indicating that the cysteines at these positions are necessary for maintenance of the biologically active conformation and may therefore be linked by a disulfide bridge. The modified IL-2 protein containing a substitution at position 125 retained full biological activity, suggesting that the cysteine at this position is not involved in a disulfide bond and that a free sulfhydryl group at that position is not necessary for receptor binding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, A -- Lu, S D -- Mark, D F -- New York, N.Y. -- Science. 1984 Jun 29;224(4656):1431-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6427925" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Cysteine/metabolism ; DNA, Recombinant/metabolism ; Escherichia coli/genetics ; Genes ; Humans ; Interleukin-2/*genetics ; *Mutation ; Receptors, Immunologic/metabolism ; Receptors, Interleukin-2 ; Serine/metabolism ; Structure-Activity Relationship
    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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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-06-29
    Description: The hormonal form of vitamin D3, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], at picomolar concentrations, inhibited the growth-promoting lymphokine interleukin-2, which is produced by human T lymphocytes activated in vitro by the mitogen phytohemagglutinin. Other metabolites of vitamin D3 were less effective than 1,25(OH)2D3 in suppressing interleukin-2; their order of potency corresponded to their respective affinity for the 1,25(OH)2D3 receptor, suggesting that the effect on interleukin-2 was mediated by this specific receptor. The proliferation of mitogen-activated lymphocytes was also inhibited by 1,25(OH)2D3. This effect of the hormone became more pronounced at later stages of the culture. These findings demonstrate that 1,25(OH)2D3 is an immunoregulatory hormone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsoukas, C D -- Provvedini, D M -- Manolagas, S C -- AM29779/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 29;224(4656):1438-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6427926" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcitriol/*pharmacology ; Cell Division/drug effects ; Cell Line ; Humans ; Immunity, Cellular/*drug effects ; Interleukin-2/antagonists & inhibitors ; Lymphocyte Activation/drug effects ; Lymphocytes/drug effects ; Mice ; Monocytes/drug effects ; Receptors, Immunologic/drug effects ; Receptors, Interleukin-2
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-05-04
    Description: Stress stimulates several adaptive hormonal responses. Prominent among these responses are the secretion of catecholamines from the adrenal medulla, corticosteroids from the adrenal cortex, and adrenocorticotropin from the anterior pituitary. A number of complex interactions are involved in the regulation of these hormones. Glucocorticoids regulate catecholamine biosynthesis in the adrenal medulla and catecholamines stimulate adrenocorticotropin release from the anterior pituitary. In addition, other hormones, including corticotropin-releasing factor, vasoactive intestinal peptide, and arginine vasopressin stimulate while the corticosteroids and somatostatin inhibit adrenocorticotropin secretion. Together these agents appear to determine the complex physiologic responses to a variety of stressors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Axelrod, J -- Reisine, T D -- New York, N.Y. -- Science. 1984 May 4;224(4648):452-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6143403" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Adrenal Cortex/metabolism ; Adrenal Medulla/metabolism ; Adrenocorticotropic Hormone/*metabolism ; Animals ; Brain/metabolism ; Catecholamines/*metabolism ; Cell Line ; Corticotropin-Releasing Hormone/metabolism ; Cyclic AMP/metabolism ; Glucocorticoids/*metabolism ; Humans ; Phospholipases A/metabolism ; Pituitary Gland, Anterior/metabolism ; Receptors, Adrenergic, alpha/metabolism ; Receptors, Adrenergic, beta/metabolism ; Receptors, Cell Surface/metabolism ; Receptors, Corticotropin-Releasing Hormone ; Receptors, Somatostatin ; Somatostatin/pharmacology ; Stress, Physiological/*metabolism ; Stress, Psychological/metabolism ; Sympathetic Nervous System/metabolism ; Vasoactive Intestinal Peptide/pharmacology ; Vasopressins/pharmacology
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  • 6
    Publication Date: 1984-08-31
    Description: Bromodeoxyuridine (BrdUrd) treatment of the prolactin nonproducing subclone of GH cells (rat pituitary tumor cells) induces amplification of a 20-kilobase DNA fragment including all of the prolactin gene coding sequences. This amplified DNA segment, which is flanked by two unamplified regions, thus designates a unit of BrdUrd-induced amplified sequence. Cloned DNA segments, 10.3 kilobases long, from the 5' end of the rat prolactin gene of BrdUrd-responsive and -nonresponsive cells, were ligated to the thymidine kinase gene of herpes simplex virus type 1 (HSV1TK), and the hybrid DNA was transferred to thymidine kinase-deficient mouse fibroblast cells by transfection. The HSV1TK gene and the rat prolactin gene were amplified together in drug-treated transfectants carrying the hybrid DNA HSV1TK gene and rat prolactin gene of BrdUrd-responsive GH cells. These results suggest that the 10.3-kilobase DNA segment at the 5' end of the rat prolactin gene of BrdUrd-responsive GH cells carries the information for drug-induced gene amplification (amplicon) and that another gene, such as the HSV1TK gene, is also amplified when the latter is placed adjacent to this segment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Biswas, D K -- Hartigan, J A -- Pichler, M H -- CA28218/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Aug 31;225(4665):941-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6089335" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Bromodeoxyuridine/*pharmacology ; Cell Line ; Cloning, Molecular ; DNA/*genetics ; DNA, Recombinant ; *Gene Amplification ; Genes, Viral ; Mice ; Prolactin/genetics ; Rats ; Simplexvirus/genetics ; Thymidine Kinase/genetics ; Transfection
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  • 7
    Publication Date: 1984-12-14
    Description: Neutrophil migration inhibition factor from T lymphocytes (NIF-T) is a lymphokine that acts to localize granulocytes. Medium conditioned by the Mo human T-lymphoblast cell line was used to purify NIF-T, a glycoprotein with a molecular weight of 22,000. The NIF-T was found to potently stimulate the growth of granulocyte and macrophage colonies from human bone marrow and colony formation by the KG-1 myeloid leukemia cell line. Thus a human lymphokine (NIF-T) that modulates the activities of mature neutrophilic granulocytes is also a colony-stimulating factor acting on precursors to induce growth and differentiation of new effector cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gasson, J C -- Weisbart, R H -- Kaufman, S E -- Clark, S C -- Hewick, R M -- Wong, G G -- Golde, D W -- CA 30280/CA/NCI NIH HHS/ -- CA 30388/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1984 Dec 14;226(4680):1339-42.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6390681" target="_blank"〉PubMed〈/a〉
    Keywords: Bone Marrow Cells ; Cell Division ; Cell Line ; Chromatography, High Pressure Liquid ; Colony-Stimulating Factors/*isolation & purification ; Electrophoresis, Polyacrylamide Gel ; Granulocytes/*cytology ; Humans ; Leukocyte Migration-Inhibitory Factors/*pharmacology ; Lymphokines/*pharmacology ; Macrophages/*cytology ; Molecular Weight
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  • 8
    Publication Date: 1984-11-23
    Description: Platelet-derived growth factor (PDGF) has been previously shown to be homologous to the transforming gene of simian sarcoma virus (v-sis), and inappropriate expression of the cellular counterpart of the v-sis gene (c-sis) has been implicated in the generation of mesenchymal tumors. The U-2 OS human osteosarcoma line was shown to contain multiple c-sis transcripts. Immunoprecipitation experiments with antiserum to PDGF identified a variety of polypeptides ranging in size from 18,000 to 165,000 daltons that were immunoprecipitated specifically from U-2 OS cell extracts. The osteosarcoma also was shown to secrete a 29,000-dalton protein having the serological and structural characteristics of PDGF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graves, D T -- Owen, A J -- Barth, R K -- Tempst, P -- Winoto, A -- Fors, L -- Hood, L E -- Antoniades, H N -- CA30101/CA/NCI NIH HHS/ -- HL27607/HL/NHLBI NIH HHS/ -- HL29583/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 23;226(4677):972-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6209798" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; DNA Replication ; Humans ; Molecular Weight ; Neoplasm Proteins/*genetics ; *Oncogenes ; Osteosarcoma/*genetics ; *Platelet-Derived Growth Factor ; Poly A/genetics/isolation & purification ; RNA/genetics/isolation & purification ; RNA, Messenger ; *Transcription, Genetic
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  • 9
    Publication Date: 1984-08-24
    Description: Infectious retroviruses have been detected in 22 of 45 randomly selected patients with acquired immune deficiency syndrome (AIDS) and in other individuals from San Francisco. The AIDS-associated retroviruses (ARV) studied in detail had a type D morphology, Mg2+-dependent reverse transcriptase, and cytopathic effects on lymphocytes. The viruses can be propagated in an established adult human T cell line, HUT-78. They cross-react with antiserum to the lymphadenopathy-associated retrovirus isolated from AIDS patients in France. Antibodies to ARV were found in all 86 AIDS patients and in a high percentage of 88 other homosexual men in San Francisco. This observation indicates the widespread presence of these lymphocytopathic retroviruses and their close association with AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levy, J A -- Hoffman, A D -- Kramer, S M -- Landis, J A -- Shimabukuro, J M -- Oshiro, L S -- CA-34980/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Aug 24;225(4664):840-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6206563" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology/*microbiology ; Antibodies, Viral/analysis ; Bone Marrow/microbiology ; California ; Cell Line ; Cells, Cultured ; Cross Reactions ; Cytopathogenic Effect, Viral ; Deltaretrovirus/immunology/*isolation & purification/physiology/ultrastructure ; *Homosexuality ; Humans ; Leukocytes/microbiology ; Lymphatic Diseases/immunology ; Male ; RNA-Directed DNA Polymerase/metabolism ; Syndrome ; T-Lymphocytes ; Virus Cultivation
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  • 10
    Publication Date: 1984-06-29
    Description: Human T lymphocytes transformed by human T cell leukemia-lymphoma viruses or activated by lectins were found to produce stimulating factors that promoted both proliferation and maturation of oligodendroglial and astroglial cells in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merrill, J E -- Kutsunai, S -- Mohlstrom, C -- Hofman, F -- Groopman, J -- Golde, D W -- CA 30388/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 29;224(4656):1428-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6610212" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Astrocytes/*drug effects ; Cell Division/*drug effects ; Cell Line ; Growth Substances/*pharmacology ; Humans ; Lymphocyte Activation ; Lymphokines/pharmacology ; Neuroglia/*drug effects ; Oligodendroglia/*drug effects ; Rats ; Receptors, Fc/metabolism ; T-Lymphocytes/*physiology
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