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  • Cell Line  (46)
  • American Association for the Advancement of Science (AAAS)  (46)
  • American Chemical Society (ACS)
  • 1990-1994
  • 1985-1989  (46)
  • 1980-1984
  • 1986  (46)
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (46)
  • American Chemical Society (ACS)
Years
  • 1990-1994
  • 1985-1989  (46)
  • 1980-1984
Year
  • 1
    Publication Date: 1986-05-02
    Description: The development of simultaneous resistance to multiple structurally unrelated drugs is a major impediment to cancer chemotherapy. Multidrug resistance in human KB carcinoma cells selected in colchicine, vinblastine, or Adriamycin is associated with amplification of specific DNA sequences (the multidrug resistance locus, mdr1). During colchicine selection resistance is initially accompanied by elevated expression of a 4.5-kilobase mdr1 messenger RNA (mRNA) without amplification of the corresponding genomic sequences. During selection for increased levels of resistance, expression of this mRNA is increased simultaneously with amplification of mdr1 DNA. Increased expression and amplification of mdr1 sequences were also found in multidrug-resistant sublines of human leukemia and ovarian carcinoma cells. These results suggest that increased expression of mdr1 mRNA is a common mechanism for multidrug resistance in human cells. Activation of the mdr1 gene by mutations or epigenetic changes may precede its amplification during the development of resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, D W -- Fojo, A -- Chin, J E -- Roninson, I B -- Richert, N -- Pastan, I -- Gottesman, M M -- New York, N.Y. -- Science. 1986 May 2;232(4750):643-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3457471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Colchicine/pharmacology ; Cricetinae ; Cricetulus ; DNA, Neoplasm/genetics ; Doxorubicin/pharmacology ; *Drug Resistance ; Female ; *Gene Amplification ; Humans ; Leukemia, Lymphoid/drug therapy ; Neoplasms/*drug therapy/genetics ; Nucleic Acid Hybridization ; Ovarian Neoplasms/drug therapy ; RNA, Messenger/genetics ; Vinblastine/pharmacology
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  • 2
    Publication Date: 1986-08-22
    Description: Continuous measurement and imaging of the intracellular free calcium ion concentration ([Ca2+]i) of mitotic and interphase PtK1 cells was accomplished with the new fluorescent Ca2+ indicator fura-2. No statistically significant difference between basal [Ca2+]i of interphase and mitotic cells was detected. However, mitotic cells showed a rapid elevation of [Ca2+]i from basal levels of 130 nM to 500 to 800 nM at the metaphase-anaphase transition. The [Ca2+]i transient was brief, lasting approximately 20 seconds and the elevated [Ca2+]i appeared uniformly distributed over the entire spindle and central region of the cell. The close temporal association of the [Ca2+]i transient with the onset of anaphase suggests that calcium may have a signaling role in this event.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Poenie, M -- Alderton, J -- Steinhardt, R -- Tsien, R -- EY04372/EY/NEI NIH HHS/ -- GM31004/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 22;233(4766):886-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3755550" target="_blank"〉PubMed〈/a〉
    Keywords: *Anaphase ; Animals ; Benzofurans ; Calcium/*metabolism ; Cell Line ; Fluorescent Dyes ; Fura-2 ; Mitosis
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  • 3
    Publication Date: 1986-03-28
    Description: The genome of the human T-lymphotropic virus type III (HTLV-III/LAV) has the potential to encode at least three polypeptides in addition to those encoded by the gag, pol, and env genes. In this study, the product of the sor (short open reading frame) region, which overlaps the 3' end of the pol gene, was found to be a protein with a molecular weight of 23,000. An assay was developed for testing the ability of cloned HTLV-III proviruses to produce viruses cytopathic for T4+ lymphocytes. In the cell line used, C8166, neither the HTLV-III sor gene product nor the complete 3'-orf gene product were necessary for the replication or cytopathic effects of the HTLV-III.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sodroski, J -- Goh, W C -- Rosen, C -- Tartar, A -- Portetelle, D -- Burny, A -- Haseltine, W -- CA07580/CA/NCI NIH HHS/ -- CA40658/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1549-53.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006244" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cytopathogenic Effect, Viral ; Deltaretrovirus/*genetics/pathogenicity ; *Genes, Viral ; Humans ; Retroviridae Proteins/genetics ; T-Lymphocytes/microbiology ; *Virus Replication
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  • 4
    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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  • 5
    Publication Date: 1986-10-24
    Description: The protein product of oncogene c-myc is believed to be important in regulation of the cell cycle. However, its direct role in DNA synthesis has not been explored. Experiments presented here show that the addition of affinity-purified antibodies against the human c-myc protein to nuclei isolated from several types of human cells reversibly inhibited DNA synthesis and DNA polymerase activity of these nuclei. This suggests that c-myc encodes a protein that is functionally involved in DNA synthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Studzinski, G P -- Brelvi, Z S -- Feldman, S C -- Watt, R A -- New York, N.Y. -- Science. 1986 Oct 24;234(4775):467-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3532322" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Nucleus/physiology ; Cell-Free System ; DNA/biosynthesis ; *DNA Replication ; Humans ; Immunologic Techniques ; Nucleic Acid Synthesis Inhibitors ; Proto-Oncogene Proteins/*physiology ; *Proto-Oncogenes
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  • 6
    Publication Date: 1986-08-29
    Description: Epstein-Barr virus (EBV), a ubiquitous human herpesvirus, has the ability to transform human B lymphocytes. No other cell type has been experimentally transformed by EBV, either by intact virions or naked viral DNA and subgenomic fragments. Two immortalized human T-lymphoblastoid cell lines have now been established by transfecting cord blood lymphocytes with purified B95-8 viral DNA enclosed in fusogenic Sendai virus envelopes (RSVE) and then exposing the cells to EBV from a P3HR-1 cell subclone. One of these lines, which has been fully characterized, is termed HBD-1. This line is positive for EBV DNA and expresses surface OKT11, OKT4, and Tac receptors, but not M-1, mu immunoglobulin chains, EBV receptors, or B-1 surface markers. The cells contain fully rearranged T-cell receptor genes and germline immunoglobulin genes. The karyotype of the cells is normal, they do not require interleukin-2 for growth, and do not contain human T-lymphotropic virus type I. However, the HBD-1 cells contain incomplete EBV genomes and express several EBV-determined antigens, including the early antigen type D, membrane antigens, but not EBV-determined nuclear antigen (EBNA). This association of the EBV genome with permanently growing hematopoietic cells of non B-cell lineage should prove useful in studies on the mechanism of EBV-mediated cell transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stevenson, M -- Volsky, B -- Hedenskog, M -- Volsky, D J -- CA33386/CA/NCI NIH HHS/ -- CA37465/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 29;233(4767):980-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3016899" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Survival ; DNA, Viral/*genetics ; Deltaretrovirus/genetics ; Herpesvirus 4, Human/*genetics ; Humans ; Nucleic Acid Hybridization ; T-Lymphocytes/*microbiology/physiology ; *Transfection
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  • 7
    Publication Date: 1986-11-21
    Description: The human T-lymphotropic retrovirus HTLV-III/LAV encodes a trans-activator that increases viral gene expression. We expressed this trans-activator in animal cells and studied its structural and functional characteristics. The putative trans-activator protein was immunoprecipitated from overproducing stable cell lines and shown to migrate as a 14-kilodalton polypeptide on sodium dodecyl sulfate-polyacrylamide gels. S1 nuclease mapping experiments showed that the trans-activator increases the levels of steady-state messenger RNA transcribed from the viral long terminal repeat promoter. Sequences within the R region of the HTLV-III/LAV long terminal repeat are essential for trans-activation. Quantitations of messenger RNA and protein showed that the protein increase was greater than the messenger RNA increase in CV1 and HeLa cells, indicating that more than one mechanism was responsible for the trans-activation and that cell type-specific factors may determine the final level of trans-activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wright, C M -- Felber, B K -- Paskalis, H -- Pavlakis, G N -- N01-CO-23909/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 21;234(4779):988-92.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3490693" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Electrophoresis, Polyacrylamide Gel ; Gene Products, rev ; HIV/*genetics ; Molecular Sequence Data ; Nucleic Acid Hybridization ; RNA, Messenger/analysis ; Retroviridae Proteins/*metabolism ; Transfection ; Viral Proteins/*biosynthesis ; Virus Activation ; rev Gene Products, Human Immunodeficiency Virus
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  • 8
    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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  • 9
    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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  • 10
    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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  • 11
    Publication Date: 1986-06-20
    Description: In many viral infections the host cell carries the viral genome without producing viral particles, a phenomenon known as viral latency. The cellular mechanisms by which viral latency is maintained or viral replication is induced are not known. The modulation of intracellular calcium concentrations by calcium ionophores induced Epstein-Barr viral antigens in lymphoblastoid cell lines that carry the virus. When calcium ionophores were used in conjunction with direct activators of protein kinase C (12-O-tetradecanoyl phorbol-13-acetate and a synthetic diacylglycerol), a greater induction of viral antigens was observed than with either agent alone. Activation of protein kinase C may be required for the expression of the viral genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faggioni, A -- Zompetta, C -- Grimaldi, S -- Barile, G -- Frati, L -- Lazdins, J -- New York, N.Y. -- Science. 1986 Jun 20;232(4757):1554-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3012779" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoquinolines ; Burkitt Lymphoma ; Calcimycin/pharmacology ; Calcium/*pharmacology ; Cell Line ; Cell Transformation, Viral/*drug effects ; Culture Media ; Ethers/pharmacology ; Fluorescent Dyes ; Genes, Viral/*drug effects ; Herpesvirus 4, Human/drug effects/*genetics ; Humans ; Ionomycin ; Kinetics ; Tetradecanoylphorbol Acetate/pharmacology
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  • 12
    Publication Date: 1986-02-07
    Description: When the human T-cell line A3.01 is infected with HTLV-III/LAV, the virus associated with the acquired immune deficiency syndrome (AIDS), most of the cells are killed. However, a small number of cells that lack the Leu-3 surface marker survive. Under normal conditions these surviving cells do not produce virus, nor can they be infected by the virus, but they can be induced to produce virus by treatment with 5-iodo-2'-deoxyuridine. This response can be induced for as long as 3 months after the initial infection, suggesting that the cells may harbor a latent form of HTLV-III/LAV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Folks, T -- Powell, D M -- Lightfoote, M M -- Benn, S -- Martin, M A -- Fauci, A S -- New York, N.Y. -- Science. 1986 Feb 7;231(4738):600-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3003906" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/genetics/microbiology ; Cell Line ; Deltaretrovirus/*growth & development ; Humans ; Idoxuridine/pharmacology ; Models, Genetic ; T-Lymphocytes/drug effects/*microbiology ; Time Factors ; *Virus Activation/drug effects
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  • 13
    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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  • 14
    Publication Date: 1986-01-24
    Description: Steady-state cellular levels of phosphatidylinositol-4,5-bisphosphate (PIP2), 1,2-diacylglycerol (DAG), and inositol phosphates have been measured in two different fibroblast cell lines (NIH 3T3 and NRK cells) before and after transformation with three different ras genes. At high cell density the ratio of DAG to PIP2 was 2.5- to 3-fold higher in the ras-transformed cells than in their untransformed counterparts. The sum of the water-soluble breakdown products of the polyphosphoinositides, inositol-1,4-bisphosphate and inositol-1,4,5-trisphosphate, was also elevated in ras-transformed NRK cells compared with nontransformed NRK cells. These findings suggest that the ras (p21) protein may act by affecting these levels, possibly as a regulatory element in the PIP2 breakdown pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fleischman, L F -- Chahwala, S B -- Cantley, L -- GM 36133/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):407-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3001936" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Transformation, Neoplastic/*analysis ; Diglycerides/analysis ; Humans ; Inositol 1,4,5-Trisphosphate ; Inositol Phosphates/analysis ; *Oncogenes ; Phosphatidylinositol 4,5-Diphosphate ; Phosphatidylinositols/*analysis ; Rats
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  • 15
    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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  • 16
    Publication Date: 1986-04-25
    Description: Monocytes are a subpopulation of peripheral blood leukocytes, which when appropriately activated by the regulatory hormones of the immune system, are capable of becoming macrophages--potent effector cells for immune response to tumors and parasites. A complementary DNA for the T lymphocyte-derived lymphokine, granulocyte-macrophage colony-stimulating factor (GM-CSF), has been cloned, and recombinant GM-CSF protein has been expressed in yeast and purified to homogeneity. This purified human recombinant GM-CSF stimulated peripheral blood monocytes in vitro to become cytotoxic for the malignant melanoma cell line A375. Another T cell-derived lymphokine, gamma-interferon (IFN-gamma), also stimulated peripheral blood monocytes to become tumoricidal against this malignant cell line. When IFN-gamma activates monocytes to become tumoricidal, additional stimulation by exogenously added lipopolysaccharide is required. No such exogenous signals were required for the activation of monocytes by GM-CSF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grabstein, K H -- Urdal, D L -- Tushinski, R J -- Mochizuki, D Y -- Price, V L -- Cantrell, M A -- Gillis, S -- Conlon, P J -- New York, N.Y. -- Science. 1986 Apr 25;232(4749):506-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3083507" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Colony-Stimulating Factors/biosynthesis/*pharmacology ; Cytotoxicity, Immunologic/*drug effects ; Humans ; Interferon-gamma/biosynthesis/pharmacology ; Macrophages/*drug effects ; Melanoma/immunology ; Monocytes/drug effects ; Neoplasms/*immunology ; Recombinant Proteins/biosynthesis/pharmacology
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  • 17
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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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  • 18
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-12-19
    Description: Thyroid hormones stimulate the rate of cell division by poorly understood mechanisms. The possibility that thyroid hormones increase cell growth by stimulating secretion of a growth factor was investigated. Thyroid hormones are nearly an absolute requirement for the division of GH4C1 rat pituitary tumor cells plated at low density. Conditioned media from cells grown with or without L-triiodothyronine (T3) were treated with an ion exchange resin to remove T3 and were tested for ability to stimulate the division of GH4C1 cells. Conditioned medium from T3-treated cells was as active as thyroid hormone at promoting GH4C1 cell growth but did not elicit other thyroid hormone responses, induction of growth hormone, and down-regulation of thyrotropin-releasing hormone receptors, as effectively as T3 did. A substance or substances associated with T3-induced growth stimulatory activity migrated at high molecular weight at neutral pH and was different from known growth-promoting hormones induced by T3. The results demonstrate that thyroid hormones stimulate the division of GH4C1 pituitary cells by stimulating the secretion of an autocrine growth factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hinkle, P M -- Kinsella, P A -- AM 32847/AM/NIADDK NIH HHS/ -- AM/NS 00827/AM/NIADDK NIH HHS/ -- CA 11198/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Dec 19;234(4783):1549-52.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3097825" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Line ; Epidermal Growth Factor/metabolism ; Growth Hormone/metabolism ; Growth Substances/*secretion ; Nerve Growth Factors/metabolism ; Pituitary Neoplasms/*metabolism/pathology ; Rats ; Thyrotropin-Releasing Hormone/metabolism ; Triiodothyronine/*pharmacology
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  • 19
    Publication Date: 1986-11-07
    Description: Lipopolysaccharide, a component of the outer membrane of Gram-negative bacteria, activates B lymphocytes and macrophages. Pertussis toxin, which inactivates several members of the G protein family of signaling components, including Gi and transducin, was found to inhibit the lipopolysaccharide-induced responses of the WEHI-231 B lymphoma cell line and the P388D1 macrophage cell line. These results, combined with the demonstration that lipopolysaccharide inhibits adenylate cyclase activity in P388D1 cells, strongly argues that lipopolysaccharide activation of cells is mediated by a Gi-like receptor-effector coupling protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jakway, J P -- DeFranco, A L -- AI-20038/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):743-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3095921" target="_blank"〉PubMed〈/a〉
    Keywords: *Adenylate Cyclase Toxin ; Antibodies, Anti-Idiotypic/immunology ; B-Lymphocytes/*physiology ; Cell Line ; Dose-Response Relationship, Drug ; Escherichia coli ; GTP-Binding Proteins/*physiology ; Immunoglobulin M/immunology ; Interleukin-1/metabolism ; Lipopolysaccharides/*antagonists & inhibitors/immunology ; Lymphocyte Activation/drug effects ; Macrophage Activation/drug effects ; Macrophages/*physiology ; *Pertussis Toxin ; Virulence Factors, Bordetella/*pharmacology
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  • 20
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    Unknown
    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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  • 21
    Publication Date: 1986-01-24
    Description: Human probes identifying the cellular homologs of the v-ets gene, Hu-ets-1 and Hu-ets-2, and two panels of rodent-human cell hybrids were used to study specific translocations occurring in acute leukemias. The human ets-1 gene was found to translocate from chromosome 11 to 4 in the t(4;11)(q21;23), a translocation characteristic of a subtype of leukemia that represents the expansion of a myeloid/lymphoid precursor cell. Similarly, the human ets-2 gene was found to translocate from chromosome 21 to chromosome 8 in the t(8;21)(q22;q22), a nonrandom translocation commonly found in patients with acute myeloid leukemia with morphology M2 (AML-M2). Both translocations are associated with expression different from the expression in normal lymphoid cells of ets genes, raising the possibility that these genes play a role in the pathogenesis of these leukemias.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sacchi, N -- Watson, D K -- Guerts van Kessel, A H -- Hagemeijer, A -- Kersey, J -- Drabkin, H D -- Patterson, D -- Papas, T S -- AG00029/AG/NIA NIH HHS/ -- HD17449/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):379-82.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3941901" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chromosomes, Human, 21-22 and Y ; Chromosomes, Human, 6-12 and X ; Cricetinae ; Cricetulus ; Humans ; Hybrid Cells ; Leukemia/*genetics ; Nucleic Acid Hybridization ; *Oncogenes ; *Translocation, Genetic
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  • 22
    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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  • 23
    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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  • 24
    Publication Date: 1986-07-18
    Description: The myb gene is the transforming oncogene of the avian myeloblastosis virus (AMV); its normal cellular homolog, c-myb, is conserved across a broad span of evolution. In humans, c-myb is expressed in malignant hematopoietic cell lines and in primary hematopoietic tumors. Partial complementary DNA clones were generated from blast cells of patients with acute myelogenous leukemia. The sequences of the clones were compared to the c-myb of other species, as well as the v-myb of AMV. In addition, the carboxyl terminal region of human c-myb was placed in an expression vector to obtain protein for the generation of antiserum, which was used to identify the human c-myb gene product. Like v-myb, this protein was found within the nucleus of leukemic cells where it was associated with the nuclear matrix. These studies provide further evidence that c-myb might be involved in human leukemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slamon, D J -- Boone, T C -- Murdock, D C -- Keith, D E -- Press, M F -- Larson, R A -- Souza, L M -- CA36827/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Jul 18;233(4761):347-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3014652" target="_blank"〉PubMed〈/a〉
    Keywords: *Aspartate Carbamoyltransferase ; Avian Leukosis Virus/*genetics ; Avian Myeloblastosis Virus/*genetics ; Base Sequence ; *Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing) ; Cell Line ; Cloning, Molecular ; DNA/analysis ; DNA Restriction Enzymes/metabolism ; *Dihydroorotase ; Escherichia coli/genetics ; Hematopoietic Stem Cells/microbiology ; Humans ; Leukemia, Myeloid, Acute/*genetics ; Molecular Weight ; *Multienzyme Complexes ; *Oncogenes ; Proteins/analysis
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  • 25
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-10-10
    Description: Polypeptide growth factors, regulatory peptides, and a variety of pharmacological agents acting alone or synergistically induce mitogenesis in cultured fibroblasts. The early signals in the membrane, cytosol, and nucleus promoted by these extracellular factors, together with their mitogenic effectiveness, are integrated in a unified hypothesis for the regulation of fibroblast growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rozengurt, E -- New York, N.Y. -- Science. 1986 Oct 10;234(4773):161-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3018928" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bombesin/pharmacology ; Cell Line ; Cell Membrane/metabolism ; Cell Nucleus/metabolism ; Cyclic AMP/metabolism ; Cytosol/metabolism ; DNA/biosynthesis ; Enzyme Activation ; Growth Substances/*pharmacology ; Interphase ; Ions/metabolism ; Mitogens/*pharmacology ; Mitosis ; Models, Biological ; Oncogenes ; Phosphorylation ; Platelet-Derived Growth Factor/*pharmacology ; Protein Kinase C/metabolism ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/metabolism
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  • 26
    Publication Date: 1986-10-31
    Description: A novel human B-lymphotropic virus (HBLV) was isolated from the peripheral blood leukocytes of six individuals: two HTLV-III seropositive patients from the United States (one with AIDS-related lymphoma and one with dermatopathic lymphadenopathy), three HTLV-III seronegative patients from the United States (one with angioimmunoblastic lymphadenopathy, one with cutaneous T-cell lymphoma, and one with immunoblastic lymphoma), and one HTLV-III seronegative patient with acute lymphocytic leukemia from Jamaica. All six isolates were closely related by antigenic analysis, and sera from all six virus-positive patients reacted immunologically with each virus isolate. In contrast, only four sera from 220 randomly selected healthy donors and none from 12 AIDS patients without associated lymphoma were seropositive. The virus selectively infected freshly isolated human B cells and converted them into large, refractile mono- or binucleated cells with nuclear and cytoplasmic inclusion bodies. HBLV is morphologically similar to viruses of the herpesvirus family but is readily distinguishable from the known human and nonhuman primate herpesviruses by host range, in vitro biological effects, and antigenic features.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salahuddin, S Z -- Ablashi, D V -- Markham, P D -- Josephs, S F -- Sturzenegger, S -- Kaplan, M -- Halligan, G -- Biberfeld, P -- Wong-Staal, F -- Kramarsky, B -- New York, N.Y. -- Science. 1986 Oct 31;234(4776):596-601.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2876520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/microbiology ; Cell Line ; Deltaretrovirus Infections/microbiology ; Fluorescent Antibody Technique ; Haplorhini ; Herpesviridae/*isolation & purification ; Herpesviridae Infections/*microbiology ; Humans ; Lymphoproliferative Disorders/*microbiology ; Microscopy, Electron ; T-Lymphocytes/microbiology
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  • 27
    Publication Date: 1986-04-04
    Description: The human metallothionein-IIA (hMT-IIA) gene contains an enhancer element within its 5' regulatory region. This enhancer element can compete with the SV40 enhancer for one or more cellular factors in vivo. The competition between the two elements is modulated by cadmium, an inducer of hMT-IIA transcription. The data presented are consistent with a model in which heavy metal ions control the ability of the hMT-IIA enhancer to bind a positive factor, leading to increased transcription. The same factor is required for maximal activity of the SV40 enhancer, which suggests that viruses utilize factors that have a normal role in cellular gene expression to control their own genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scholer, H -- Haslinger, A -- Heguy, A -- Holtgreve, H -- Karin, M -- ES03222/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):76-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006253" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Animals ; Base Sequence ; Cadmium/pharmacology ; Cell Line ; Cercopithecus aethiops ; Chloramphenicol O-Acetyltransferase ; *Enhancer Elements, Genetic ; *Genes ; *Genes, Regulator ; *Genes, Viral ; Humans ; Kidney ; Kinetics ; Metallothionein/*genetics ; Plasmids ; Simian virus 40/*genetics ; Transcription, Genetic/drug effects ; Transfection
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  • 28
    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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  • 29
    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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  • 30
    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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  • 31
    Publication Date: 1986-11-07
    Description: This work was aimed at understanding the mechanisms of T-lymphocyte function by studying the cellular distribution and traffic of molecules of the T-cell receptor complex. The accumulation of specific molecules in intracytoplasmic vesicles is related to the activation of T lymphocytes. Some of these molecules include acid hydrolases, the transferrin receptor, and class I antigens of the major histocompatibility complex. Molecules of the T-cell receptor complex have now also been found in intracytoplasmic vesicles in a human T-cell line derived from a lymphoblastic leukemia. Such vesicles were tightly associated with the cytoplasmic microtubule network. One functional aspect of this association is a cellular pathway by which vesicles traveling to and from the cell surface converge in an area of the cells that is rich in processing enzymes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tse, D B -- Al-Haideri, M -- Pernis, B -- Cantor, C R -- Wang, C Y -- CA39782/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):748-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3490690" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Cell Compartmentation ; Cell Line ; Cytoplasmic Granules/metabolism ; HLA Antigens/metabolism ; Humans ; Microtubules/ultrastructure ; Receptors, Antigen, T-Cell/*metabolism ; Receptors, Transferrin/metabolism ; T-Lymphocytes/immunology/*metabolism
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  • 32
    Publication Date: 1986-11-14
    Description: The expression of the cellular src gene product pp60c-src was examined in an embryonal carcinoma cell line that differentiates in vitro into neuronlike cells after being treated with retinoic acid. Quantitative and qualitative changes in c-src expression accompanied the events associated with neuronal differentiation. The levels of pp60c-src increased 8- to 20-fold during the period when the cells elaborated neuritic processes and expressed neuron-specific proteins. The electrophoretic mobility of pp60c-src induced in these cells was retarded in comparison with that in untreated cells or in treated cells before neurite elaboration. The shift in electrophoretic mobility was due to an alteration in the amino terminal 16,000 daltons of pp60c-src and similar to an alteration of c-src protein found in neural tissues and in pure primary cultures of neuronal cells. These results indicate that expression of pp60c-src induced by retinoic acid in these embryonal carcinoma cells mimics the expression of c-src in developing neurons. Therefore, this embryonal carcinoma cell line provides a model system to investigate the function of the src protein in neuronal differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lynch, S A -- Brugge, J S -- Levine, J M -- CA 28146/CA/NCI NIH HHS/ -- NS 21198/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 14;234(4778):873-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3095923" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation/drug effects ; Cell Line ; Embryonal Carcinoma Stem Cells ; Gene Expression Regulation ; Neoplastic Stem Cells/cytology/*metabolism ; Neurons/cytology ; Oncogene Protein pp60(v-src) ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Retroviridae Proteins/genetics/*metabolism ; Tretinoin/pharmacology
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  • 33
    Publication Date: 1986-01-24
    Description: Human T-lymphotropic virus type III (HTLV-III) or lymphadenopathy-associated virus (LAV) is tropic for human T cells with the helper-inducer phenotype, as defined by reactivity with monoclonal antibodies specific for the T4 molecule. Treatment of T4+ T cells with monoclonal antibodies to T4 antigen blocks HTLV-III/LAV binding, syncytia formation, and infectivity. Thus, it has been inferred that the T4 molecule itself is a virus receptor. In the present studies, the surfaces of T4+ T cells were labeled radioactively, and then the cells were exposed to virus. After the cells were lysed, HTLV-III/LAV antibodies were found to precipitate a surface protein with a molecular weight of 58,000 (58K). By blocking and absorption experiments, this 58K protein was identified as the T4 molecule. No cell-surface structures other than the T4 molecule were involved in the antibody-antigen complex formation. Two monoclonal antibodies, each reactive with a separate epitope of the T4 molecule, were tested for their binding capacities in the presence of HTLV-III/LAV. When HTLV-III/LAV was bound to T4+ T cells, the virus blocked the binding of one of the monoclonal antibodies, T4A (OKT4A), but not of the other, T4 (OKT4). When HTLV-III/LAV was internally radiolabeled and bound to T4+ T cells which were then lysed, a viral glycoprotein of 110K (gp110) coprecipitated with the T4 molecule. The binding of gp110 to the T4 molecule may thus be a major factor in HTLV-III/LAV tropism and may prove useful in developing therapeutic or preventive measures for the acquired immune deficiency syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDougal, J S -- Kennedy, M S -- Sligh, J M -- Cort, S P -- Mawle, A -- Nicholson, J K -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):382-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3001934" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/microbiology ; Antibodies, Monoclonal ; Cell Line ; Deltaretrovirus/*metabolism ; Humans ; T-Lymphocytes/metabolism/*microbiology ; Viral Proteins/*metabolism
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  • 34
    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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  • 35
    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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  • 36
    Publication Date: 1986-12-05
    Description: Transient stimulation of target tissues by sex steroids can cause long-lasting changes that may facilitate or alter responses to subsequent hormonal treatment. How these altered characteristics are propagated during cell division in the absence of the stimulating hormone is unknown. The human hepatocarcinoma cell line HepG2 was used as a model to examine the effects of estrogen on the synthesis of serum apolipoproteins in vitro. Treatment with low concentrations of estrogen for 24 to 48 hours resulted in long-lasting alterations in the kinetics with which the cells responded to subsequent stimulation with estrogen. Manifestation of this memory effect was correlated quantitatively with the induction and propagation of a moderate-affinity, nuclear, estrogen-binding protein with the characteristics of a type II estrogen receptor. The data indicate that transient exposure of these cells to estrogen can induce changes in their response characteristics and composition of nuclear proteins that are inherited by daughter cells grown in the absence of hormone for more than ten generations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tam, S P -- Hache, R J -- Deeley, R G -- New York, N.Y. -- Science. 1986 Dec 5;234(4781):1234-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3022381" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoproteins B/pharmacology ; Apolipoproteins E/pharmacology ; Carcinoma, Hepatocellular/metabolism ; Cell Division ; Cell Line ; Chick Embryo ; Estradiol/pharmacology ; Estrogens/*pharmacology ; Humans ; Liver/*cytology/drug effects ; Liver Neoplasms/metabolism ; Receptors, Estrogen/drug effects
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  • 37
    Publication Date: 1986-02-28
    Description: Differentiation of lymphoid precursor cells in a variety of species is induced by polypeptide hormones such as thymopoietin for T cells and bursin for B cells. In the present experiments, bursin isolated from the bursa of Fabricius of chicken was found to induce the phenotypic differentiation of mammalian and avian B precursor cells but not of T precursor cells in vitro. Similarly, bursin increased cyclic guanosine monophosphate in cells of the human B-cell line Daudi but not in cells of the human T-cell line CEM. These inducing properties of bursin are the reverse of the inducing properties of thymopoietin produced by the thymus and are appropriate to a physiological B-cell-inducing hormone. A tripeptide sequence (lysyl-histidyl-glycyl-amide) was determined for bursin and confirmed by synthesizing this proposed structure and demonstrating chemical identity of the natural and synthetic peptides. Similarity of biological action was indicated in induction assays by elevation of cyclic adenosine monophosphate and guanosine monophosphate in Daudi B cells but not in CEM T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Audhya, T -- Kroon, D -- Heavner, G -- Viamontes, G -- Goldstein, G -- New York, N.Y. -- Science. 1986 Feb 28;231(4741):997-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3484838" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*physiology ; Bursa of Fabricius/*physiology ; Cell Line ; Chickens ; Chromatography, High Pressure Liquid ; Chromatography, Thin Layer ; Humans ; Mass Spectrometry ; Oligopeptides/*isolation & purification/pharmacology/physiology ; Rats ; T-Lymphocytes/drug effects
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  • 38
    Publication Date: 1986-05-16
    Description: The human T-lymphotropic viruses types I and II (HTLV-I and -II) have been etiologically linked with certain T-cell leukemias and lymphomas that characteristically display membrane receptors for interleukin-2. The relation of these viruses to this growth factor receptor has remained unexplained. It is demonstrated here that introduction of the trans-activator (tat) gene of HTLV-II into the Jurkat T-lymphoid cell line results in the induction of both interleukin-2 receptor and interleukin-2 gene expression. The coexpression of these cellular genes may play a role in the altering T-cell growth following retroviral infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greene, W C -- Leonard, W J -- Wano, Y -- Svetlik, P B -- Peffer, N J -- Sodroski, J G -- Rosen, C A -- Goh, W C -- Haseltine, W A -- 1R01CA369974-01AI/CA/NCI NIH HHS/ -- CA07580/CA/NCI NIH HHS/ -- CA40658/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 May 16;232(4752):877-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3010456" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Deltaretrovirus/*genetics ; Gene Expression Regulation ; *Genes, Viral ; Humans ; Interleukin-2/biosynthesis/*genetics ; Leukemia/microbiology ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Receptors, Immunologic/*genetics ; Receptors, Interleukin-2
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  • 39
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-08-01
    Description: The relative stability of amplified DNA in drug-resistant Leishmania major was previously reported to be dependent on location, that is, unstable amplified DNA was extrachromosomal and stable amplified DNA was chromosomal. Leishmanial chromosomes have now been directly examined by means of orthogonal-field-alternation gel electrophoresis (OFAGE). The amplified DNA's in three resistant cell lines displayed unusual migration and were clearly extrachromosomal, regardless of whether the amplified DNA's were stable or unstable. Thus, contrary to conclusions from earlier studies of drug resistance in cultured animal cells, stable amplified DNA in Leishmania can be extrachromosomal. In addition, these amplified DNA's were shown to be circular on the basis of their resistance to exonuclease III digestion and their behavior on OFAGE. Their mobility was also greatly changed after treatment with topoisomerase II, suggesting that the amplified DNA's were either supercoiled or concatenated circles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garvey, E P -- Santi, D V -- New York, N.Y. -- Science. 1986 Aug 1;233(4763):535-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726545" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chromosomes ; DNA/*genetics ; Drug Resistance, Microbial ; Electrophoresis ; *Extrachromosomal Inheritance ; Gene Amplification/drug effects ; Leishmania tropica/drug effects/*genetics ; Methotrexate/pharmacology ; Nucleic Acid Hybridization
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  • 40
    Publication Date: 1986-09-26
    Description: The potential utility of cultured neuroblastoma cells as donor tissue for neutral implants into the mammalian brain has been examined. Cells from a human neuroblastoma cell line, IMR-32, were labeled with [3H]thymidine and chemically rendered amitotic. These differentiated IMR-32 cells were grafted into the hippocampi of five adult African Green monkeys, and graft survival was evaluated for up to 270 days after transplantation. Autoradiographically labeled grafted cells were identified in four animals. Processes from grafted cells could be followed for distances of up to 150 micrometers into the host brain. No evidence for neoplastic growth of the transplant was found. Thus, grafted neuroblastoma cells can survive for prolonged periods in the primate brain and may serve as a practical source of donor tissue for neural implants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gash, D M -- Notter, M F -- Okawara, S H -- Kraus, A L -- Joynt, R J -- New York, N.Y. -- Science. 1986 Sep 26;233(4771):1420-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3749886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoradiography ; Brain/*cytology ; Cell Line ; Cercopithecus aethiops ; DNA Replication ; Female ; Humans ; Male ; Neoplasm Transplantation ; Neuroblastoma/*pathology ; Neurons/*transplantation ; Thymidine/metabolism ; Tritium
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  • 41
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-10-03
    Description: Cholinergic agonists rapidly and transiently induced transcription of the c-fos protooncogene and one or more actin genes in neuronally differentiated PC12 cells. Transcription was activated within minutes after stimulation of the nicotinic acetylcholine receptor and required an influx of extracellular Ca2+ ions through voltage-sensitive calcium channels. Nicotine activation proceeded by a different pathway from activation by nerve growth factor, whose stimulation of these genes is independent of extracellular Ca2+ ions. These findings suggest that neurotransmitters may rapidly activate specific gene transcription in nondividing neuronally differentiated cells. They also suggest a functional role for neurotransmitter induction of c-fos and actin expression in the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greenberg, M E -- Ziff, E B -- Greene, L A -- GM 30760/GM/NIGMS NIH HHS/ -- NS16036/NS/NINDS NIH HHS/ -- P30 CA 16087/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Oct 3;234(4772):80-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3749894" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Adrenal Gland Neoplasms/metabolism ; Animals ; Calcium/metabolism ; Cell Line ; Dose-Response Relationship, Drug ; Nerve Growth Factors/pharmacology ; Nicotine/pharmacology ; Pheochromocytoma/metabolism ; Rats ; Receptors, Cholinergic/*drug effects ; Transcription, Genetic/*drug effects
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  • 42
    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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  • 43
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-03-21
    Description: The bovine leukemia virus, like the human T-cell leukemia viruses (HTLV-I and HTLV-II), are unusual biologically in that viral transcripts are not detected in tumors or infected tissues. The bovine leukemia virus long terminal repeat (BLV LTR) functions as a transcriptional promoter only in cell lines productively infected with BLV. Deletion mapping indicated that at least two regions of the LTR, on the 5' and 3' sides of the RNA start site, influenced gene expression. An analysis has now been made of the effects of coupling sequences from these LTR regions to a heterologous core promoter derived from the SV40 early promoter unit. Through the use of the transient expression of the bacterial chloramphenicol acetyltransferase (CAT) gene to monitor transcriptional activity in vivo, two independent, regulatory elements were identified in the BLV LTR. One was present in a fragment of 75 base pairs derived from the U3 region of the LTR and behaved much like other enhancer elements. It may be a major determinant of BLV expression in productively infected cell lines, since it enhanced transcription controlled by the heterologous core promoter only in these cells. The second element was contained in a 250-bp fragment derived from LTR sequences in the R region, located downstream from the RNA start site. Its activation of CAT expression was not dependent on BLV infection and was evident only when the fragment was located immediately downstream from the RNA start site. BLV expression thus appears to be regulated in part by a cell-specific enhancer element upstream from the core promoter and a novel sequence downstream from the RNA initiation site in the viral LTR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Derse, D -- Casey, J W -- CA07392/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Mar 21;231(4744):1437-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006241" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cell Line ; Cercopithecus aethiops ; DNA, Recombinant ; DNA, Viral/genetics ; Deltaretrovirus/genetics ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; *Genes, Regulator ; Genes, Viral ; Humans ; Leukemia Virus, Bovine/*genetics ; Plasmids ; *Promoter Regions, Genetic ; RNA, Messenger/genetics ; *Repetitive Sequences, Nucleic Acid ; Retroviridae/*genetics ; Transcription, Genetic
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  • 44
    Publication Date: 1986-11-21
    Description: The chromosomal breakpoint involved in the t(8;14)(q24;q11) chromosome translocation in the SKW-3 cell line, which directly involves the 3' flanking region of the c-myc gene, was cloned and sequenced. The breakpoint on chromosome 8 mapped to a position 3 kb 3' of c-myc while the chromosome 14 breakpoint occurred 36 kb 5' of the gene for the constant region of the alpha chain of the T-cell receptor (TCR). The translocation resulted in a precise rearrangement of sequences on chromosome 8 and what appears to be a functional J alpha segment on chromosome 14. Signal sequences for V-J joining occurred at the breakpoint positions on both chromosomes 14 and 8, suggesting that the translocation occurs during TCR gene rearrangement and that it is catalyzed by the enzymatic systems involved in V-J joining reactions. The involvement of c-myc in the translocation and the association of joining signals at the breakpoints provides a parallel to the situation observed in the translocations involving c-myc and the immunoglobulin loci in B-cell neoplasms and suggests that common mechanisms of translocation and oncogene deregulation are involved in B- and T-cell malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finger, L R -- Harvey, R C -- Moore, R C -- Showe, L C -- Croce, C M -- CA 09485/CA/NCI NIH HHS/ -- CA 39860/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 21;234(4779):982-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3490692" target="_blank"〉PubMed〈/a〉
    Keywords: *B-Lymphocytes ; Base Sequence ; Cell Line ; Chromosomes, Human, 13-15 ; Chromosomes, Human, 6-12 and X ; Humans ; Leukemia/*genetics ; Nucleic Acid Hybridization ; Proto-Oncogenes ; Receptors, Antigen, T-Cell/genetics ; *T-Lymphocytes ; *Translocation, Genetic
    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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  • 45
    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
    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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  • 46
    Publication Date: 1986-07-25
    Description: Remarkable similarities in the intracellular and genetic events occur when lymphoid and hematopoietic cells are exposed to their specific growth factors. The interleukin-2 (IL-2) receptor, whose cell-surface expression is an absolute requirement for the growth and differentiation of lymphoid cells, was detected on various nonlymphoid hematopoietic cell types in this study. Cell lines consisting either of granulocyte-macrophage precursors or mast cells, which are dependent on interleukin-3 (IL-3) for their growth, expressed high levels of the IL-2 receptor on their surface. Analysis of the binding characteristics of these receptors with 125I-labeled recombinant IL-2 revealed that only receptors with low affinity for IL-2 were present on these cells. Addition of purified recombinant IL-3 to these cell lines led to an increase in IL-2 receptor gene expression within 1 hour in isolated nuclei. This IL-3--induced increase in the number of IL-2 receptors on the cell surface is maximal within 24 hours. Addition of 10,000 units of IL-2 to these cells had no apparent effect on their growth or differentiation. The presence of the receptor with only low affinity for IL-2 on hematopoietic cells and the regulation by IL-3 suggest that this receptor is involved in some important metabolic event in hematopoiesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Birchenall-Sparks, M C -- Farrar, W L -- Rennick, D -- Kilian, P L -- Ruscetti, F W -- New York, N.Y. -- Science. 1986 Jul 25;233(4762):455-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3088729" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Hematopoiesis/drug effects ; Hematopoietic Stem Cells/*drug effects/metabolism ; Humans ; Interleukin-2/pharmacology ; Interleukin-3 ; Lymphokines/*pharmacology ; Macrophages/drug effects/metabolism ; Mice ; Receptors, Immunologic/*biosynthesis/drug effects/genetics ; Receptors, Interleukin-2 ; T-Lymphocytes, Cytotoxic/drug effects/metabolism
    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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