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  • Cell Line  (43)
  • American Association for the Advancement of Science (AAAS)  (43)
  • American Association of Petroleum Geologists (AAPG)
  • 1985-1989  (43)
  • 1987  (43)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (43)
  • American Association of Petroleum Geologists (AAPG)
Years
  • 1985-1989  (43)
Year
  • 1
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    Brain damage by AIDS under active study (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-03-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, D M -- New York, N.Y. -- Science. 1987 Mar 27;235(4796):1574-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3103218" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*complications/drug therapy ; Antigens, Differentiation, T-Lymphocyte ; Antigens, Surface/analysis ; Cell Line ; Cell Transformation, Viral ; Encephalitis/*etiology/microbiology ; Glioma/microbiology ; Histocytochemistry ; Humans ; Macrophages/microbiology ; Membrane Proteins ; Microscopy, Electron ; Neuroglia/microbiology ; T-Lymphocytes/microbiology ; Thymidine/analogs & derivatives/therapeutic use ; Viral Proteins/analysis ; Zidovudine
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Transformation of rat fibroblasts by FSV rapidly increases glucose transporter gene transcription (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-03-20
    Description: Elevation of glucose transport is an alteration common to most virally induced tumors. Rat fibroblasts transformed with wild-type or a temperature-sensitive Fujinami sarcoma virus (FSV) were studied in order to determine the mechanisms underlying the increased transport. Five- to tenfold increases in total cellular glucose transporter protein in response to transformation were accompanied by similar increases in transporter messenger RNA levels. This, in turn, was preceded by an absolute increase in the rate of glucose transporter gene transcription within 30 minutes after shift of the temperature-sensitive FSV-transformed cells to the permissive temperature. The transporter messenger RNA levels in transformed fibroblasts were higher than those found in proliferating cells maintained at the nonpermissive temperature. The activation of transporter gene transcription by transformation represents one of the earliest known effects of oncogenesis on the expression of a gene encoding a protein of well-defined function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Birnbaum, M J -- Haspel, H C -- Rosen, O M -- AM35430-01/AM/NIADDK NIH HHS/ -- DK 35158/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 20;235(4795):1495-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3029870" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avian Sarcoma Viruses ; Cell Division ; Cell Line ; *Cell Transformation, Viral ; Fibroblasts ; Gene Expression Regulation ; Kinetics ; Monosaccharide Transport Proteins/*genetics ; RNA, Messenger/genetics ; Rats ; Transcription, Genetic
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  • 3
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    erbB-2 is a potent oncogene when overexpressed in NIH/3T3 cells (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-10
    Description: A wide variety of human tumors contain an amplified or overexpressed erbB-2 gene, which encodes a growth factor receptor-like protein. When erbB-2 complementary DNA was expressed in NIH/3T3 cells under the control of the SV40 promoter, the gene lacked transforming activity despite expression of detectable levels of the erbB-2 protein. A further five- to tenfold increase in its expression under influence of the long terminal repeat of Moloney murine leukemia virus was associated with activation of erbB-2 as a potent oncogene. The high levels of the erbB-2 product associated with malignant transformation of NIH/3T3 cells were observed in human mammary tumor cells that overexpressed this gene. These findings demonstrate a new mechanism for acquisition of oncogenic properties by genes encoding growth factor receptor-like proteins and provide a functional basis for the role of their overexpression in the development of human malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Fiore, P P -- Pierce, J H -- Kraus, M H -- Segatto, O -- King, C R -- Aaronson, S A -- New York, N.Y. -- Science. 1987 Jul 10;237(4811):178-82.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2885917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/genetics ; Cell Line ; *Cell Transformation, Neoplastic/genetics ; DNA/genetics ; Fibroblasts/*metabolism ; Gene Expression Regulation ; Genes, Viral ; Humans ; Mice ; Moloney murine leukemia virus/genetics ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/biosynthesis/genetics/*physiology ; Rats ; Receptor, Epidermal Growth Factor ; Receptor, ErbB-2 ; Receptors, Cell Surface/genetics ; Recombinant Fusion Proteins/biosynthesis/genetics/physiology ; Simian virus 40/genetics ; Tumor Stem Cell Assay
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  • 4
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    Cytokine-induced expression of HIV-1 in a chronically infected promonocyte cell line (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-06
    Description: A model system for cytokine-induced up-regulation of human immunodeficiency virus type 1 (HIV-1) expression in chronically infected promonocyte clones was established. The parent promonocyte cell line U937 was chronically infected with HIV-1 and from this line a clone, U1, was derived. U1 showed minimal constitutive expression of HIV-1, but virus expression was markedly up-regulated by a phytohemagglutinin-induced supernatant containing multiple cytokines and by recombinant granulocyte/macrophage colony-stimulating factor alone. Recombinant interleukin-1 (IL-1), IL-2, interferon-gamma, and tumor necrosis factor-alpha did not up-regulate virus expression. Concomitant with the cytokine-induced up-regulation of HIV-1, expression of membrane-bound IL-1 beta was selectively induced in U1 in the absence of induction of other surface membrane proteins. This cytokine up-regulation of IL-1 beta was not seen in the uninfected parent U937 cell line. These studies have implications for the understanding of the mechanism of progression from a latent or low-level HIV-1 infection to a productive infection with resulting immunosuppression. In addition, this model can be used to delineate the potential mechanisms whereby HIV-1 infection regulates cellular gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Folks, T M -- Justement, J -- Kinter, A -- Dinarello, C A -- Fauci, A S -- New York, N.Y. -- Science. 1987 Nov 6;238(4828):800-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3313729" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Products/*pharmacology ; Cell Line ; Clone Cells ; Cytokines ; HIV/drug effects/genetics/*growth & development ; Monocytes ; Recombinant Proteins/pharmacology
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  • 5
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    Identification and localization of mutations at the Lesch-Nyhan locus by ribonuclease A cleavage (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-17
    Description: Many mutations leading to human disease are the result of single DNA base pair changes that cannot be identified by Southern analysis. This has prompted the development of alternative assays for point mutation detection. The recently described ribonuclease A cleavage procedure, with a polyuridylic acid-paper affinity chromatography step, has been used to identify the mutational lesions in the hypoxanthine phosphoribosyltransferase (HPRT) messenger RNAs of patients with Lesch-Nyhan syndrome. Distinctive ribonuclease A cleavage patterns were identified in messenger RNA from 5 of 14 Lesch-Nyhan patients who were chosen because no HPRT Southern or Northern blotting pattern changes had been found. This approach now allows HPRT mutation detection in 50 percent of the cases of Lesch-Nyhan syndrome. The polyuridylic acid-paper affinity procedure provides a general method for analysis of low abundance messenger RNAs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbs, R A -- Caskey, C T -- New York, N.Y. -- Science. 1987 Apr 17;236(4799):303-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563511" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chromosome Deletion ; HeLa Cells/enzymology ; Humans ; Hypoxanthine Phosphoribosyltransferase/*genetics ; Lesch-Nyhan Syndrome/*genetics ; *Mutation ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Ribonuclease, Pancreatic
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  • 6
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    Identification of an amplified, highly expressed gene in a human glioma (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-03
    Description: A gene, termed gli, was identified that is amplified more than 50-fold in a malignant glioma. The gene is expressed at high levels in the original tumor and its derived cell line and is located at chromosome 12 position (q13 to q14.3). The gli gene is a member of a select group of cellular genes that are genetically altered in primary human tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kinzler, K W -- Bigner, S H -- Bigner, D D -- Trent, J M -- Law, M L -- O'Brien, S J -- Wong, A J -- Vogelstein, B -- CA-09243/CA/NCI NIH HHS/ -- CA-43722/CA/NCI NIH HHS/ -- NS-20023/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Apr 3;236(4797):70-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563490" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Chromosomes, Human, Pair 12 ; Cloning, Molecular ; DNA, Neoplasm/*genetics ; *Gene Amplification ; Gene Expression Regulation ; Glioma/*genetics ; Humans ; RNA, Messenger/genetics ; RNA, Neoplasm/genetics
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  • 7
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    The raf oncogene is associated with a radiation-resistant human laryngeal cancer (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-28
    Description: In order to identify the genetic factors associated with the radiation-resistant human laryngeal carcinoma cell line (SQ-20B), tumor cell DNA was transfected into NIH/3T3 cells. A high incidence (six out of six) of raf sequences was found in transfected NIH/3T3 clones and the tumorigenic potential of SQ-20B DNA could be linked to genomic fragments that represent most of the kinase domain of human c-raf-1. An apparently unaltered 3.5-kilobase pair (kb) human c-raf transcript was identified in SQ-20B cells but was not observed in the transfected NIH/3T3 cell clones. Two new transcripts (4.2 kb and 2.6 kb) were found in tumorigenic clones; the large transcript was missing in a very poorly tumorigenic clone. Cytogenetic analysis indicated that the normal autosomes of chromosome 3 were absent in SQ-20B karyotypes and had formed apparently stable marker chromosomes. Unlike the recipient NIH/3T3 cell line, 30 percent of the transformed clone-1 metaphases had minute and double-minute chromosomes representative of amplified DNA sequences. The frequency of the c-raf-1 identification by NIH/3T3 transfection of SQ-20B DNA suggests the presence of some genetic abnormality within this locus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kasid, U -- Pfeifer, A -- Weichselbaum, R R -- Dritschilo, A -- Mark, G E -- CA425969/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):1039-41.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616625" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA, Neoplasm/genetics ; Humans ; Karyotyping ; Laryngeal Neoplasms/*genetics/radiotherapy ; Mice ; Mice, Nude ; Nucleic Acid Hybridization ; Oncogenes/*radiation effects ; Proto-Oncogenes/radiation effects ; *Radiation Tolerance
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  • 8
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    Identification of nuclear receptors for VIP on a human colonic adenocarcinoma cell line (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-11
    Description: Vasoactive intestinal peptide (VIP) is a neuropeptide with broad tissue distribution. Although its precise function is unknown, it is thought to exert its effect, at least in part, by interacting with cell surface receptors. Nuclear receptors for VIP have now been identified by specific binding of 125I-labeled VIP to nuclei of a human colonic adenocarcinoma cell line (HT29) and by cross-linking of 125I-labeled VIP to its receptor on intact nuclei. In contrast, 125I-labeled transferrin shows only background binding to nuclei but significant binding to intact cells. Purity of the isolated nuclei was further substantiated by electron microscopy. The apparent molecular sizes of the VIP--cross-linked nuclear and cell surface receptors are similar but not identical.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Omary, M B -- Kagnoff, M F -- DK07202/DK/NIDDK NIH HHS/ -- DK35108/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1578-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2825352" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/*metabolism/ultrastructure ; Cell Line ; Cell Nucleus/*metabolism/ultrastructure ; Colonic Neoplasms/*metabolism/ultrastructure ; Humans ; Kinetics ; Microscopy, Electron ; Receptors, Gastrointestinal Hormone/*metabolism ; Receptors, Vasoactive Intestinal Peptide ; Vasoactive Intestinal Peptide/*metabolism
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  • 9
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    Protein-DNA interactions in vivo upstream of a cell cycle-regulated human H4 histone gene (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-06-05
    Description: Cell cycle-dependent histone genes are transcribed at a basal level throughout the cell cycle, with a three- to fivefold increase during early S phase. Protein-DNA interactions in the 5' promoter region of a cell cycle-regulated human H4 histone gene have been analyzed at single-nucleotide resolution in vivo. This region contains two sites, with four potential protein-binding domains, at which the DNA is protected from reaction with dimethyl sulfate in cells and from digestion with deoxyribonuclease I in nuclei. These protein-DNA interactions persist during all phases of the cell cycle and dissociate with 0.16 to 0.2M sodium chloride.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pauli, U -- Chrysogelos, S -- Stein, G -- Stein, J -- Nick, H -- GM32010/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jun 5;236(4806):1308-11.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3035717" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Cycle ; Cell Line ; Dna ; DNA Restriction Enzymes ; Deoxyribonuclease I ; Gene Expression Regulation ; Histones/*genetics ; Humans ; Nucleic Acid Hybridization ; *Promoter Regions, Genetic ; Protein Binding ; Sulfuric Acid Esters
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  • 10
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    Primary structure and biochemical properties of an M2 muscarinic receptor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-01
    Description: A partial amino acid sequence obtained for porcine atrial muscarinic acetylcholine receptor was used to isolate complementary DNA clones containing the complete receptor coding region. The deduced 466-amino acid polypeptide exhibits extensive structural and sequence homology with other receptors coupled to guanine nucleotide binding (G) proteins (for example, the beta-adrenergic receptor and rhodopsins); this similarity predicts a structure of seven membrane-spanning regions distinguished by the disposition of a large cytoplasmic domain. Stable transfection of the Chinese hamster ovary cell line with the atrial receptor complementary DNA leads to the binding of muscarinic antagonists in these cells with affinities characteristic of the M2 receptor subtype. The atrial muscarinic receptor is encoded by a unique gene consisting of a single coding exon and multiple, alternatively spliced 5' noncoding regions. The atrial receptor is distinct from the cerebral muscarinic receptor gene product, sharing only 38% overall amino acid homology and possessing a completely nonhomologous large cytoplasmic domain, suggesting a role for the latter region in differential effector coupling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peralta, E G -- Winslow, J W -- Peterson, G L -- Smith, D H -- Ashkenazi, A -- Ramachandran, J -- Schimerlik, M I -- Capon, D J -- CA16417/CA/NCI NIH HHS/ -- HL23632/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 May 1;236(4801):600-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107123" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA/genetics ; Exons ; GTP-Binding Proteins/metabolism ; Heart Atria/analysis ; Immunosorbent Techniques ; Membrane Proteins ; Molecular Weight ; Nucleic Acid Hybridization ; Peptide Fragments/metabolism ; Quinuclidinyl Benzilate/metabolism ; Receptors, Muscarinic/*genetics/metabolism ; Sequence Homology, Nucleic Acid ; Swine ; Transfection
    Print ISSN: 0036-8075
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  • 11
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    erg, a human ets-related gene on chromosome 21: alternative splicing, polyadenylation, and translation (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-07
    Description: The avian acute leukemia virus E26 induces a mixed erythroid-myeloid leukemia in chickens and carries two distinct oncogenes, v-myb and v-ets. Recently, a novel gene named erg, closely related to the v-ets oncogene, was identified in human COLO 320 cells and the nucleotide sequence of its approximately 5.0-kilobase transcript, erg 1 was determined. In the present study, the nucleotide sequence of the alternatively spliced transcript, erg 2, was found to differ from erg 1 by a splicing event that causes a coding frameshift near the amino terminus, resulting in an additional 99-amino acid insertion at the amino-terminus. Expression of complementary DNAs for the two transcripts in vitro resulted in synthesis of polypeptides of approximately 41 and 52 kilodaltons, suggesting the use of alternative translation initiation codons in the case of erg proteins. The erg gene was localized by somatic cell genetic analysis to human chromosome 21. It is proposed that alternative sites of splicing and polyadenylation, together with alternative sites of translation initiation, allow the synthesis of two related polypeptides from a single erg gene transcriptional unit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rao, V N -- Papas, T S -- Reddy, E S -- New York, N.Y. -- Science. 1987 Aug 7;237(4815):635-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3299708" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; *Chromosomes, Human, Pair 21 ; Cloning, Molecular ; Humans ; Oncogenes ; Plasmids ; Poly A/metabolism ; *Protein Biosynthesis ; Proto-Oncogene Proteins/biosynthesis ; *Proto-Oncogenes ; *RNA Splicing ; RNA, Messenger ; Sequence Homology, Nucleic Acid
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  • 12
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    Activated oncogenes in B6C3F1 mouse liver tumors: implications for risk assessment (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-09-11
    Description: The validity of mouse liver tumor end points in assessing the potential hazards of chemical exposure to humans is a controversial but important issue, since liver neoplasia in mice is the most frequent tumor target tissue end point in 2-year carcinogenicity studies. The ability to distinguish between promotion of background tumors versus a genotoxic mechanism of tumor initiation by chemical treatment would aid in the interpretation of rodent carcinogenesis data. Activated oncogenes in chemically induced and spontaneously occurring mouse liver tumors were examined and compared as one approach to determine the mechanism by which chemical treatment caused an increased incidence of mouse liver tumors. Data suggest that furan and furfural caused an increased incidence in mouse liver tumors at least in part by induction of novel weakly activating point mutations in ras genes even though both chemicals did not induce mutations in Salmonella assays. In addition to ras oncogenes, two activated raf genes and four non-ras transforming genes were detected. The B6C3F1 mouse liver may thus provide a sensitive assay system to detect various classes of proto-oncogenes that are susceptible to activation by carcinogenic insult. As illustrated with mouse liver tumors, analysis of activated oncogenes in spontaneously occurring and chemically induced rodent tumors will provide information at a molecular level to aid in the use of rodent carcinogenesis data for risk assessment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reynolds, S H -- Stowers, S J -- Patterson, R M -- Maronpot, R R -- Aaronson, S A -- Anderson, M W -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1309-16.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3629242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Liver Neoplasms/*genetics ; Mice ; Mutation ; Nucleic Acid Hybridization ; *Oncogenes ; *Proto-Oncogenes ; Risk
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  • 13
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    A chimeric, ligand-binding v-erbB/EGF receptor retains transforming potential (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-10
    Description: Comparison of amino acid sequences from human epidermal growth factor (EGF) receptor and avian erythroblastosis virus erbB oncogene product suggests that v-erbB represents a truncated avian EGF receptor gene product. Although both proteins are transmembrane tyrosine kinases, the v-erbB protein lacks most of the extracellular ligand-binding domain and a 32-amino acid cytoplasmic sequence present in the human EGF receptor. To test the validity of the proposed origin of v-erbB and to investigate the functional significance of the deleted extracellular sequences, a chimeric gene encoding the extracellular and the transmembrane domain of the human EGF receptor joined to sequences coding for the cytoplasmic domain of the avian erbB oncogene product was constructed. When expressed in Rat1 fibroblasts, this reconstituted gene product (HER-erbB) was transported to the cell surface and bound EGF. Its autophosphorylation activity was stimulated by interaction with the ligand. Expression of the HER-erbB chimera led to anchorage-independent cell growth in soft agar and EGF-induced focus formation in Rat1 monolayers. Thus, it appears that v-erbB protein sequences in the chimeric receptor retain their transforming activity under the influence of the human extracellular EGF-binding domain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riedel, H -- Schlessinger, J -- Ullrich, A -- New York, N.Y. -- Science. 1987 Apr 10;236(4798):197-200.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3494307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cell Line ; *Cell Transformation, Neoplastic ; DNA, Recombinant ; Epidermal Growth Factor/*physiology ; Humans ; *Oncogenes ; Phosphorylation ; Protein-Tyrosine Kinases/*genetics ; Rats ; Receptor, Epidermal Growth Factor/*genetics
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  • 14
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    The fragile X site in somatic cell hybrids: an approach for molecular cloning of fragile sites (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-24
    Description: Fragile X syndrome is a common form of mental retardation associated with a fragile site on the human X chromosome. Although fragility at this site is usually evident as a nonstaining chromatid gap, it remains unclear whether or not actual chromosomal breakage occurs. By means of somatic cell hybrids containing either a normal human X or a fragile X chromosome and utilizing two genes that flank the fragile site as markers of chromosome integrity, segregation of these markers was shown to be more frequent if they encompass the fragile site under appropriate culture conditions. Hybrid cells that reveal marker segregation were found to contain rearranged X chromosomes involving the region at or near the fragile site, thus demonstrating true chromosomal breakage within this area. Two independent translocation chromosomes were identified involving a rodent chromosome joined to the human X at the location of the fragile site. DNA analysis of closely linked, flanking loci was consistent with the position of the breakpoint being at or very near the fragile X site. Fragility at the translocation junctions was observed in both hybrids, but at significantly lower frequencies than that seen in the intact X of the parental hybrid. This observation suggests that the human portion of the junctional DNA may contain part of a repeated fragility sequence. Since the translocation junctions join heterologous DNA, the molecular cloning of the fragile X sequence should now be possible.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warren, S T -- Zhang, F -- Licameli, G R -- Peters, J F -- CA31777/CA/NCI NIH HHS/ -- HD20521/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 24;237(4813):420-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603029" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chromosome Banding ; *Cloning, Molecular ; Female ; Fragile X Syndrome/*genetics ; Glucosephosphate Dehydrogenase/genetics ; Humans ; Hybrid Cells/cytology ; Hypoxanthine Phosphoribosyltransferase/genetics ; Male ; Sex Chromosome Aberrations/*genetics ; Translocation, Genetic
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  • 15
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    Activation of the HIV-1 LTR by T cell mitogens and the trans-activator protein of HTLV-I (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-11
    Description: To investigate the mechanism by which immune activation augments replication of the human immunodeficiency virus type 1 (HIV-1) in infected T cells, four different classes of T cell mitogens were evaluated for their effects on the HIV-1 long terminal repeat (LTR). Phytohemagglutinin (PHA), a mitogenic lectin; phorbol 12-myristic 13-acetate, a tumor promoter; ionomycin, a calcium ionophore; and tat-1, the trans-activator protein from the human T cell leukemia/lymphoma virus type I (HTLV-I) each stimulated the HIV-1 LTR. Studies of deleted forms of the LTR supported a central role in these responses for the HIV-1 enhancer, which alone was sufficient for mitogen inducibility, but also suggested that other 5' positive and negative regulatory elements contribute to the overall magnitude of the response. Synergistic activation of the HIV-1 LTR (up to several thousandfold) was observed with combinations of these mitogens and the HIV-1--derived tat-III protein. Cyclosporin A, an immunosuppressive agent, inhibited PHA-mediated activation of the HIV-1 LTR but was without effect in the presence of other mitogens. Thus, HIV-1 gene expression and replication appear to be regulated, via the HIV-1 LTR, by the same mitogenic signals that induce T cell activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Siekevitz, M -- Josephs, S F -- Dukovich, M -- Peffer, N -- Wong-Staal, F -- Greene, W C -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1575-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Duke University School of Medicine, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2825351" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cyclosporins/pharmacology ; Deltaretrovirus/*physiology ; Genes, Viral ; HIV/drug effects/genetics/*growth & development ; Mitogens/*pharmacology ; Retroviridae Proteins/*physiology ; T-Lymphocytes/*immunology ; Trans-Activators ; Transcription Factors/*physiology ; Transcription, Genetic ; *Virus Activation/drug effects
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  • 16
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    Downregulation of L3T4+ cytotoxic T lymphocytes by interleukin-2 (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-16
    Description: Proliferation of activated cytotoxic T lymphocytes (CTLs) that recognize foreign histocompatibility antigens is induced by interleukin-2, a potent immunoregulatory molecule originally described as T cell growth factor. Interleukin-2 (IL-2) is widely used to isolate and induce clonal expansion of CTLs for functional studies in vitro and in vivo. However, in studies with CTLs specific for class I and class II histocompatibility antigens, IL-2 rapidly downregulated the lytic activity of some class II-specific CTLs in a time- and dose-dependent manner. Lytic activity of L3T4+ CTLs specific for the murine class II antigen I-Ek was repeatedly up- and downregulated in vitro by alternate exposure to specific (alloantigen) and nonspecific (recombinant IL-2) signals, respectively. These results demonstrate that some CTLs modulate their functional property (cytolysis) while undergoing IL-2-driven cell proliferation without loss of antigen specificity or ability to revert to a lytic phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shih, C C -- Truitt, R L -- AI-22312/AI/NIAID NIH HHS/ -- CA-39854/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 16;238(4825):344-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee 53233.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2443976" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, Differentiation, T-Lymphocyte/genetics ; Cell Line ; Clone Cells/immunology ; Cytotoxicity, Immunologic ; Epitopes ; H-2 Antigens/immunology ; Interleukin-2/*physiology ; Isoantigens/immunology ; *Lymphocyte Activation ; Mice ; Phenotype ; T-Lymphocytes, Cytotoxic/*immunology
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  • 17
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    Blocking of HIV-1 infectivity by a soluble, secreted form of the CD4 antigen (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-18
    Description: The initial event in the infection of human T lymphocytes, macrophages, and other cells by human immunodeficiency virus (HIV-1) is the attachment of the HIV-1 envelope glycoprotein gp120 to its cellular receptor, CD4. As a step toward designing antagonists of this binding event, soluble, secreted forms of CD4 were produced by transfection of mammalian cells with vectors encoding versions of CD4 lacking its transmembrane and cytoplasmic domains. The soluble CD4 so produced binds gp120 with an affinity and specificity comparable to intact CD4 and is capable of neutralizing the infectivity of HIV-1. These studies reveal that the high-affinity CD4-gp120 interaction does not require other cell or viral components and may establish a novel basis for therapeutic intervention in the acquired immune deficiency syndrome (AIDS).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, D H -- Byrn, R A -- Marsters, S A -- Gregory, T -- Groopman, J E -- Capon, D J -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1704-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Genentech, Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3500514" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; Animals ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Cell Line ; HIV/immunology/*pathogenicity/physiology ; Humans ; Receptors, Virus/immunology/*physiology ; Recombinant Proteins/immunology ; T-Lymphocytes/*immunology ; Viral Envelope Proteins/immunology/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Mitogens and oncogenes can block the induction of specific voltage-gated ion channels (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-01
    Description: The mechanisms underlying the ontogeny of voltage-gated ion channels in muscle are unknown. Whether expression of voltage-gated channels is dependent on mitogen withdrawal and growth arrest, as is generally true for the induction of muscle-specific gene products, was investigated in the BC3H1 muscle cell line by patch-clamp techniques. Differentiated BC3H1 myocytes expressed functional Ca2+ and Na+ channels that correspond to those found in T tubules of skeletal muscle. However, Ca2+ and Na+ channels were first detected after about 5 days of mitogen withdrawal. In order to test whether cellular oncogenes, as surrogates for exogenous growth factors, could prevent the expression of ion channels whose induction was contingent on mitogen withdrawal, BC3H1 cells were modified by stable transfection with oncogene expression vectors. Expression vectors containing v-erbB, or c-myc under the control of the SV40 promoter, delayed but did not prevent the appearance of functional Ca2+ and Na+ channels. In contrast, transfection with a Val12 c-H-ras vector, or cotransfection of c-myc together with v-erbB, suppressed the formation of functional Ca2+ and Na+ channels for greater than or equal to 4 weeks. Potassium channels were affected neither by mitogenic medium nor by transfected oncogenes. Thus, the selective effects of certain oncogenes on ion channel induction corresponded to the suppressive effects of mitogenic medium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caffrey, J M -- Brown, A M -- Schneider, M D -- HL36475/HL/NHLBI NIH HHS/ -- HL37044/HL/NHLBI NIH HHS/ -- RR-05425/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 May 1;236(4801):570-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2437651" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium/metabolism ; Cell Line ; Electric Conductivity ; Growth Substances/physiology ; Ion Channels/*physiology ; Mitogens/*pharmacology ; Muscles/*physiology ; *Oncogenes ; Potassium/metabolism ; Sodium/metabolism ; Transfection
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  • 19
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    Clonal gene therapy: transplanted mouse fibroblast clones express human alpha 1-antitrypsin gene in vivo (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-14
    Description: A retroviral vector was used to insert human alpha 1-antitrypsin (alpha 1AT) complementary DNA into the genome of mouse fibroblasts to create a clonal population of mouse fibroblasts secreting human alpha 1AT. After demonstrating that this clone of fibroblasts produced alpha 1AT after more than 100 population doublings in the absence of selection pressure, the clone was transplanted into the peritoneal cavities of nude mice. When the animals were evaluated 4 weeks later, human alpha 1AT was detected in both sera and the epithelial surface of the lungs. The transplanted clone of fibroblasts could be recovered from the peritoneal cavities of those mice and demonstrated to still be producing human alpha 1AT. Thus, even after removal of selective pressure, a single clone of retroviral vector-infected cells that expressed an exogenous gene in vitro, continued to do so in vivo, and when recovered, continued to produce the product of the exogenous gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garver, R I Jr -- Chytil, A -- Courtney, M -- Crystal, R G -- New York, N.Y. -- Science. 1987 Aug 14;237(4816):762-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3497452" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Clone Cells/metabolism ; DNA/*genetics ; DNA, Recombinant ; Fibroblasts/metabolism/*transplantation ; Humans ; Lung/metabolism ; Mice ; Mice, Nude ; Peritoneal Cavity ; Retroviridae/genetics ; *Transformation, Genetic ; alpha 1-Antitrypsin/biosynthesis/*genetics
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  • 20
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    The CML-specific P210 bcr/abl protein, unlike v-abl, does not transform NIH/3T3 fibroblasts (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-31
    Description: The v-abl oncogene of the Abelson murine leukemia virus (A-MuLV) is known to efficiently transform NIH/3T3 fibroblasts in vitro and to cause an acute lymphosarcoma in susceptible murine hosts. The role of its relative, the bcr/abl gene product, in the etiology of human chronic myelogenous leukemia (CML) remains speculative. To assess the transforming properties of the bcr/abl gene product, complementary DNA clones encoding the CML-specific P210 bcr/abl protein were expressed in NIH/3T3 fibroblasts. In contrast to the v-abl oncogene product P160, the P210 bcr/abl gene product did not transform NIH/3T3 cells. Cell lines were isolated that expressed high levels of the P210 bcr/abl protein but were morphologically normal. During the course of these experiments, a transforming recombinant of bcr/abl was isolated which fuses gag determinants derived from helper virus to the NH2-terminus of the bcr/abl protein. This suggests that a property of viral gag sequences, probably myristylation-dependent membrane localization, must be provided to bcr/abl for it to transform fibroblasts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daley, G Q -- McLaughlin, J -- Witte, O N -- Baltimore, D -- 2T 32 GM07753-07/GM/NIGMS NIH HHS/ -- CA27507/CA/NCI NIH HHS/ -- CA38497/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 31;237(4814):532-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2440107" target="_blank"〉PubMed〈/a〉
    Keywords: Abelson murine leukemia virus/physiology ; Animals ; Cell Line ; *Cell Transformation, Neoplastic ; Cell Transformation, Viral ; Epitopes ; Fibroblasts/pathology ; Fusion Proteins, bcr-abl ; Gene Products, gag ; Leukemia, Myeloid/*genetics ; Neoplasm Proteins/*genetics/physiology ; Oncogene Proteins, Viral/*physiology ; Recombinant Fusion Proteins/*genetics/physiology ; Recombinant Proteins/*genetics ; Retroviridae Proteins/physiology ; Transfection ; Viral Proteins/*physiology
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  • 21
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    Beta 1-6 branching of Asn-linked oligosaccharides is directly associated with metastasis (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-01
    Description: Neoplastic transformation has been associated with a variety of structural changes in cell surface carbohydrates, most notably increased sialylation and beta 1-6-linked branching of complex-type asparagine (Asn)-linked oligosaccharides (that is, -GlcNAc beta 1-6Man alpha 1-6Man beta 1-). However, little is known about the relevant glycoproteins or how these transformation-related changes in oligosaccharide biosynthesis may affect the malignant phenotype. Here it is reported that a cell surface glycoprotein, gp 130, is a major target of increased beta 1-6-linked branching and that the expression of these oligosaccharide structures is directly related to the metastatic potential of the cells. Glycosylation mutants of a metastatic tumor cell line were selected that are deficient in both beta 1-6 GlcNAc transferase V activity and metastatic potential in situ. Moreover, induction of increased beta 1-6 branching in clones of a nonmetastatic murine mammary carcinoma correlated strongly with acquisition of metastatic potential. The results indicate that increased beta 1-6-linked branching of complex-type oligosaccharides on gp 130 may be an important feature of tumor progression related to increased metastatic potential.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dennis, J W -- Laferte, S -- Waghorne, C -- Breitman, M L -- Kerbel, R S -- R0I-CA41233/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 May 1;236(4801):582-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2953071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Asparagine ; Carbohydrate Conformation ; Cell Line ; Cell Transformation, Neoplastic ; Glucosyltransferases/metabolism ; Glycosylation ; Lysosome-Associated Membrane Glycoproteins ; *Membrane Glycoproteins ; Membrane Proteins/metabolism ; Mice ; Mutation ; *N-Acetylglucosaminyltransferases ; *Neoplasm Metastasis ; Neoplasms, Experimental/genetics/metabolism ; *Oligosaccharides/biosynthesis ; Structure-Activity Relationship
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  • 22
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    Insulin rapidly increases diacylglycerol by activating de novo phosphatidic acid synthesis (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-01
    Description: The mechanisms whereby insulin increases diacylglycerol in BC3H-1 myocytes were examined. When [3H]arachidonate labeling of phospholipids was used as an indicator of phospholipase C activation, transient increases in [3H]diacylglycerol were observed between 0.5 and 10 minutes after the onset of insulin treatment. With [3H]glycerol labeling as an indicator of de novo phospholipid synthesis, [3H]diacylglycerol was increased maximally at 1 minute and remained elevated for 20 minutes. [3H]Glycerol-labeled diacylglycerol was largely derived directly from phosphatidic acid. Insulin increased de novo phosphatidic acid synthesis within 5 to 10 seconds; within 1 minute, this synthesis was 60 times greater than that of controls. Thus, the initial increase in diacylglycerol is due to both increased hydrolysis of phospholipids and a burst of de novo phosphatidic acid synthesis. After 5 to 10 minutes, de novo phosphatidic acid synthesis continues as a major source of diacylglycerol. Both phospholipid effects of insulin seem important for generating diacylglycerol and other phospholipid-derived intracellular signaling substances.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farese, R V -- Konda, T S -- Davis, J S -- Standaert, M L -- Pollet, R J -- Cooper, D R -- AM18608/AM/NIADDK NIH HHS/ -- HD22248/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 May 1;236(4801):586-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107122" target="_blank"〉PubMed〈/a〉
    Keywords: Arachidonic Acid ; Arachidonic Acids/metabolism ; Cell Line ; Diglycerides/*metabolism ; Enzyme Activation ; Glycerides/*metabolism ; Glycerol/metabolism ; Insulin/*pharmacology ; Kinetics ; Muscles/drug effects/*metabolism ; Phosphatidic Acids/*biosynthesis ; Phosphatidylinositols/metabolism ; Phospholipids/metabolism ; Type C Phospholipases/metabolism
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  • 23
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    Restoration of LDL receptor activity in mutant cells by intercellular junctional communication (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-02
    Description: Exchange of small molecules between cells through intercellular junctions is a widespread phenomenon implicated in many physiological and developmental processes. This type of intercellular communication can restore the activity of low-density lipoprotein (LDL) receptors in mammalian cells that are deficient in the enzyme UDP-Gal/UDP-GalNAc 4-epimerase. Pure cultures of the 4-epimerase mutant are unable to synthesize normal carbohydrate chains on LDL receptors and many other glycoproteins and therefore do not express LDL receptor activity. When these cells are cocultivated with cells expressing normal 4-epimerase activity, the structure and function of LDL receptors are restored to normal by the transfer of this enzyme's products through intercellular junctions. The formation of functional junctions does not require normal glycosylation of membrane proteins. Because many convenient assays and selections for LDL receptor activity are available, this mutant can provide a powerful new tool for biochemical and genetic studies of intercellular junctional communication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hobbie, L -- Kingsley, D M -- Kozarsky, K F -- Jackman, R W -- Krieger, M -- New York, N.Y. -- Science. 1987 Jan 2;235(4784):69-73.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3798096" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Communication/drug effects ; Cell Line ; Cricetinae ; Genetic Complementation Test ; Intercellular Junctions/*physiology ; Receptors, LDL/*physiology ; Tretinoin/pharmacology ; UDPglucose 4-Epimerase/metabolism ; Uridine Diphosphate Galactose/*metabolism ; Uridine Diphosphate N-Acetylgalactosamine/*metabolism ; Uridine Diphosphate Sugars/*metabolism
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  • 24
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    Interleukin-1 stimulates the secretion of hypothalamic corticotropin-releasing factor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-23
    Description: There is now evidence that the immune system, during times of infectious challenge, can stimulate the secretion of glucocorticoids, the adrenal steroids that mediate important aspects of the response to stress. Specifically, secretion of interleukin-1 (IL-1), a monocyte lymphokine secreted after infection, appears at least in part responsible for this effect. Glucocorticoids are secreted in response to a neuroendocrine cascade involving, first, the brain, then the pituitary, and finally the adrenal gland. In this report, human IL-1 is shown to activate the adrenocortical axis at the level of the brain, stimulating the release of the controlling hormone corticotropin-releasing factor (CRF) from the hypothalamus. Infusion of IL-1 induced a significant secretion of CRF into the circulation exiting the hypothalamus, whereas immunoneutralization of CRF blocked the stimulatory effect of IL-1 on glucocorticoid secretion. IL-1 appeared to have no acute direct stimulatory effects on the pituitary or adrenal components of this system. Furthermore, IL-1 did not cause a nonspecific release of other hypothalamic hormones. Thus, the lymphokine acts in a specific manner to activate the adrenocortical axis at the level of the brain; this effect appears to be unrelated to the known pyrogenic effects of IL-1 within the hypothalamus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sapolsky, R -- Rivier, C -- Yamamoto, G -- Plotsky, P -- Vale, W -- AA06420/AA/NIAAA NIH HHS/ -- AM26741/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):522-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821621" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex/physiology ; Adrenocorticotropic Hormone/secretion ; Animals ; Cell Line ; Corticosterone/secretion ; Corticotropin-Releasing Hormone/*secretion ; Hypothalamus/*secretion ; Immunologic Techniques ; Interleukin-1/*physiology ; Male ; Pituitary Gland, Anterior/secretion ; Pituitary Neoplasms/secretion ; Rats ; Rats, Inbred Strains
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  • 25
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    Measuring the human T cell receptor gamma-chain locus (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-09-04
    Description: The human T cell receptor gamma locus, including eleven variable-region, five joining-region, and two constant-region segments, is contained in 160 kilobases. During T cell somatic development these genes undergo rearrangement by deletion of the sequences separating the variable and joining regions. The molecular map of this locus was completely defined by deletion mapping and restriction mapping. Restriction fragments were resolved by standard agarose electrophoresis and field inversion electrophoresis. These studies demonstrate that the deletions in this locus, which occur during the formation of a functional T cell receptor gamma-chain gene, range from 50 to 145 kilobases in length. These studies also provide a structural basis for understanding the development of the gamma-chain peptide repertoire, and extends the potential of the emerging pulsed-field electrophoretic technology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strauss, W M -- Quertermous, T -- Seidman, J G -- AI18436/AI/NIAID NIH HHS/ -- T32-07208/PHS HHS/ -- New York, N.Y. -- Science. 1987 Sep 4;237(4819):1217-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3498213" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chromosome Deletion ; *Genes ; Genetic Linkage ; Humans ; Macromolecular Substances ; Receptors, Antigen, T-Cell/*genetics ; T-Lymphocytes/*immunology
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  • 26
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    Genetic reconstitution of functional acetylcholine receptor channels in mouse fibroblasts (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-18
    Description: Foreign genes can be stably integrated into the genome of a cell by means of DNA-mediated gene transfer techniques, and large quantities of homogenous cells that continuously express these gene products can then be isolated. Such an expression system can be used to study the functional consequences of introducing specific mutations into genes and to study the expressed protein in the absence of cellular components with which it is normally in contact. All four Torpedo acetylcholine receptor (AChR) subunit complementary DNA's were introduced into the genome of a mouse fibroblast cell by DNA-mediated gene transfer. A clonal cell line that stably produced high concentrations of correctly assembled cell surface AChR's and formed proper ligand-gated ion channels was isolated. With this new expression system, recombinant DNA, biochemical, pharmacological, and electrophysiological techniques were combined to study Torpedo AChR's in a single intact system. The physiological and pharmacological profiles of Torpedo AChR's expressed in mouse fibroblast cells differ in some details from those described earlier, and may provide a more accurate reflection of the properties of this receptor in its natural environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Claudio, T -- Green, W N -- Hartman, D S -- Hayden, D -- Paulson, H L -- Sigworth, F J -- Sine, S M -- Swedlund, A -- NS 07102/NS/NINDS NIH HHS/ -- NS 21501/NS/NINDS NIH HHS/ -- NS 21714/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1688-94.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3686008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/physiology ; Fibroblasts/metabolism ; *Genes ; Kinetics ; Mice ; Receptors, Cholinergic/*genetics/metabolism ; Torpedo ; *Transfection
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  • 27
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    Glucocorticoid receptor-like antigen in lymphoma cell membranes: correlation to cell lysis (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-24
    Description: S-49 mouse lymphoma cells undergo lysis when treated with glucocorticoids; the mechanism of this effect is not understood. A protein was detected in the plasma membrane of these cells by means of direct immunofluorescent labeling with a monoclonal antibody to the soluble glucocorticoid receptor. Cellular heterogeneity in the content of this glucocorticoid receptor-like molecule was evident. By immunoadsorption to antibody-coated tissue culture plates, the cells were separated into populations positive (100%) and depleted (38%) for this membrane antigen. Gel electrophoresis, specific immunoblot, and autoradiographic (binding of [3H]dexamethasone mesylate) analysis of the membrane proteins from the membrane antigen-positive group revealed multiple protein bands ranging in size from 85 to 145 kilodaltons. Furthermore, comparison of the glucocorticoid sensitivity of these groups of cells showed complete lysis of the membrane antigen-positive cells and only partial lysis of the antigen-deficient group, which suggests that the lysis response of cells to glucocorticoids is mediated by a glucocorticoid receptor-like molecule located in the plasma membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gametchu, B -- CA17701/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Apr 24;236(4800):456-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563523" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/*analysis ; Antigens, Surface/*analysis ; Cell Line ; Cell Membrane/immunology/metabolism ; Cell Nucleus/metabolism ; Cell Survival/drug effects ; Cytoplasm/metabolism ; Dexamethasone/metabolism/pharmacology ; Lymphoma/*immunology ; Mice ; Molecular Weight ; Receptors, Glucocorticoid/*immunology/metabolism
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  • 28
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    Mutations in diphtheria toxin separate binding from entry and amplify immunotoxin selectivity (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-23
    Description: Monoclonal antibodies linked to toxic proteins (immunotoxins) can selectively kill some tumor cells in vitro and in vivo. However, reagents that combine the full potency of the native toxins with the high degree of cell type selectivity of monoclonal antibodies have not previously been designed. Two heretofore inseparable activities on one polypeptide chain of diphtheria toxin and ricin account for the failure to construct optimal reagents. The B chains (i) facilitate entry of the A chain to the cytosol, which allows immunotoxins to efficiently kill target cells, and (ii) bind to receptors present on most cells, which imparts to immunotoxins a large degree of non-target cell toxicity. This report identifies point mutations in the B polypeptide chain of diphtheria toxin that block binding but allow cytosol entry. Three mutants of diphtheria toxin have 1/1,000 to 1/10,000 the toxicity and 1/100 to 1/8,000 the binding activity of diphtheria toxin. Linking of either of two of the inactivated mutant toxins (CRM103, Phe508; CRM107, Phe390, Phe525) to a monoclonal antibody specific for human T cells reconstitutes full target-cell toxicity--indistinguishable from that of the native toxin linked to the same antibody--without restoring non-target cell toxicity. This separation of the entry function from the binding function generates a uniquely potent and cell type-specific immunotoxin that retains full diphtheria toxin toxicity, yet is four to five orders of magnitude less toxic than the native toxin is to nontarget cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greenfield, L -- Johnson, V G -- Youle, R J -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):536-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbial Genetics, Cetus Corporation, Emeryville, CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3498987" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigens, Differentiation, T-Lymphocyte/immunology ; Antigens, Surface/immunology ; Cell Line ; Cell Survival/drug effects ; Chemical Phenomena ; Chemistry ; Diphtheria Toxin/genetics/*metabolism/pharmacology ; Heparin-binding EGF-like Growth Factor ; Immunotoxins/*pharmacology ; Intercellular Signaling Peptides and Proteins ; *Mutation ; *Receptors, Cell Surface ; Receptors, Cholinergic/metabolism ; Ricin/metabolism ; Structure-Activity Relationship ; T-Lymphocytes/immunology ; Vero Cells
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  • 29
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    Lipoprotein uptake by neuronal growth cones in vitro (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-22
    Description: Macrophages that rapidly enter injured peripheral nerve synthesize and secrete large quantities of apolipoprotein E. This protein may be involved in the redistribution of lipid, including cholesterol released during degeneration, to the regenerating axons. To test this postulate, apolipoprotein E-associated lipid particles released from segments of injured rat sciatic nerve and apolipoprotein E-containing lipoproteins from plasma were used to determine whether sprouting neurites, specifically their growth cones, possessed lipoprotein receptors. Pheochromocytoma (PC12) cells, which can be stimulated to produce neurites in vitro, were used as a model system. Apolipoprotein E-containing lipid particles and lipoproteins, which had been labeled with fluorescent dye, were internalized by the neurites and their growth cones; the unmetabolized dye appeared to be localized to the lysosomes. The rapid rate of accumulation in the growth cones precludes the possibility of orthograde transport of the fluorescent particles from the PC12 cell bodies. Thus, receptor-mediated lipoprotein uptake is performed by the apolipoprotein B,E(LDL) (low density lipoprotein) receptors, and in the regenerating peripheral nerve apolipoprotein E may deliver lipids to the neurites and their growth cones for membrane biosynthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ignatius, M J -- Shooter, E M -- Pitas, R E -- Mahley, R W -- MH 17047/MH/NIMH NIH HHS/ -- NS 04270/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 May 22;236(4804):959-62.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3576212" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Gland Neoplasms ; Animals ; Apolipoproteins E/*metabolism ; Axons/ultrastructure ; Cell Line ; Cells, Cultured ; Neurons/*cytology/metabolism ; Pheochromocytoma ; Rats ; Sciatic Nerve/*cytology/metabolism
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  • 30
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    A nerve growth factor-induced gene encodes a possible transcriptional regulatory factor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-06
    Description: Nerve growth factor (NGF) is a trophic agent that promotes the outgrowth of nerve fibers from sympathetic and sensory ganglia. The neuronal differentiation stimulated by this hormone was examined in the NGF-responsive cell line PC12. Differential hybridization was used to screen a complementary DNA library constructed from PC12 cells treated with NGF and cycloheximide. One of the complementary DNA clones that was rapidly induced by NGF was found to have a nucleotide sequence that predicts a 54-kilodalton protein with homology to transcriptional regulatory proteins. This clone, NGFI-A, contains three tandemly repeated copies of the 28- to 30-amino acid "zinc finger" domain present in Xenopus laevis TFIIIA and other DNA-binding proteins. It also contains another highly conserved unit of eight amino acids that is repeated at least 11 times. The NGFI-A gene is expressed at relatively high levels in the brain, lung, and superior cervical ganglion of the adult rat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Milbrandt, J -- NS01018/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 6;238(4828):797-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3672127" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Gland Neoplasms ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cycloheximide/pharmacology ; DNA/metabolism ; Genes/*drug effects ; Genes, Regulator/drug effects ; Molecular Sequence Data ; Molecular Weight ; Nerve Growth Factors/*pharmacology ; Pheochromocytoma ; Sequence Homology, Nucleic Acid ; Transcription Factors/*genetics
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    Tissue distribution and developmental expression of the messenger RNA encoding angiogenin (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-17
    Description: New blood vessel growth occurs during normal fetal development and in diseases such as cancer and diabetes. The polypeptide angiogenin induces new blood vessel growth in two biological assays and may play a role in the vascular development of the fetus and in the neovascularization that accompanies diseases and wound healing. A complementary DNA probe for human angiogenin was used to examine the tissue distribution of angiogenin messenger RNA (mRNA) in the developing rat and in selected transformed cell lines. Angiogenin mRNA was detected predominantly in adult liver but was also detectable at low levels in other tissues. The expression of the angiogenin gene in rat liver was found to be developmentally regulated; mRNA levels were low in the developing fetus, increased in the neonate, and maximal in the adult. The amount of angiogenin mRNA in human HT-29 colon carcinoma and SK-HEP hepatoma cells was not greater than that in normal rat liver. These results demonstrate that angiogenin is predominantly expressed in adult liver, that the pattern of angiogenin gene expression is not temporally related to vascular development in the rat, and that the transformed cells studied do not contain more angiogenin mRNA than does normal liver. If angiogenin activity is controlled at the transcriptional level, the results of this study suggest that the primary function of angiogenin in vivo may be in processes other than the regulation of vascular growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiner, H L -- Weiner, L H -- Swain, J L -- HL26831/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):280-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2440105" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Animals ; Cell Line ; Gene Expression Regulation ; Humans ; Liver/physiology ; Neoplasm Proteins/*genetics ; Neovascularization, Pathologic ; RNA, Messenger/genetics ; Rats ; *Ribonuclease, Pancreatic ; Tissue Distribution
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    Acylation of proteins with myristic acid occurs cotranslationally (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-27
    Description: Several proteins of viral and cellular origin are acylated with myristic acid early during their biogenesis. To investigate the possibility that myristylation occurred cotranslationally, the BC3H1 muscle cell line, which contains a broad array of myristylated proteins, was pulse-labeled with [3H]myristic acid. Nascent polypeptide chains covalently associated with transfer RNA were isolated subsequently by ion-exchange chromatography. [3H]Myristate was attached to nascent chains through an amide linkage and was identified by thin-layer chromatography after its release from nascent chains by acid methanolysis. Inhibition of cellular protein synthesis with puromycin resulted in cessation of [3H]myristate-labeling of nascent chains, in agreement with the dependence of this modification on protein synthesis in vivo. These data represent a direct demonstration that myristylation of proteins is a cotranslational modification.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilcox, C -- Hu, J S -- Olson, E N -- New York, N.Y. -- Science. 1987 Nov 27;238(4831):1275-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Texas, M.D. Anderson Hospital and Tumor Institute at Houston 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685978" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Animals ; Cell Line ; Kinetics ; Methionine/metabolism ; Muscles ; Myristic Acid ; Myristic Acids/*metabolism ; *Protein Biosynthesis ; Proteins/*genetics/metabolism ; Sulfur Radioisotopes ; Tritium
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  • 33
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    A parathyroid hormone-related protein implicated in malignant hypercalcemia: cloning and expression (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-21
    Description: Humoral hypercalcemia of malignancy is a common complication of lung and certain other cancers. The hypercalcemia results from the actions of tumor factors on bone and kidney. We report here the isolation of full-length complementary DNA clones of a putative hypercalcemia factor, and the expression from the cloned DNA of the active protein in mammalian cells. The clones encode a prepro peptide of 36 amino acids and a mature protein of 141 amino acids that has significant homology with parathyroid hormone in the amino-terminal region. This previously unrecognized hormone may be important in normal as well as abnormal calcium metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suva, L J -- Winslow, G A -- Wettenhall, R E -- Hammonds, R G -- Moseley, J M -- Diefenbach-Jagger, H -- Rodda, C P -- Kemp, B E -- Rodriguez, H -- Chen, E Y -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):893-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616618" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Line ; Cloning, Molecular ; DNA/genetics ; Gene Expression Regulation ; Humans ; Hypercalcemia/*genetics ; Lung Neoplasms/complications/*genetics ; Neoplasm Proteins/*genetics ; Parathyroid Hormone/genetics ; Parathyroid Hormone-Related Protein
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    An M2 muscarinic receptor subtype coupled to both adenylyl cyclase and phosphoinositide turnover (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-10-30
    Description: To investigate whether a particular receptor subtype can be coupled to multiple effector systems, recombinant M2 muscarinic receptors were expressed in cells lacking endogenous receptor. The muscarinic agonist carbachol both inhibited adenylyl cyclase and stimulated phosphoinositide hydrolysis. The stimulation of phosphoinositide hydrolysis was significantly less efficient and more dependent on receptor levels than the inhibition of adenylyl cyclase. Both responses were mediated by guanine nucleotide binding proteins, as evidenced by their inhibition by pertussis toxin; the more efficiently coupled adenylyl cyclase response was significantly more sensitive. Thus, individual subtypes of a given receptor are capable of regulating multiple effector pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ashkenazi, A -- Winslow, J W -- Peralta, E G -- Peterson, G L -- Schimerlik, M I -- Capon, D J -- Ramachandran, J -- CA16417/CA/NCI NIH HHS/ -- HL23632/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 30;238(4827):672-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Genentech, Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2823384" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylate Cyclase Toxin ; Adenylyl Cyclases/*metabolism ; Animals ; Carbachol/pharmacology ; Cell Line ; Cricetinae ; Cyclic AMP/biosynthesis ; GTP-Binding Proteins/*metabolism ; Gene Expression Regulation ; Guanosine 5'-O-(3-Thiotriphosphate) ; Guanosine Triphosphate/analogs & derivatives/metabolism ; Oxotremorine/pharmacology ; Pertussis Toxin ; Phosphatidylinositols/*metabolism ; Receptors, Muscarinic/*metabolism ; Recombinant Proteins ; Thionucleotides/metabolism ; Virulence Factors, Bordetella/metabolism
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  • 35
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    Immunochemical proof that a novel rearranging gene encodes the T cell receptor delta subunit (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-30
    Description: The T cell receptor (TCR) delta protein is expressed as part of a heterodimer with TCR gamma, in association with the CD3 polypeptides on a subset of functional peripheral blood T lymphocytes, thymocytes, and certain leukemic T cell lines. A monoclonal antibody directed against TCR delta was produced that binds specifically to the surface of several TCR gamma delta cell lines and immunoprecipitates the TCR gamma delta as a heterodimer from Triton X-100 detergent lysates and also immunoprecipitates the TCR delta subunit alone after chain separation. A candidate human TCR delta complementary DNA clone (IDP2 O-240/38), reported in a companion paper, was isolated by the subtractive library approach from a TCR gamma delta cell line. This complementary DNA clone was used to direct the synthesis of a polypeptide that is specifically recognized by the monoclonal antibody to TCR delta. This complementary DNA clone thus corresponds to the gene that encodes the TCR delta subunit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Band, H -- Hochstenbach, F -- McLean, J -- Hata, S -- Krangel, M S -- Brenner, M B -- 1-KO1-AMO1598/AM/NIADDK NIH HHS/ -- 5RO1-AI15669/AI/NIAID NIH HHS/ -- SO7RR5526-24/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 30;238(4827):682-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Tumor Virology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3672118" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal/*immunology ; Antibody Specificity ; Cell Line ; Cloning, Molecular ; DNA/genetics ; Glycoproteins/genetics/immunology ; Humans ; Receptors, Antigen, T-Cell/*genetics/immunology ; Recombinant Proteins/immunology
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  • 36
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    Signal for attachment of a phospholipid membrane anchor in decay accelerating factor (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-27
    Description: Decay accelerating factor (DAF) belongs to a novel group of membrane proteins anchored to the cell surface by a glycophospholipid membrane anchor that is covalently attached to the carboxyl terminus of the protein. The last 37 amino acids of membrane DAF, when fused to the carboxyl terminus of a secreted protein, are sufficient to target the fusion protein to the plasma membrane by means of a glycophospholipid anchor. This approach provides a novel means of targeting proteins to the cell-surface membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caras, I W -- Weddell, G N -- Davitz, M A -- Nussenzweig, V -- Martin, D W Jr -- AI-08499/AI/NIAID NIH HHS/ -- AI-23276/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 27;238(4831):1280-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genentech, Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2446389" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD55 ; Cell Line ; Cell Membrane/physiology ; DNA/metabolism ; Membrane Lipids/*metabolism ; Membrane Proteins/genetics/*metabolism ; Phospholipids/*metabolism ; Transfection
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  • 37
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    Mutations in the first exon are associated with altered transcription of c-myc in Burkitt lymphoma (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-27
    Description: The c-myc proto-oncogene is involved in chromosomal translocations that are specifically and consistently found in Burkitt lymphoma. Although these translocations are thought to lead to a deregulation of c-myc expression, the structural and functional basis of this phenomenon has not been identified. Mutations in a specific region spanning approximately 70 base pairs and located at the 3' border of the first exon of translocated c-myc alleles were consistently detected in Burkitt lymphoma cells carrying classic (8:14) as well as variant (8:22 and 2:8) translocations. These structural alterations were accompanied by an altered pattern of c-myc transcription, namely, the removal of a block to transcriptional elongation that has been mapped to the same region. Thus, specific c-myc mutations leading to the alleviation of this block to transcriptional elongation may represent a general mechanism causing c-myc activation in Burkitt lymphoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cesarman, E -- Dalla-Favera, R -- Bentley, D -- Groudine, M -- NCI 28151/CI/NCPDCID CDC HHS/ -- NCI 37165/CI/NCPDCID CDC HHS/ -- NCI 37195/CI/NCPDCID CDC HHS/ -- New York, N.Y. -- Science. 1987 Nov 27;238(4831):1272-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, New York University School of Medicine, NY 10016.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685977" target="_blank"〉PubMed〈/a〉
    Keywords: Burkitt Lymphoma/*genetics ; Cell Line ; Chromosomes, Human, Pair 14 ; Chromosomes, Human, Pair 2 ; Chromosomes, Human, Pair 22 ; Chromosomes, Human, Pair 8 ; *Exons ; Humans ; *Mutation ; *Proto-Oncogenes ; *Transcription, Genetic ; *Translocation, Genetic
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    Interaction of a liver-specific nuclear factor with the fibrinogen and alpha 1-antitrypsin promoters (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-30
    Description: The orderly and sequential activation of genes during development is hypothesized to be related to the selective expression of groups of regulatory proteins acting primarily at the level of transcription. A nuclear protein was found in hepatocytes, but not other cell types, that binds to a sequence required for hepatocyte-specific transcription of the gene for the beta chain of fibrinogen. This protein, hepatocyte nuclear factor 1 (HNF1), also interacts with homologous sequences required for optimal promoter function of the genes for the alpha chain of fibrinogen and alpha 1-antitrypsin. The promoter or enhancer regions for several viral and cellular genes not expressed in the liver did not compete for this binding. The restricted expression of HNF1 and its selective interaction with the control regions of several liver-specific genes indicate that it is involved in developmentally regulated gene expression in the liver.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Courtois, G -- Morgan, J G -- Campbell, L A -- Fourel, G -- Crabtree, G R -- CA39612/CA/NCI NIH HHS/ -- HL33942/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 30;238(4827):688-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3499668" target="_blank"〉PubMed〈/a〉
    Keywords: Albumins/genetics ; Base Sequence ; Binding, Competitive ; Cell Line ; DNA-Binding Proteins/*genetics ; Deoxyribonuclease I ; Fibrinogen/*genetics ; *Gene Expression Regulation ; Liver/*physiology ; Nuclear Proteins/*physiology ; *Promoter Regions, Genetic ; Regulatory Sequences, Nucleic Acid ; Transcription Factors/*genetics ; alpha 1-Antitrypsin/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 39
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    Phagocytosis of Candida albicans enhances malignant behavior of murine tumor cells (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-11
    Description: Murine tumor cells were induced to phagocytize either Candida albicans or group A streptococcal cells. The presence of microbial particles within the tumor cell cytoplasm had no effect on in vitro tumor cell growth. However, when Candida albicans-infected tumor cells were injected into syngeneic mice, they formed tumors that grew faster, invaded the surrounding normal tissue more rapidly and metastasized more rapidly than control tumor cells. Tumor cells infected with group A streptococcal particles did not grow faster or show increased malignant behavior. These data indicate that the in vivo behavior of malignant tumor cells can be modulated by microbial particles, which are often present in the microenvironment of the growing tumor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ginsburg, I -- Fligiel, S E -- Kunkel, R G -- Riser, B L -- Varani, J -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1573-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oral Biology, Hebrew University--Hadassah School of Dental Medicine, Jerusalem, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3317835" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Candida albicans ; Cell Line ; Fibrosarcoma/pathology/*physiopathology ; Mice ; Mice, Inbred C57BL ; *Phagocytosis ; Streptococcus pyogenes
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 40
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    Tumor cell rejection through terminal cell differentiation (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-27
    Description: Leukemic cells cultured in the presence of various conditioned media differentiate into macrophages. This finding suggested that the maintenance of undifferentiated state and self-renewal in vivo may be related to the inability of the host to generate an appropriate level of differentiation factor (DF). Evidence for this hypothesis was derived from experiments in vitro and in vivo with myeloid leukemia of rat. The following results were obtained: (i) in vitro, the percentage of cell differentiation at a fixed concentration of DF was inversely related to the concentration of cells; (ii) leukemic cell inoculates that were lethal to 7-day-old rats were rejected by 21-day-old rats; (iii) leukemic cells in diffusion chambers underwent differentiation in 21-day-old rats but not in 7-day-old rats; (iv) organs from 21-day-old rats contained more DF activity than those of 7-day-old rats; (v) treatment of rats with DF in diffusion chambers resulted in leukemic cell differentiation inside the chamber; and (vi) the development of leukemia in 7-day-old rats was aborted by treatment with DF. These results show that the differentiation of rat leukemia cells requires the appropriate level of DF. The proliferation of transplanted leukemia cells in 7-day-old rats goes unchecked because of inadequate generation of DF. Conversely, in the 21-day-old rats, rejection is accomplished by differentiation of the transplanted cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jimenez, J J -- Yunis, A A -- AM 07114/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 27;238(4831):1278-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Miami School of Medicine, FL 33101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685979" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cell Differentiation ; Cell Division ; Cell Line ; Cell Survival ; *Graft Rejection ; Leukemia, Experimental/*pathology ; Neoplasm Transplantation ; Phagocytosis ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 41
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    Identification of a T3-associated gamma delta T cell receptor on Thy-1+ dendritic epidermal Cell lines (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-15
    Description: The murine epidermis contains a subpopulation of bone marrow-derived lymphocytes that have a dendritic morphology and that express Thy-1 and T3 cell-surface antigens but not other markers (L3T4 or Lyt-2) characteristic of mature peripheral T lymphocytes. An alternative type of T cell receptor was earlier identified on a subpopulation of murine thymocytes with a similar phenotype (T3+, L3T4-, Lyt-2-), but not on peripheral murine T lymphocytes. Two independently derived Thy-1+, L3T4-, and Lyt-2- dendritic cell lines of epidermal origin that express a T3-associated disulfide-linked heterodimer composed of a 34-kilodalton gamma-chain and 46-kilodalton partner (the delta chain) have now been identified. Analysis of N-linked glycosylation revealed that this receptor is similar to that detected on thymocytes. These results demonstrate that Thy-1+ dendritic epidermal cell lines can express gamma delta T cell receptors in vitro and suggest that Thy-1+ dendritic epidermal cells express such receptors in vivo. The localization of these gamma delta T cell receptor-expressing cells in the epidermis may be of importance for understanding the function of these receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koning, F -- Stingl, G -- Yokoyama, W M -- Yamada, H -- Maloy, W L -- Tschachler, E -- Shevach, E M -- Coligan, J E -- F32AM07219-03/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 May 15;236(4803):834-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2883729" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/*analysis ; Antigens, Thy-1 ; Bone Marrow/immunology ; Cell Line ; Mice ; Molecular Weight ; Receptors, Antigen, T-Cell/*analysis ; T-Lymphocytes/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 42
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    Ribavirin antagonizes the effect of azidothymidine on HIV replication (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-03-13
    Description: Azidothymidine and ribavirin both inhibit replication of human immunodeficiency virus in vitro and show promise of clinical utility in patients infected with this virus. In this study, the possible interactions of these drugs were examined in vitro, and a reproducible antagonism between azidothymidine and ribavirin was found to occur under a variety of experimental conditions. The mechanism responsible for this antagonism appeared to be inhibition of azidothymidine phosphorylation by ribavirin. Because similar effects may occur in vivo, clinical trials of these two drugs in combination must be performed only under carefully controlled conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogt, M W -- Hartshorn, K L -- Furman, P A -- Chou, T C -- Fyfe, J A -- Coleman, L A -- Crumpacker, C -- Schooley, R T -- Hirsch, M S -- CA 09382-04/CA/NCI NIH HHS/ -- CA 12464/CA/NCI NIH HHS/ -- CA 27569/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 13;235(4794):1376-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2435003" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; HIV/*drug effects/physiology ; Humans ; Lymphocytes/microbiology ; Monocytes/microbiology ; Phosphorylation ; Phytohemagglutinins/pharmacology ; RNA-Directed DNA Polymerase/metabolism ; Ribavirin/*pharmacology ; Ribonucleosides/*pharmacology ; Thymidine/*analogs & derivatives/antagonists & inhibitors/pharmacology ; Virus Replication/drug effects ; Zidovudine
    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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  • 43
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    Nuclear reassembly excludes large macromolecules (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-23
    Description: Interphase nucleus and cytoplasm are distinct compartments, whose soluble macromolecular contents mix when the nuclear envelope disassembles at mitosis. To determine how their interphase identities are reestablished, fibroblasts were loaded with fluorescent dextrans and then allowed to divide. Large dextrans (molecular weight of 40,000 or more) were excluded from condensed mitotic chromosomes and from newly formed, postmitotic interphase nuclei. Therefore, postmitotic reassembly of the nucleus as a compartment distinct from cytoplasm occurs by exclusion not only of organelles but also of soluble macromolecules. This might occur by exclusion of macromolecules from condensed chromatin throughout mitosis and completion of nuclear envelope assembly before nuclear expansion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Swanson, J A -- McNeil, P L -- R01 CA42275/CA/NCI NIH HHS/ -- R23 CA44328/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):548-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Cellular Biology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2443981" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane Permeability ; Cell Nucleus/metabolism/*ultrastructure ; Cytoplasm/ultrastructure ; Dextrans/*metabolism ; Fibroblasts/ultrastructure ; *Fluorescein-5-isothiocyanate/*analogs & derivatives ; Fluoresceins/metabolism ; Fluorescent Dyes ; *Interphase ; Macromolecular Substances ; Mitosis ; Molecular Weight ; Nuclear Envelope/ultrastructure ; Xanthenes
    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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