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  • Gene Expression Regulation  (165)
  • American Association for the Advancement of Science (AAAS)  (165)
  • American Association of Petroleum Geologists (AAPG)
  • 1985-1989  (165)
  • 1955-1959
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (165)
  • American Association of Petroleum Geologists (AAPG)
Years
Year
  • 1
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    Isolation and expression of functional high-affinity Fc receptor complementary DNAs (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-01-20
    Description: Human and murine mononuclear phagocytes express a high-affinity receptor for immunoglobulin G that plays a central role in macrophage antibody-dependent cellular cytotoxicity and clearance of immune complexes. The receptor (FcRI) may also be involved in CD4-independent infection of human macrophages by human immunodeficiency virus. This report describes the isolation of cDNA clones encoding the human FcRI by a ligand-mediated selection technique. Expression of the cDNAs in COS cells gave rise to immunoglobulin G binding of the expected affinity and subtype specificity. RNA blot analysis revealed expression of a 1.7-kilobase transcript in macrophages and in cells of the promonocytic cell line U937 induced with interferon-gamma. The extracellular region of FcRI consists of three immunoglobulin-like domains, two of which share homology with low-affinity receptor domains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allen, J M -- Seed, B -- New York, N.Y. -- Science. 1989 Jan 20;243(4889):378-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital, Boston 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2911749" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Cercopithecus aethiops ; Cloning, Molecular ; DNA/genetics ; Gene Expression Regulation ; Humans ; Molecular Sequence Data ; Molecular Weight ; Polymorphism, Genetic ; Receptors, Fc/*genetics ; Transfection
    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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    AP1/jun function is differentially induced in promotion-sensitive and resistant JB6 cells (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-05-05
    Description: Tumor promoters may bring about events that lead to neoplastic transformation by inducing specific promotion-relevant effector genes. Functional activation of the transacting transcription factor AP-1 by the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) may play an essential role in this process. Clonal genetic variants of mouse epidermal JB6 cells that are genetically susceptible (P+) or resistant (P-) to promotion of transformation by TPA were transfected with 3XTRE-CAT, a construct that has AP-1 cis-enhancer sequences attached to a reporter gene encoding chloramphenicol acetyltransferase (CAT). Transfected JB6 P+, but not P- variants, showed TPA-inducible CAT synthesis. Epidermal growth factor, another transformation promoter in JB6 cells, also caused P+ specific induction of CAT gene expression. These results demonstrate an association between induced AP-1 function and sensitivity to promotion of neoplastic transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bernstein, L R -- Colburn, N H -- New York, N.Y. -- Science. 1989 May 5;244(4904):566-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins University, Department of Biology, Baltimore, MD 21218.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2541502" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Transformation, Neoplastic ; Chloramphenicol O-Acetyltransferase/genetics ; Cloning, Molecular ; DNA-Binding Proteins/genetics/*physiology ; Epidermal Growth Factor/pharmacology ; Epidermis ; Gene Expression Regulation ; Genetic Variation ; Kinetics ; Mice ; Nucleic Acid Hybridization ; Plasmids ; Promoter Regions, Genetic ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-jun ; Simplexvirus/genetics ; Tetradecanoylphorbol Acetate/*pharmacology ; Transcription Factors/genetics/*physiology ; Transfection
    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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  • 3
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    Expression of functional nerve growth factor receptors after gene transfer (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-01-20
    Description: Nerve growth factor (NGF) interacts with both high affinity (Kd = 10(-10)-10(-11)M) and low affinity (Kd = 10(-8)-10(-9)M) receptors; the binding of NGF to the high affinity receptor is correlated with biological actions of NGF. To determine whether a single NGF binding protein is common to both forms of the receptor, a full-length receptor cDNA was introduced in the NR18 cell line, an NGF receptor-deficient variant of the PC12 pheochromocytoma cell line. The transformant displayed (i) both high and low affinity receptors detectable by receptor binding; (ii) an affinity cross-linking pattern with 125I-labeled NGF similar to that of the parent PC12 cell line; and (iii) biological responsiveness to NGF as assayed by induction of c-fos transcription. These findings support the hypothesis that a single binding protein is common to both forms of the NGF receptor and suggest that an additional protein is required to produce the high affinity form of the NGF receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hempstead, B L -- Schleifer, L S -- Chao, M V -- HD23315/HD/NICHD NIH HHS/ -- NS-21072/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1989 Jan 20;243(4889):373-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2536190" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blotting, Northern ; Cloning, Molecular ; Gene Expression Regulation ; Nerve Growth Factors/pharmacology ; Pheochromocytoma ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins c-fos ; Rats ; Receptors, Cell Surface/*genetics/metabolism ; Receptors, Nerve Growth Factor ; Transformation, Genetic ; Tumor Cells, Cultured
    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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  • 4
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    Bacterial blight of soybean: regulation of a pathogen gene determining host cultivar specificity (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-09-22
    Description: Soybean cultivars resistant to Pseudomonas syringae pathovar glycinea (Psg), the causal agent of bacterial blight, exhibit a hypersensitive (necrosis) reaction (HR) to infection. Psg strains carrying the avrB gene elicit the HR in soybean cultivars carrying the resistance gene Rpg1. Psg expressing avrB at a high level and capable of eliciting the HR in the absence of de novo bacterial RNA synthesis have been obtained in in vitro culture. Nutritional signals and regions within the Psg hrp gene cluster, an approximately 20-kilobase genomic region also necessary for pathogenicity, control avrB transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huynh, T V -- Dahlbeck, D -- Staskawicz, B J -- New York, N.Y. -- Science. 1989 Sep 22;245(4924):1374-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Pathology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2781284" target="_blank"〉PubMed〈/a〉
    Keywords: Cloning, Molecular ; DNA Mutational Analysis ; Gene Expression Regulation ; Genes, Bacterial ; *Plant Diseases ; Promoter Regions, Genetic ; Pseudomonas/*genetics/growth & development/pathogenicity ; Regulatory Sequences, Nucleic Acid ; Restriction Mapping ; Soybeans/*genetics/microbiology ; Transcription, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Golf: an olfactory neuron specific-G protein involved in odorant signal transduction (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-05-19
    Description: Biochemical and electrophysiological studies suggest that odorants induce responses in olfactory sensory neurons via an adenylate cyclase cascade mediated by a G protein. An olfactory-specific guanosine triphosphate (GTP)-binding protein alpha subunit has now been characterized and evidence is presented suggesting that this G protein, termed Golf, mediates olfaction. Messenger RNA that encodes Golf alpha is expressed in olfactory neuroephithelium but not in six other tissues tested. Moreover, within the olfactory epithelium, Golf alpha appears to be expressed only by the sensory neurons. Specific antisera were used to localize Golf alpha protein to the sensory apparatus of the receptor neurons. Golf alpha shares extensive amino acid identity (88 percent) with the stimulatory G protein, Gs alpha. The expression of Golf alpha in S49 cyc- kin- cells, a line deficient in endogenous stimulatory G proteins, demonstrates its capacity to stimulate adenylate cyclase in a heterologous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, D T -- Reed, R R -- New York, N.Y. -- Science. 1989 May 19;244(4906):790-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Biology and Genetic Johns Hopkins School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2499043" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; GTP-Binding Proteins/analysis/genetics/*physiology ; Gene Expression Regulation ; Immunoblotting ; Immunohistochemistry ; Molecular Sequence Data ; Neurons, Afferent/analysis/*physiology ; *Odors ; Olfactory Bulb/physiology ; Olfactory Mucosa/analysis/*innervation ; RNA, Messenger/analysis/genetics ; Rats ; Sequence Homology, Nucleic Acid ; *Signal Transduction ; Tissue Distribution ; Transfection
    Print ISSN: 0036-8075
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  • 6
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    Switch protein alters specificity of RNA polymerase containing a compartment-specific sigma factor (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-01-27
    Description: During sporulation in Bacillus subtilis, expression of developmental genes spoIVCB and cotD is induced in the mother cell compartment of the sporangium at morphological stages IV and V, respectively. A 27-kilodalton RNA polymerase sigma factor called sigma K (or sigma 27) has been found that causes weak transcription of spoIVCB and strong transcription of cotD. A 14-kD protein was also discovered that changes the specificity of sigma K-containing RNA polymerase, greatly stimulating spoIVCB transcription and markedly repressing cotD transcription. Both sigma K and the 14-kD protein are products of genes known to be required for expression of specific genes in the mother cell. Thus, sigma K directs gene expression in the mother cell and it is proposed that inactivation or sequestering of the 14-kD protein switches the temporal pattern of gene expression during the transition from stages IV to V of development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kroos, L -- Kunkel, B -- Losick, R -- GM18568/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1989 Jan 27;243(4890):526-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Developmental Biology, Harvard University, Cambridge, Massachusetts 02138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2492118" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacillus subtilis/*genetics/physiology ; Cloning, Molecular ; DNA-Directed RNA Polymerases/*genetics/isolation & purification ; Electrophoresis, Polyacrylamide Gel ; Gene Expression Regulation ; Molecular Sequence Data ; Promoter Regions, Genetic ; Sigma Factor/*genetics/isolation & purification ; Spores, Bacterial/genetics ; Transcription Factors/*genetics ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 7
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    Are tissues a patch quilt of ectopic gene expression? (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-10-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Linsk, R -- Gottesman, M -- Pernis, B -- New York, N.Y. -- Science. 1989 Oct 13;246(4927):261.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2799388" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Expression Regulation ; Genes, MHC Class I/physiology ; Immune Tolerance/*genetics ; Organ Specificity/*genetics ; Thymus Gland/physiology
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  • 8
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    Regulation of lymphokine messenger RNA stability by a surface-mediated T cell activation pathway (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-04-21
    Description: Quiescent T cells can be induced to express many genes by mitogen or antigen stimulation. The messenger RNAs of some of these genes undergo relatively rapid degradation compared to messenger RNAs from constitutively expressed genes. A T cell activation pathway that specifically regulates the stability of messenger RNAs for the lymphokines interleukin-2, interferon-gamma, tumor necrosis factor-alpha, and granulocyte-macrophage colony-stimulating factor is induced by stimulation of the CD28 surface molecule. This pathway does not directly affect the steady-state messenger RNA level, transcription, or messenger RNA half-life of other T cell activation genes, including c-myc, c-fos, IL-2 receptor, and the 4F2HC surface antigen. These data show that stimuli received at the cell surface can alter gene expression by inducing specific changes in messenger RNA degradation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lindstein, T -- June, C H -- Ledbetter, J A -- Stella, G -- Thompson, C B -- New York, N.Y. -- Science. 1989 Apr 21;244(4902):339-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Michigan, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2540528" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD28 ; Antigens, CD3 ; Antigens, Differentiation, T-Lymphocyte/immunology ; Colony-Stimulating Factors/genetics ; Drug Stability ; Gene Expression Regulation ; Granulocyte-Macrophage Colony-Stimulating Factor ; Growth Substances/genetics ; Interferon-gamma/genetics ; Interleukin-2/genetics ; *Lymphocyte Activation ; Lymphokines/*genetics ; RNA, Messenger/genetics/*metabolism ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/*immunology ; Transcription, Genetic ; Tumor Necrosis Factor-alpha/genetics
    Print ISSN: 0036-8075
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  • 9
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    Human KGF is FGF-related with properties of a paracrine effector of epithelial cell growth (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-08-18
    Description: Keratinocyte growth factor (KGF) is a human mitogen that is specific for epithelial cells. The complementary DNA sequence of KGF demonstrates that it is a member of the fibroblast growth factor family. The KGF transcript was present in stromal cells derived from epithelial tissues. By comparison with the expression of other epithelial cell mitogens, only KGF, among known human growth factors, has the properties of a stromal mediator of epithelial cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finch, P W -- Rubin, J S -- Miki, T -- Ron, D -- Aaronson, S A -- New York, N.Y. -- Science. 1989 Aug 18;245(4919):752-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2475908" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Division ; Codon ; DNA/genetics/isolation & purification ; Epithelial Cells ; Epithelium/analysis/metabolism ; Fibroblast Growth Factor 10 ; Fibroblast Growth Factor 7 ; *Fibroblast Growth Factors/genetics ; Fibroblasts/metabolism ; Gene Expression Regulation ; Growth Substances/*genetics/physiology ; Humans ; Mesoderm/metabolism ; Mice ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Oligonucleotide Probes ; RNA/analysis ; Sequence Homology, Nucleic Acid ; Skin/analysis ; Tissue Distribution ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 10
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    Gene signals relapse of breast, ovarian cancers (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-05-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1989 May 12;244(4905):654-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2566202" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics/pathology ; Female ; *Gene Amplification ; Gene Expression Regulation ; Humans ; Lymph Nodes/pathology ; *Neoplasm Recurrence, Local ; Ovarian Neoplasms/*genetics ; Prognosis ; Proto-Oncogene Proteins/*genetics ; *Proto-Oncogenes ; Receptor, ErbB-2
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Brain protein yields clues to Alzheimer's disease (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-03-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1989 Mar 31;243(4899):1664-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2494699" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*etiology/genetics/pathology ; *Amyloid/genetics/physiology ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Gene Expression Regulation ; Humans ; Interleukin-1/physiology ; Nerve Growth Factors/physiology ; Neurons/pathology ; Protease Inhibitors ; *Protein Precursors/genetics/physiology
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  • 12
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    Transformation and plasmacytoid differentiation of EBV-infected human B lymphoblasts by ras oncogenes (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-02-03
    Description: The biological effects of ras oncogene activation in B cells were studied by using amphotropic retroviral vectors to introduce H- or N-ras oncogenes into human B lymphoblasts immortalized by Epstein-Barr virus. Expression of both H- and N-ras oncogenes led to malignant transformation of these cells, as shown by clonogenicity in semisolid media and tumorigenicity in immunodeficient mice. In addition, terminal differentiation into plasma cells was detectable as specific changes in morphology, immunoglobulin secretion, and cell surface antigen expression. This combined effect, promoting growth and differentiation in human lymphoblasts, represents a novel biological action of ras oncogenes and has implications for the pathogenesis of terminally differentiated B-lymphoid malignancies such as multiple myeloma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seremetis, S -- Inghirami, G -- Ferrero, D -- Newcomb, E W -- Knowles, D M -- Dotto, G P -- Dalla-Favera, R -- CA-37165/CA/NCI NIH HHS/ -- CA49236/CA/NCI NIH HHS/ -- EY 06337/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1989 Feb 3;243(4891):660-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, New York University, NY 10016.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2536954" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/metabolism/*pathology ; Cell Differentiation ; *Cell Transformation, Neoplastic ; *Cell Transformation, Viral ; DNA Replication ; Flow Cytometry ; Fluorescent Antibody Technique ; Gene Expression Regulation ; *Genes, ras ; *Herpesvirus 4, Human ; Humans ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplasms, Experimental/etiology ; Phenotype ; Plasma Cells/*pathology
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  • 13
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    Parasitic protozoa and helminths: biological and immunological challenges (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-11-24
    Description: Parasitic protozoans and helminths pose considerable medical as well as scientific challenges. Investigations of the complex and very different life cycles of these organisms, their adaptation to the obligate parasitic mode of life, and their ability to face the hostile host environment have resulted in many exciting discoveries. Invasion of host erythrocytes by plasmodial sporozoites and intact skin by schistosomal cercariae are outlined as examples of the elaborate mechanisms of parasitism. Isolation and characterization of single protective antigens or subunit vaccines from these two organisms are examined as models for vaccine development. Finally, developments in exploring gene regulation in protozoans and free and parasitic nematodes are briefly outlined.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mahmoud, A A -- New York, N.Y. -- Science. 1989 Nov 24;246(4933):1015-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH 44106.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2686024" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Eukaryota/genetics/pathogenicity/*physiology ; Gene Expression Regulation ; Helminthiasis/*immunology ; Helminths/genetics/pathogenicity/*physiology ; Humans ; Molecular Sequence Data ; Protozoan Infections/*immunology
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  • 14
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    Metastatic hibernomas in transgenic mice expressing an alpha-amylase-SV40 T antigen hybrid gene (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-04-28
    Description: Mice transgenic for a hybrid gene containing the liver promoter of the mouse amylase gene (Amy-1a) fused to the SV40 tumor antigen coding region unexpected developed malignant brown adipose tissue tumors (malignant hibernomas). Expression of the alpha-amylase gene had previously been thought to be confined to the liver parotid, and pancreas; however, analysis of white and brown adipose tissue from nontransgenic mice revealed expression of the endogenous Amy-1a gene in these tissues. Gene constructs driven by the Amy-1a liver promoter thus provide a means of targeting gene expression to the adipocyte cell lineage in transgenic mice. Moreover the high frequency of metastases in the liver, lungs, spleen, heart, and adrenals of these mice provides an experimental system in which to study the development of disseminated malignancy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fox, N -- Crooke, R -- Hwang, L H -- Schibler, U -- Knowles, B B -- Solter, D -- CA-10815/CA/NCI NIH HHS/ -- CA-18470/CA/NCI NIH HHS/ -- CA-21124/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Apr 28;244(4903):460-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute, Philadelphia, PA 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2785714" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism/pathology ; *Adipose Tissue, Brown/metabolism/pathology ; Animals ; Antigens, Polyomavirus Transforming/*genetics ; Cloning, Molecular ; Gene Expression Regulation ; Liver/metabolism ; Mice ; Mice, Transgenic ; Neoplasm Metastasis ; Neoplasms, Experimental/*genetics/pathology ; Nucleic Acid Hybridization ; Promoter Regions, Genetic ; RNA, Messenger/metabolism ; Tissue Distribution ; Transcription, Genetic ; alpha-Amylases/*genetics
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  • 15
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    Interferon-alpha but not AZT suppresses HIV expression in chronically infected cell lines (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-05-05
    Description: Promonocytic (U1) and T lymphocytic (ACH-2) cell lines chronically infected with human immunodeficiency virus type 1 (HIV-1) constitutively express low levels of virus, but expression can be induced by phorbol esters and cytokines. Whereas ACH-2 cells produce infectious virions, U1 cells produce defective, noninfectious particles. Although 3'-azido-3'-deoxythimidine (AZT) prevented acute HIV infection of susceptible cells, it did not prevent the induction of HIV expression in the infected cell lines. In contrast, interferon alpha (IFN-alpha) inhibited the release of reverse transcriptase and viral antigens into the culture supernatant after phorbol ester stimulation of both cell lines. Further, IFN-alpha suppressed the production or release (or both) of whole HIV virions, but had no effect on the amount of cell-associated viral proteins. Also, after phorbol ester stimulation of ACH-2 cells, IFN-alpha reduced the number of infectious viral particles secreted into the culture supernatant, but had no effect on the infectivity of cell-associated virus. These findings lend support to the combined use of antiviral agents that have action at both the early (AZT) and the late (IFN-alpha) stages of HIV replication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Poli, G -- Orenstein, J M -- Kinter, A -- Folks, T M -- Fauci, A S -- New York, N.Y. -- Science. 1989 May 5;244(4904):575-7.〈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/2470148" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/therapy ; Cell Line ; Cell Membrane/microbiology ; Drug Therapy, Combination ; Gene Expression Regulation ; HIV-1/drug effects/*physiology/ultrastructure ; Immunoblotting ; Interferon Type I/administration & dosage/*pharmacology ; Microscopy, Electron ; Monocytes/microbiology ; RNA-Directed DNA Polymerase/metabolism ; Recombinant Proteins ; T-Lymphocytes/microbiology ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription, Genetic ; Vacuoles/microbiology ; Virion/drug effects/physiology/ultrastructure ; Virus Replication/*drug effects ; Zidovudine/administration & dosage/*pharmacology
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  • 16
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    Transfer of a protein encoded by a single nucleus to nearby nuclei in multinucleated myotubes (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-06-02
    Description: Specialized regions of muscle fibers may result from differential gene expression within a single fiber. In order to investigate the range of action of individual nuclei in multinucleated myotubes, C2 myoblasts were transfected to obtain stable cell lines that express a reporter protein that is targeted to the nucleus. Hybrid myotubes were then formed containing one or a few transfected nuclei as well as a large number of nuclei from the parental strain. In order to determine how far the products of a single nucleus extend, transfected nuclei were labeled with [3H]thymidine before fusion and the myotubes were stained to identify the reporter protein. In such myotubes the fusion protein was not confined to its nucleus of origin, but was restricted to nearby nuclei.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ralston, E -- Hall, Z W -- NS 20107/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 2;244(4908):1066-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, School of Medicine, University of California, San Francisco 94143-0444.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2543074" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Nucleus/*metabolism ; Cloning, Molecular ; Cytoplasm/metabolism ; Enhancer Elements, Genetic ; Escherichia coli/genetics ; Fluorescent Antibody Technique ; Gene Expression Regulation ; Globins/genetics ; Mice ; Muscle Proteins/*genetics/metabolism ; Muscles/*ultrastructure ; Plasmids ; Promoter Regions, Genetic ; Receptors, Glucocorticoid/genetics ; Simian virus 40/genetics ; *Transfection ; beta-Galactosidase/genetics
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  • 17
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    Adipsin and complement factor D activity: an immune-related defect in obesity (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-06-23
    Description: Adipsin is a serine protease that is secreted by adipocytes into the bloodstream; it is deficient in several animal models of obesity, representing a striking example of defective gene expression in this disorder. Recombinant mouse adipsin was purified and its biochemical and enzymatic properties were studied in order to elucidate the function of this protein. Activated adipsin has little or no proteolytic activity toward most substrates but has the same activity as human complement factor D, cleaving complement factor B when it is complexed with activated complement component C3. Like authentic factor D, adipsin can activate the alternative pathway of complement, resulting in red blood cell lysis. Decreased (58 to 80 percent) complement factor D activity, relative to lean controls, was observed as a common feature of several experimental models of obesity, including the ob/ob, db/db, and monosodium glutamate (MSG)-injected mouse and the fa/fa rat. These results suggest that adipsin and the alternative pathway of complement may play an unexpected but important role in the regulation of systemic energy balance in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosen, B S -- Cook, K S -- Yaglom, J -- Groves, D L -- Volanakis, J E -- Damm, D -- White, T -- Spiegelman, B M -- DK31403/DK/NIDDK NIH HHS/ -- DK34605/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 23;244(4911):1483-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2734615" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Amino Acid Sequence ; Animals ; Cell Line ; Complement Activating Enzymes/*metabolism ; Complement Factor D/*metabolism ; Complement Pathway, Alternative ; Cricetinae ; DNA/genetics ; Gene Expression Regulation ; Humans ; Immunoblotting ; Mice ; Molecular Sequence Data ; Obesity/genetics/*immunology/metabolism ; RNA, Messenger/metabolism ; Recombinant Proteins ; Serine Endopeptidases/genetics/isolation & purification/*metabolism ; Substrate Specificity ; Transfection
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  • 18
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    Reciprocal effects of hyper- and hypoactivity mutations in the Drosophila pattern gene torso (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-02-24
    Description: In Drosophila, five "terminal" polarity genes must be active in females in order for them to produce embryos with normal anterior and posterior ends. Hypoactivity mutations in one such gene, torso, result in the loss of the most posterior domain of fushi tarazu expression and the terminal cuticular structures. In contrast, a torso hyperactivity mutation causes the loss of central fushi tarazu expression and central cuticular structures. Cytoplasmic leakage, transplantation, and temperature-shift experiments suggest that the latter effect is caused by abnormal persistence of the torso product in the central region of the embryo during early development. Thus, the amount and timing of torso activity is key to distinguishing the central and terminal regions of the embryo. Mutations in the tailless terminal gene act as dominant maternal suppressors of the hyperactive torso allele, indicating that the torso product acts through, or in concert with, the tailless product.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strecker, T R -- Halsell, S R -- Fisher, W W -- Lipshitz, H D -- GM07616/GM/NIGMS NIH HHS/ -- HD23099/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1989 Feb 24;243(4894 Pt 1):1062-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2922596" target="_blank"〉PubMed〈/a〉
    Keywords: Abdomen ; Alleles ; Animals ; Cytoplasm/physiology ; Drosophila/anatomy & histology/embryology/*genetics ; Female ; Gene Expression Regulation ; Mutation ; Phenotype ; Suppression, Genetic ; Thorax
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  • 19
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    Developmental biology of T cell receptors (1989)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1989-05-26
    Description: T cell receptors are the antigen-recognizing elements found on the effector cells of the immune system. Two isotypes have been discovered, TCR-gamma delta and TCR-alpha beta, which appear in that order during ontogeny. The maturation of prothymocytes that colonize the thymic rudiment at defined gestational stages occurs principally within the thymus, although some evidence for extrathymic maturation also exists. The maturation process includes the rearrangement and expression of the T cell receptor genes. Determination of these mechanisms, the lineages of the cells, and the subsequent thymic selection that results in self-tolerance is the central problem in developmental immunology and is important for the understanding of autoimmune diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strominger, J L -- New York, N.Y. -- Science. 1989 May 26;244(4907):943-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, MA 02138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2658058" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Differentiation, T-Lymphocyte/analysis ; Gene Expression Regulation ; Humans ; Receptors, Antigen, T-Cell/genetics/immunology/*physiology ; T-Lymphocytes/*immunology ; Thymus Gland/embryology/*growth & development/immunology
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  • 20
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    Progress toward human gene therapy (1989)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1989-06-16
    Description: Current therapies for most human genetic diseases are inadequate. In response to the need for effective treatments, modern molecular genetics is providing tools for an unprecedented new approach to disease treatment through an attack directly on mutant genes. Recent results with several target organs and gene transfer techniques have led to broad medical and scientific acceptance of the feasibility of this "gene therapy" concept for disorders of the bone marrow, liver, and central nervous system; some kinds of cancer; and deficiencies of circulating enzymes, hormones, and coagulation factors. The most well-developed models involve alteration of mutant target genes by gene transfer with recombinant pathogenic viruses in order to express new genetic information and to correct disease phenotypes--the conversion of the swords of pathology into the plowshares of therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Friedmann, T -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1275-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, School 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/2660259" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/physiology ; Brain/physiology ; Ethics, Medical ; Gene Expression Regulation ; Genetic Diseases, Inborn ; Genetic Therapy/*methods/trends ; Genetic Vectors ; Humans ; Liver/physiology ; Neoplasms/genetics ; Risk Assessment ; Transfection
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  • 21
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    Interleukin-2 receptor beta chain gene: generation of three receptor forms by cloned human alpha and beta chain cDNA's (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-05-05
    Description: Interleukin-2 (IL-2) binds to two distinct receptor molecules, the IL-2 receptor alpha (IL-2R alpha, p55) chain and the newly identified IL-2 receptor beta (IL-2R beta, p70-75) chain. The cDNA encoding the human IL-2R beta chain has now been isolated. The overall primary structure of the IL-2R beta chain shows no apparent homology to other known receptors. Unlike the IL-2R alpha chain, the IL-2R beta chain has a large cytoplasmic region in which a functional domain (or domains) mediating an intracellular signal transduction pathway (or pathways) may be embodied. The cDNA-encoded beta chain binds and internalizes IL-2 when expressed on T lymphoid cells but not fibroblast cells. Furthermore, the cDNA gives rise to the generation of high-affinity IL-2 receptor when co-expressed with the IL-2R alpha chain cDNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hatakeyama, M -- Tsudo, M -- Minamoto, S -- Kono, T -- Doi, T -- Miyata, T -- Miyasaka, M -- Taniguchi, T -- New York, N.Y. -- Science. 1989 May 5;244(4904):551-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular and Cellular Biology, Osaka University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2785715" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; *Cloning, Molecular ; Cross-Linking Reagents ; DNA/*genetics/isolation & purification ; Fibroblasts/metabolism ; Gene Expression Regulation ; Humans ; Interleukin-2/metabolism ; Leukemia ; Molecular Sequence Data ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Receptors, Interleukin-2/*genetics/metabolism ; Recombinant Proteins ; Sequence Homology, Nucleic Acid ; Signal Transduction ; Succinimides ; T-Lymphocytes/metabolism ; Transfection ; Tumor Cells, Cultured
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  • 22
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    Isolation of a novel receptor cDNA establishes the existence of two PDGF receptor genes (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-02-10
    Description: A genomic sequence and cloned complementary DNA has been identified for a novel receptor-like gene of the PDGF receptor/CSF1 receptor subfamily (platelet-derived growth factor receptor/colony-stimulating factor type 1 receptor). The gene recognized a 6.4-kilobase transcript that was coexpressed in normal human tissues with the 5.3-kilobase PDGF receptor messenger RNA. Introduction of complementary DNA of the novel gene into COS-1 cells led to expression of proteins that were specifically detected with antiserum directed against a predicted peptide. When the new gene was transfected into COS-1 cells, a characteristic pattern of binding of the PDGF isoforms was observed, which was different from the pattern observed with the known PDGF receptor. Tyrosine phosphorylation of the receptor in response to the PDGF isoforms was also different from the known receptor. The new PDGF receptor gene was localized to chromosome 4q11-4q12. The existence of genes encoding two PDGF receptors that interact in a distinct manner with three different PDGF isoforms likely confers considerable regulatory flexibility in the functional responses to PDGF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsui, T -- Heidaran, M -- Miki, T -- Popescu, N -- La Rochelle, W -- Kraus, M -- Pierce, J -- Aaronson, S -- New York, N.Y. -- Science. 1989 Feb 10;243(4892):800-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2536956" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cells, Cultured ; *Chromosomes, Human, Pair 4 ; Cloning, Molecular ; DNA/genetics ; Gene Expression Regulation ; *Genes ; Humans ; Molecular Sequence Data ; Multigene Family ; Platelet-Derived Growth Factor/*physiology ; Protein-Tyrosine Kinases/genetics ; RNA, Messenger/genetics ; Receptors, Cell Surface/*genetics ; Receptors, Platelet-Derived Growth Factor ; Tissue Distribution
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  • 23
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    Transcriptional regulation in mammalian cells by sequence-specific DNA binding proteins (1989)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1989-07-28
    Description: The cloning of genes encoding mammalian DNA binding transcription factors for RNA polymerase II has provided the opportunity to analyze the structure and function of these proteins. This review summarizes recent studies that define structural domains for DNA binding and transcriptional activation functions in sequence-specific transcription factors. The mechanisms by which these factors may activate transcriptional initiation and by which they may be regulated to achieve differential gene expression are also discussed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mitchell, P J -- Tjian, R -- New York, N.Y. -- Science. 1989 Jul 28;245(4916):371-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2667136" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; Cloning, Molecular ; DNA-Binding Proteins/*genetics/metabolism ; Gene Expression Regulation ; Molecular Sequence Data ; Protein Processing, Post-Translational ; RNA Polymerase II/*genetics/metabolism ; Repetitive Sequences, Nucleic Acid ; Transcription Factors/*genetics/metabolism ; *Transcription, Genetic
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  • 24
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    Interleukin-1 costimulatory activity on the interleukin-2 promoter via AP-1 (1989)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1989-10-13
    Description: Interleukin-1 (IL-1) is a major regulator of inflammation and immunity. IL-1 induces T lymphocyte growth by acting as a second signal (together with antigen) in enhancing the production of interleukin-2 (IL-2). An IL-1-responsive element in the promoter region of the human IL-2 gene was similar to the binding site for the transcription factor AP-1. IL-1 enhanced expression of c-jun messenger RNA, whereas the antigenic signal enhanced messenger RNA expression of c-fos. Thus, the two components of the AP-1 factor are independently regulated and the AP-1 factor may serve as a nuclear mediator for the many actions of IL-1 on cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muegge, K -- Williams, T M -- Kant, J -- Karin, M -- Chiu, R -- Schmidt, A -- Siebenlist, U -- Young, H A -- Durum, S K -- 5-T32-CA-09140/CA/NCI NIH HHS/ -- AI-R01-23879/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Oct 13;246(4927):249-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunoregulation, Program Resources Inc., Frederick, MD 21701.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2799385" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chloramphenicol O-Acetyltransferase/genetics ; Gene Expression Regulation ; Humans ; Interleukin-1/*physiology ; Interleukin-2/*genetics ; Mice ; Promoter Regions, Genetic/genetics ; Proto-Oncogene Proteins c-jun/*genetics ; Tetradecanoylphorbol Acetate/pharmacology ; Transfection ; Tumor Cells, Cultured
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  • 25
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    Enhancement of bacteriophage T4 late transcription by components of the T4 DNA replication apparatus (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-09-01
    Description: The expression of the late genes in bacteriophage T4 development is closely connected to viral DNA replication. Three T4-encoded DNA polymerase accessory proteins are shown to stimulate transcription at T4 late promoters in an adenosine triphosphate (ATP) hydrolysis-requiring process. The properties of the activation resemble those found for enhancers of eukaryotic transcription. However, the nature of the enhancer of T4 late transcription is novel in that it is a structure--a break in the nontranscribed DNA stand--to which the three replication proteins bind, rather than a sequence. Since the three DNA polymerase accessory proteins are carried on the moving replication fork as part of the replisome, we postulate that viral DNA replication forks act, in vivo, as the mobile enhancers of T4 late gene transcription. Whereas Escherichia coli RNA polymerase bearing the T4 gene 55 protein can selectively recognize T4 late promoters, it is only capable of responding to the transcription-enhancing activity of the three replication proteins on acquiring an additional T4-specific modification.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herendeen, D R -- Kassavetis, G A -- Barry, J -- Alberts, B M -- Geiduschek, E P -- New York, N.Y. -- Science. 1989 Sep 1;245(4921):952-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Center for Molecular Genetics, 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/2672335" target="_blank"〉PubMed〈/a〉
    Keywords: *DNA Replication ; DNA, Viral/*genetics ; DNA-Directed DNA Polymerase/metabolism ; DNA-Directed RNA Polymerases/metabolism ; *Enhancer Elements, Genetic ; Escherichia coli/*genetics ; Gene Expression Regulation ; *Genes, Viral ; Plasmids ; Promoter Regions, Genetic ; T-Phages/*genetics ; *Transcription, Genetic
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  • 26
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    Sindbis virus: an efficient, broad host range vector for gene expression in animal cells (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-03-03
    Description: Sindbis virus, an enveloped virus with a single-stranded RNA genome, was engineered to express a bacterial protein, chloramphenicol acetyltransferase (CAT), in cultured insect, avian, and mammalian cells. The vectors were self-replicating and gene expression was efficient and rapid; up to 10(8) CAT polypeptides were produced per infected cell in 16 to 20 hours. CAT expression could be made temperature-sensitive by means of a derivative that incorporated a temperature-sensitive mutation in viral RNA synthesis. Vector genomic RNAs were packaged into infectious particles when Sindbis helper virus was used to supply virion structural proteins. The vector RNAs were stable to at least seven cycles of infection. The expression of CAT increased about 10(3)-fold, despite a 10(15)-fold dilution during the passaging. Sindbis virus vectors should prove useful for expressing large quantities of gene products in a variety of animal cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiong, C -- Levis, R -- Shen, P -- Schlesinger, S -- Rice, C M -- Huang, H V -- AG05681/AG/NIA NIH HHS/ -- AI11377/AI/NIAID NIH HHS/ -- AI24134/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Mar 3;243(4895):1188-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, 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/2922607" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes ; Animals ; Bacteria/enzymology ; Cells, Cultured ; Chick Embryo ; Chloramphenicol O-Acetyltransferase/*genetics ; Codon ; Cricetinae ; DNA/genetics ; Drosophila ; Gene Amplification ; Gene Expression Regulation ; *Genetic Engineering ; *Genetic Vectors ; Humans ; Quail ; RNA, Viral/*genetics ; Sindbis Virus/*genetics ; Transcription, Genetic ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 27
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    Studies of the HER-2/neu proto-oncogene in human breast and ovarian cancer (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-05-12
    Description: Carcinoma of the breast and ovary account for one-third of all cancers occurring in women and together are responsible for approximately one-quarter of cancer-related deaths in females. The HER-2/neu proto-oncogene is amplified in 25 to 30 percent of human primary breast cancers and this alteration is associated with disease behavior. In this report, several similarities were found in the biology of HER-2/neu in breast and ovarian cancer, including a similar incidence of amplification, a direct correlation between amplification and over-expression, evidence of tumors in which overexpression occurs without amplification, and the association between gene alteration and clinical outcome. A comprehensive study of the gene and its products (RNA and protein) was simultaneously performed on a large number of both tumor types. This analysis identified several potential shortcomings of the various methods used to evaluate HER-2/neu in these diseases (Southern, Northern, and Western blots, and immunohistochemistry) and provided information regarding considerations that should be addressed when studying a gene or gene product in human tissue. The data presented further support the concept that the HER-2/neu gene may be involved in the pathogenesis of some human cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slamon, D J -- Godolphin, W -- Jones, L A -- Holt, J A -- Wong, S G -- Keith, D E -- Levin, W J -- Stuart, S G -- Udove, J -- Ullrich, A -- CA 36827/CA/NCI NIH HHS/ -- CA 48780/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1989 May 12;244(4905):707-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, U.C.L.A. School of Medicine 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2470152" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers, Tumor ; Breast Neoplasms/*genetics ; Cloning, Molecular ; DNA/analysis ; Female ; Gene Amplification ; Gene Expression Regulation ; Humans ; Immunohistochemistry ; Nucleic Acid Hybridization ; Ovarian Neoplasms/*genetics ; Prognosis ; Protein Kinases ; Proto-Oncogene Proteins/*genetics ; *Proto-Oncogenes ; RNA/analysis ; Receptor, ErbB-2
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  • 28
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    Leucine repeats and an adjacent DNA binding domain mediate the formation of functional cFos-cJun heterodimers (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-03-31
    Description: The discovery that the AP-1 family of enhancer binding factors includes a complex of the cellular Fos (cFos) and cellular Jun (cJun) proteins established a direct and important link between oncogenesis and transcriptional regulation. Homodimeric cJun protein synthesized in vitro is capable of binding selectively to AP-1 recognition sites, whereas the cFos polypeptide is not. When cotranslated, the cFos and cJun proteins can form a stable, heterodimeric complex with the DNA binding properties of AP-1/cJun. The related proteins Jun B and vJun are also able to form DNA binding complexes with cFos. Directed mutagenesis of the cFos protein reveals that a leucine repeat structure is required for binding to cJun, in a manner consistent with the proposed function of the "leucine zipper." A novel domain adjacent to, but distinct from, the leucine repeat of cFos is required for DNA binding by cFos-cJun heterodimers. Thus experimental evidence is presented that leucine repeats can mediate complex formation between heterologous proteins and that promotes further understanding of the molecular mechanisms underlying the function of two proto-oncogene products.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turner, R -- Tjian, R -- New York, N.Y. -- Science. 1989 Mar 31;243(4899):1689-94.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2494701" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Chromatography, Affinity ; DNA/*metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Gene Expression Regulation ; Humans ; *Leucine ; Macromolecular Substances ; Molecular Sequence Data ; Mutation ; Oncogenes ; Protein Biosynthesis ; Proto-Oncogene Proteins/genetics/*metabolism ; Proto-Oncogene Proteins c-fos ; Proto-Oncogene Proteins c-jun ; Rats ; Repetitive Sequences, Nucleic Acid ; Structure-Activity Relationship ; Transcription Factors/genetics/*metabolism
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  • 29
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    Neurotoxicity of a fragment of the amyloid precursor associated with Alzheimer's disease (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-07-28
    Description: Amyloid deposition in senile plaques and the cerebral vasculature is a marker of Alzheimer's disease. Whether amyloid itself contributes to the neurodegenerative process or is simply a by-product of that process is unknown. Pheochromocytoma (PC12) and fibroblast (NIH 3T3) cell lines were transfected with portions of the gene for the human amyloid precursor protein. Stable PC12 cell transfectants expressing a specific amyloid-containing fragment of the precursor protein gradually degenerated when induced to differentiate into neuronal cells with nerve growth factor. Conditioned medium from these cells was toxic to neurons in primary hippocampal cultures, and the toxic agent could be removed by immunoabsorption with an antibody directed against the amyloid polypeptide. Thus, a peptide derived from the amyloid precursor may be neurotoxic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yankner, B A -- Dawes, L R -- Fisher, S -- Villa-Komaroff, L -- Oster-Granite, M L -- Neve, R L -- HD 18655/HD/NICHD NIH HHS/ -- HD 18658/HD/NICHD NIH HHS/ -- NS 01240/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Jul 28;245(4916):417-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Harvard Medical School, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2474201" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*etiology/pathology ; Amyloid/genetics/*physiology ; Blotting, Northern ; Cell Line ; Fibroblasts ; Gene Expression Regulation ; Humans ; Immunoblotting ; Neurons/pathology ; Nucleic Acid Hybridization ; Pheochromocytoma ; Protein Precursors/genetics/*physiology ; RNA/analysis/genetics ; Restriction Mapping ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 30
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    Mechanism of interleukin-2 signaling: mediation of different outcomes by a single receptor and transduction pathway (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-02-10
    Description: The T cell lymphokine, interleukin-2 (IL-2), plays a pivotal role in an immune response by stimulating antigen-activated B lymphocytes to progress through the cell cycle and to differentiate into antibody-secreting cells. An IL-2 inducible B lymphoma line, in which the growth and differentiation responses are uncoupled, provides a model system for dissecting the signaling mechanisms operating in each response. This system was used to show that both signals are initiated by IL-2 binding to a single, unifunctional receptor complex. Moreover, both signals are transduced by a pathway that does not involve any known second messenger system and that can be blocked by a second T cell lymphokine, interleukin 4. These findings suggest that the pleiotrophic effects of IL-2 are determined by different translations of the signal in the nucleus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tigges, M A -- Casey, L S -- Koshland, M E -- AI07079/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Feb 10;243(4892):781-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chiron Corporation, Emeryville, CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2492678" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody Formation ; B-Lymphocytes/*physiology ; Calcium/physiology ; Gene Expression Regulation ; Immunoglobulin J-Chains/genetics ; Interleukin-2/*physiology ; Interleukin-4 ; Interleukins/pharmacology ; Lymphocyte Activation ; Mice ; Protein Kinase C/physiology ; Receptors, Interleukin-2/*physiology ; Tumor Cells, Cultured
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  • 31
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    Genetic engineering of filamentous fungi (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-06-16
    Description: Filamentous fungi are important in medicine, industry, agriculture, and basic biological research. For example, some fungal species are pathogenic to humans, whereas others produce beta-lactam antibiotics (penicillin and cephalosporin). Industrial strains produce large amounts of enzymes, such as glucoamylase and proteases, and low molecular weight compounds, such as citric acid. The largest and most economically important group of plant pathogens are fungi. Several fungal species have biological properties and genetic systems that make them ideally suited for basic biological research. Recently developed techniques for genetic engineering of filamentous fungi make it possible to alter their detrimental and beneficial activities in novel ways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Timberlake, W E -- Marshall, M A -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1313-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, University of Georgia, Athens 30602.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2525275" target="_blank"〉PubMed〈/a〉
    Keywords: Aspergillus nidulans/*genetics ; Forecasting ; Gene Expression Regulation ; Genetic Engineering/*methods/trends ; Mutation ; Neurospora/*genetics ; Neurospora crassa/*genetics ; Transformation, Genetic
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    Signal transduction by the platelet-derived growth factor receptor (1989)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1989-03-24
    Description: When platelet-derived growth factor (PDGF) binds to its receptor on a quiescent fibroblast or smooth muscle cell, it stimulates a remarkably diverse group of biochemical responses, including changes in ion fluxes, activation of several kinases, alterations in cell shape, increased transcription of a number of genes, and stimulation of enzymes that regulate phospholipid metabolism. These and other reactions culminate, hours later, in DNA replication and cell division. How does the receptor for PDGF recognize and bind its specific ligand and then transduce this signal across the cell membrane via a single membrane-spanning region? Which of the immediate cellular responses are directly involved in the biochemical pathways that lead to DNA synthesis? How does the PDGF receptor trigger a diverse group of responses? Recent studies of the PDGF receptor have provided insight into these issues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, L T -- HL-32898/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Mar 24;243(4898):1564-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California, San Francisco 94143-0724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2538922" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Gene Expression Regulation ; Humans ; Membrane Proteins/physiology/ultrastructure ; Molecular Structure ; Platelet-Derived Growth Factor/*physiology ; Protein-Tyrosine Kinases/physiology ; Receptors, Cell Surface/*physiology/ultrastructure ; Receptors, Platelet-Derived Growth Factor
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  • 33
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    Purification of growth hormone-specific transcription factor GHF-1 containing homeobox (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-02-10
    Description: Pituitary-specific expression of the growth hormone (GH) gene is governed by a transcription factor, GHF-1, that binds to two sites within its promoter. Recently, GHF-1 was shown to be a member of the homeobox family of DNA-binding proteins. An important question is whether GHF-1 controls the expression of other pituitary specific genes, such as prolactin (Prl), expressed in closely related cell types. To this end, GHF-1 was purified from extracts of GH- and Prl-expressing pituitary tumor cells and identified as a 33-kilodalton polypeptide. Although GHF-1 bound to and activated the GH promoter, it did not recognize the Prl promoter. However, at least one other factor in the same extracts, which was easily separated from GHF-1, bound to several sites within the Prl but not the GH promoter. Antibodies to GHF-1 did not react with the Prl binding activity. These results imply that the pituitary-specific expression of GH and Prl is governed by two distinct trans-acting factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Castrillo, J L -- Bodner, M -- Karin, M -- DK-38527/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1989 Feb 10;243(4892):814-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School 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/2563596" target="_blank"〉PubMed〈/a〉
    Keywords: DNA-Binding Proteins/*genetics ; Gene Expression Regulation ; *Genes, Homeobox ; Growth Hormone/*genetics ; Humans ; Molecular Weight ; Peptide Mapping ; Pituitary Gland/physiology ; Prolactin/genetics ; Promoter Regions, Genetic ; Transcription Factors/*genetics ; Tumor Cells, Cultured
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    The story so far--chronology, dramatis personae (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-04-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culliton, B J -- New York, N.Y. -- Science. 1989 Apr 28;244(4903):413.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2655080" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Fraud/legislation & jurisprudence ; Gene Expression Regulation ; Genes, Immunoglobulin ; History, 20th Century ; Mice ; Mice, Transgenic ; Publishing/*standards ; Research/*standards ; Research Personnel ; United States
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  • 35
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    Cloning and expression of a Xenopus embryonic gap junction protein (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-03-03
    Description: Gap junctions in the early amphibian embryo may play a fundamental role in the regulation of differentiation by mediating the cell-to-cell transfer of chemical signals. A complementary DNA encoding a gap junction present in Xenopus oocytes and early embryos has now been cloned and sequenced. This protein sequence is homologous to the well-characterized gap junction structural proteins rat connexin32 and connexin43. RNA blot analysis of total Xenopus oocyte RNA showed hybridization to a single 1.6-kilobase band. This messenger RNA is abundant in oocytes, decreases to levels below the sensitivity of our assay by stage 15 (18 hours), and is not detectable in RNA from a number of adult organs. To confirm that the oocyte cDNA encodes a gap junction channel, the protein was over expressed in Xenopus oocytes by injection of RNA synthesized in vitro. Pairs of RNA-injected oocytes formed many more time- and voltage-sensitive cell-cell channels than water-injected pairs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ebihara, L -- Beyer, E C -- Swenson, K I -- Paul, D L -- Goodenough, D A -- GM18974/GM/NIGMS NIH HHS/ -- GM37751/GM/NIGMS NIH HHS/ -- HL28958-06/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Mar 3;243(4895):1194-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2466337" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Communication ; *Cloning, Molecular ; Connexins ; DNA Probes ; Electric Conductivity ; Female ; Gene Expression Regulation ; Intercellular Junctions/physiology ; Membrane Proteins/*genetics/physiology ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Oocytes/analysis/physiology ; RNA/analysis ; RNA, Messenger/analysis ; Rats ; Tissue Distribution ; Xenopus/*embryology
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  • 36
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    Limbic seizures increase neuronal production of messenger RNA for nerve growth factor (1989)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1989-08-18
    Description: Nerve growth factor (NGF) produced by telencephalic neurons provides critical trophic support for cholinergic neurons of the basal forebrain. In situ hybridization and nuclease protection analyses demonstrate that limbic seizures dramatically increase the amount of messenger RNA for NGF in the neurons of the hippocampal dentate gyrus within 1 hour of seizure onset and in broadly distributed neocortical and olfactory forebrain neurons some hours later. The increased messenger RNA species is indistinguishable from messenger RNA for transcript B of the beta subunit of NGF from mouse submandibular gland. Thus, the expression of a known growth factor is affected by unusual physiological activity, suggesting one route through which trophic interactions between neurons in adult brain can be modified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gall, C M -- Isackson, P J -- NS00915/NS/NINDS NIH HHS/ -- NS24747/NS/NINDS NIH HHS/ -- NS26748/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1989 Aug 18;245(4919):758-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, University of California, Irvine 92717.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2549634" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoradiography ; Endonucleases ; Gene Expression Regulation ; Guinea Pigs ; Hippocampus/physiopathology ; Limbic System/*physiopathology ; Mice ; Nerve Growth Factors/*genetics ; Neurons/*metabolism ; Nucleic Acid Hybridization ; RNA Probes ; RNA, Messenger/*biosynthesis ; Rats ; Seizures/*metabolism ; Single-Strand Specific DNA and RNA Endonucleases ; Telencephalon/metabolism ; Tissue Distribution
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  • 37
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    G1/S transition in normal human T-lymphocytes requires the nuclear protein encoded by c-myb (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-07-14
    Description: Exposure of peripheral blood mononuclear cells (PBMC) to an 18-base c-myb antisense oligomer before mitogen or antigen stimulation resulted in almost complete inhibition of c-myb messenger RNA and protein synthesis and blockade of T lymphocyte proliferation. Expression of early and late activation markers, interleukin-2 receptor and transferrin receptor, respectively, by PBMC was unaffected by antisense oligomer exposure as was the expression of c-myc messenger RNA. In contrast, histone H3 messenger RNA levels and DNA content were selectively decreased. These results suggest that c-myb protein deprivation does not perturb T lymphocyte activation or early molecular events that may prepare the cell for subsequent proliferation. Rather, it appears to specifically block cells in late G1 or early S phase of the cell cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gewirtz, A M -- Anfossi, G -- Venturelli, D -- Valpreda, S -- Sims, R -- Calabretta, B -- CA01324/CA/NCI NIH HHS/ -- CA36896/CA/NCI NIH HHS/ -- CA46782/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1989 Jul 14;245(4914):180-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Temple University School of Medicine, Philadelphia, PA 19140.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2665077" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division/drug effects ; DNA/biosynthesis ; Fluorescent Antibody Technique ; Gene Expression Regulation ; Humans ; Image Processing, Computer-Assisted ; *Interphase ; *Lymphocyte Activation/drug effects ; Oligonucleotides/pharmacology ; Oligonucleotides, Antisense ; Proto-Oncogene Proteins/biosynthesis/*genetics/physiology ; Proto-Oncogene Proteins c-myb ; Proto-Oncogenes ; RNA, Messenger/biosynthesis/*genetics ; Receptors, Interleukin-2/biosynthesis ; Receptors, Transferrin/biosynthesis ; T-Lymphocytes/*cytology/metabolism
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  • 38
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    Endothelial leukocyte adhesion molecule 1: an inducible receptor for neutrophils related to complement regulatory proteins and lectins (1989)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1989-03-03
    Description: Focal adhesion of leukocytes to the blood vessel lining is a key step in inflammation and certain vascular disease processes. Endothelial leukocyte adhesion molecule-1 (ELAM-1), a cell surface glycoprotein expressed by cytokine-activated endothelium, mediates the adhesion of blood neutrophils. A full-length complementary DNA (cDNA) for ELAM-1 has now been isolated by transient expression in COS cells. Cells transfected with the ELAM-1 clone express a surface structure recognized by two ELAM-1 specific monoclonal antibodies (H4/18 and H18/7) and support the adhesion of isolated human neutrophils and the promyelocytic cell line HL-60. Expression of ELAM-1 transcripts in cultured human endothelial cells is induced by cytokines, reaching a maximum at 2 to 4 hours and decaying by 24 hours; cell surface expression of ELAM-1 protein parallels that of the mRNA. The primary sequence of ELAM-1 predicts an amino-terminal lectin-like domain, an EGF domain, and six tandem repetitive motifs (about 60 amino acids each) related to those found in complement regulatory proteins. A similar domain structure is also found in the MEL-14 lymphocyte cell surface homing receptor, and in granule-membrane protein 140, a membrane glycoprotein of platelet and endothelial secretory granules that can be rapidly mobilized (less than 5 minutes) to the cell surface by thrombin and other stimuli. Thus, ELAM-1 may be a member of a nascent gene family of cell surface molecules involved in the regulation of inflammatory and immunological events at the interface of vessel wall and blood.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bevilacqua, M P -- Stengelin, S -- Gimbrone, M A Jr -- Seed, B -- P01 HL-36028/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Mar 3;243(4895):1160-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Brigham and Women's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2466335" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Adhesion ; DNA/genetics ; E-Selectin ; Endothelium, Vascular/metabolism ; Gene Expression Regulation ; Humans ; Immunoassay ; Interleukin-1/pharmacology ; *Membrane Glycoproteins ; Molecular Sequence Data ; Neutrophils/*physiology ; Nucleic Acid Hybridization ; Recombinant Proteins ; Sequence Homology, Nucleic Acid ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/pharmacology
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    Contingent genetic regulatory events in T lymphocyte activation (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-01-20
    Description: Interaction of antigen in the proper histocompatibility context with the T lymphocyte antigen receptor leads to an orderly series of events resulting in morphologic change, proliferation, and the acquisition of immunologic function. In most T lymphocytes two signals are required to initiate this process, one supplied by the antigen receptor and the other by accessory cells or agents that activate protein kinase C. Recently, DNA sequences have been identified that act as response elements for one or the other of the two signals, but do not respond to both signals. The fact that these sequences lie within the control regions of the same genes suggests that signals originating from separate cell membrane receptors are integrated at the level of the responsive gene. The view is put forth that these signals initiate a contingent series of gene activations that bring about proliferation and impart immunologic function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crabtree, G R -- CA 39612/CA/NCI NIH HHS/ -- HL 33942/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Jan 20;243(4889):355-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Stanford University Medical School, CA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2783497" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Expression Regulation ; Humans ; Interleukin-2/genetics ; *Lymphocyte Activation ; Mice ; Oncogenes ; Protein-Tyrosine Kinases/genetics ; T-Lymphocytes/*physiology ; Time Factors
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    Dingell v. Baltimore (1989)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1989-04-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culliton, B J -- New York, N.Y. -- Science. 1989 Apr 28;244(4903):412-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2655079" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biomedical Research ; Federal Government ; Fraud/legislation & jurisprudence ; Gene Expression Regulation ; Genes, Immunoglobulin ; History, 20th Century ; Mice ; Mice, Transgenic ; Publishing/*standards ; Research/*standards ; Research Personnel ; United States
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    Mammalian glucocorticoid receptor derivatives enhance transcription in yeast (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-19
    Description: In mammalian cells, the glucocorticoid receptor binds specifically to glucocorticoid response element (GRE) DNA sequences and enhances transcription from linked promoters. It is shown here that derivatives of the glucocorticoid receptor also enhance transcription when expressed in yeast. Receptor-mediated enhancement in yeast was observed in fusions of GRE sequences to the yeast cytochrome c1 (CYC1) promoter; the CYC1 upstream activator sequences were not essential, since enhancement was observed in fusions of GREs to mutant CYC1 promoters retaining only the TATA region and transcription startpoints. It is concluded that the receptor operates by a common, highly conserved mechanism in yeast and mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schena, M -- Yamamoto, K R -- CA20535-12/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 19;241(4868):965-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3043665" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA/metabolism ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; Immunoassay ; Plasmids ; Promoter Regions, Genetic ; Rats ; Receptors, Glucocorticoid/*genetics ; Saccharomyces cerevisiae/*genetics ; *Transcription, Genetic
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    DNA looping (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-04-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schleif, R -- New York, N.Y. -- Science. 1988 Apr 8;240(4849):127-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Brandeis University, Waltham, Massachusetts 02254.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3353710" target="_blank"〉PubMed〈/a〉
    Keywords: DNA/*genetics ; DNA-Binding Proteins/physiology ; Eukaryotic Cells/physiology ; Gene Expression Regulation ; Nucleic Acid Conformation ; Prokaryotic Cells/physiology ; Regulatory Sequences, Nucleic Acid
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    Cloning of a lymphoid-specific cDNA encoding a protein binding the regulatory octamer DNA motif (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-29
    Description: An octamer DNA sequence plays a critical role in directing transcription of immunoglobulin genes in B lymphocytes. A new technique of direct binding of radioactive DNA was used to screen a complementary DNA expression library from the BJAB cell line in lambda gt11 phage to derive molecular cDNA clones representing a putative B lymphocyte-specific octamer binding protein. The plaques were screened with DNA containing four copies of the octamer sequence and positive phage recombinants were identified. The fusion protein produced on inducing a lysogen of one phage bound to a monomeric octamer probe. The cDNA insert from this phage hybridized to messenger RNA found in B lymphocytes, but not in most other cells. Thus, this cDNA derives from a gene (oct-2) that specifies an octamer binding protein expressed preferentially in B lymphocytes, proving that, for at least one gene, a cell-specific transcription factor exists and its amount is controlled through messenger RNA availability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Staudt, L M -- Clerc, R G -- Singh, H -- LeBowitz, J H -- Sharp, P A -- Baltimore, D -- P01-CA42063/CA/NCI NIH HHS/ -- P30-CAL4051/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):577-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3399892" target="_blank"〉PubMed〈/a〉
    Keywords: Cloning, Molecular ; DNA/genetics ; DNA-Binding Proteins/*physiology ; Gene Expression Regulation ; *Genes ; Humans ; Lymphocytes/*physiology ; *Regulatory Sequences, Nucleic Acid ; Transcription Factors/*physiology
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    The effect of histone gene deletions on chromatin structure in Saccharomyces cerevisiae (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-11-04
    Description: As a way of studying nucleosome assembly and maintenance in Saccharomyces cerevisiae, mutants bearing deletions or duplications of the genes encoding histones H2A and H2B were analyzed. Previous genetic analysis had shown that only one of these mutants exhibited dramatic and pleiotropic phenotypes. This mutant was also the only one that contained disrupted chromatin, suggesting that the original phenotypes were attributable to alterations in chromosome structure. The chromatin disruption in the mutant, however, did not extend over the entire genome, but rather was localized to specific regions. Thus, while the arrangement of nucleosomes over the HIS4 and GAL1 genes, the telomeres, and the long terminal repeats (delta sequences) of Ty retrotransposons appeared essentially normal, nucleosomes over the CYH2 and UBI4 genes and the centromere of chromosome III were dramatically disrupted. The observation that the mutant exhibited localized chromatin disruptions implies that the assembly or maintenance of nucleosomes differs over different parts of the yeast genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Norris, D -- Dunn, B -- Osley, M A -- GM40118/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 4;242(4879):759-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2847314" target="_blank"〉PubMed〈/a〉
    Keywords: Centromere/ultrastructure ; Chromatin/physiology/*ultrastructure ; Chromosome Deletion ; DNA Transposable Elements ; Galactose ; Gene Expression Regulation ; Genes, Fungal ; Histidine ; Histones/*genetics ; Mutation ; Phenotype ; RNA, Messenger/genetics ; Repetitive Sequences, Nucleic Acid ; Saccharomyces cerevisiae/genetics/*ultrastructure ; Transcription, Genetic
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    A transcriptional enhancer 3' of C beta 2 in the T cell receptor beta locus (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-07-08
    Description: Run-on transcription experiments were used to demonstrate that transcription of T cell receptor beta chain V genes is activated by DNA rearrangement, in a manner similar to immunoglobulin genes. A transcriptional enhancer likely to be involved in this activation has been identified. A 25-kilobase region from J beta 1 to V beta 14 was tested for enhancer activity by transient transfections, and an enhancer was found 7.5 kilobases 3' of C beta 2. The beta enhancer has low activity relative to the simian virus 40 viral enhancer, does not display a preference for V beta promoters, has a T cell-specific activity, and binds two purified immunoglobulin heavy chain enhancer factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDougall, S -- Peterson, C L -- Calame, K -- GM29361/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 8;241(4862):205-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, UCLA School of Medicine 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2968651" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; Genes, Immunoglobulin ; Immunoglobulin Heavy Chains/genetics ; In Vitro Techniques ; Mice ; Nuclear Proteins/physiology ; Receptors, Antigen, T-Cell/*genetics ; Receptors, Antigen, T-Cell, alpha-beta ; *Regulatory Sequences, Nucleic Acid ; Transcription Factors/physiology ; Transcription, Genetic
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    Vasopressin mRNA in the suprachiasmatic nuclei: daily regulation of polyadenylate tail length (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-07-15
    Description: Daily variation has been found in the length of the polyadenylate tail attached to vasopressin messenger RNA in the suprachiasmatic nuclei, which is the location of an endogenous circadian pacemaker in mammals. No such variation was found in the supraoptic or paraventricular nuclei. This variation in the length of the polyadenylate tail may underlie the circadian rhythm of vasopressin peptide levels in cerebrospinal fluid and is a unique example of a daily rhythm in messenger RNA structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robinson, B G -- Frim, D M -- Schwartz, W J -- Majzoub, J A -- 1P50HL36568/HL/NHLBI NIH HHS/ -- R01NS24542/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 15;241(4863):342-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3388044" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine Vasopressin/*physiology ; Biological Clocks ; Circadian Rhythm ; Gene Expression Regulation ; Poly A/*physiology ; RNA, Messenger/*physiology ; Rats ; Suprachiasmatic Nucleus/*physiology
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    Molecular cloning of two types of GAP complementary DNA from human placenta (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-12-23
    Description: The ras p21 GTPase-activating protein (GAP) was purified from human placental tissue. Internal amino acid sequence was obtained from this 120,000-dalton protein and, by means of this sequence, two types of complementary DNA clones were isolated and characterized. One type encoded GAP with a predicted molecular mass of 116,000 daltons and 96% identity with bovine GAP. The messenger RNA of this GAP was detected in human lung, brain, liver, leukocytes, and placenta. The second type appeared to be generated by a differential splicing mechanism and encoded a novel form of GAP with a predicted molecular mass of 100,400 daltons. This protein lacks the hydrophobic amino terminus characteristic of the larger species, but retains GAP activity. The messenger RNA of this type was abundantly expressed in placenta and in several human cell lines, but not in adult tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trahey, M -- Wong, G -- Halenbeck, R -- Rubinfeld, B -- Martin, G A -- Ladner, M -- Long, C M -- Crosier, W J -- Watt, K -- Koths, K -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1697-700.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Cetus Corp., Emeryville, CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201259" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Brain Chemistry ; *Cloning, Molecular ; DNA/*genetics/isolation & purification ; Female ; GTPase-Activating Proteins ; Gene Expression Regulation ; Humans ; Leukocytes/analysis ; Liver/analysis ; Lung/analysis ; Molecular Sequence Data ; Molecular Weight ; Nucleic Acid Hybridization ; Oligonucleotide Probes ; Placenta/*analysis ; Pregnancy ; Proteins/*genetics/isolation & purification ; RNA, Messenger/analysis/genetics ; Sequence Homology, Nucleic Acid ; ras GTPase-Activating Proteins
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    Germline transformation used to define key features of heat-shock response elements (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-03-04
    Description: The heat-shock consensus element (HSE), CTNGAANNTTCNAG, is found in multiple copies upstream of all heat-shock genes. Here, the sequence requirements for heat-shock induction are tested by Drosophila germline transformation with an hsp70-lacZ gene fused to a pair of synthetic HSEs. Certain single-base substitutions in either HSE cause a dramatic reduction (forty-fold) in expression. Surprisingly, variations in sequences immediately flanking the HSEs also reduced levels of induction. One such variant that contains two perfect 14-base pair HSEs, which are correctly spaced relative to each other and the TATA box, retained only 7% of wild type-induced expression. These and additional analyses indicate that the heat-shock regulatory element includes sequences beyond the 14-base pair HSE and may be better described as a dimer of a 10-base pair sequence, NTTCNNGAAN.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiao, H -- Lis, J T -- GM25232/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 4;239(4844):1139-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, NY 14853.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3125608" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Composition ; DNA, Recombinant ; Drosophila melanogaster/*genetics ; Gene Expression Regulation ; Heat-Shock Proteins/*genetics ; Hot Temperature ; Mutation ; Nucleic Acid Conformation ; Promoter Regions, Genetic ; *Regulatory Sequences, Nucleic Acid ; Repetitive Sequences, Nucleic Acid ; Transcription Factors/*metabolism ; *Transformation, Genetic
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    A point mutation in the c-myc locus of a Burkitt lymphoma abolishes binding of a nuclear protein (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-06-24
    Description: A 20-base pair region in the first intron of the human c-myc gene was identified as the binding site of a nuclear protein. This binding site is mutated in five out of seven Burkitt lymphomas sequenced to date. To investigate the protein-recognition region in greater detail, the abnormal c-myc allele from a Burkitt lymphoma line (PA682) that carries a t(8;22) chromosomal translocation was used. A point mutation in the binding region of the PA682 c-myc DNA abolished binding of this nuclear protein. This protein may be an important factor for control of c-myc expression, and mutations in its recognition sequence may be associated with c-myc activation in many cases of Burkitt lymphoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zajac-Kaye, M -- Gelmann, E P -- Levens, D -- New York, N.Y. -- Science. 1988 Jun 24;240(4860):1776-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medicine Branch, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2454510" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Burkitt Lymphoma/*genetics ; DNA-Binding Proteins/*metabolism ; Gene Expression Regulation ; Humans ; Molecular Sequence Data ; Mutation ; Nuclear Proteins/*metabolism ; *Oncogenes ; Proto-Oncogene Proteins/*genetics ; RNA/genetics ; RNA, Antisense ; Transcription, Genetic
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    Independent molecular pathways in initiation and loss of hormone responsiveness of breast carcinomas (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-04-22
    Description: These studies were set up to determine whether those oncogenes participating in the initiation of mammary carcinogenesis (for example, ras oncogenes) play a direct role in the outcome of events associated with the late stages of tumor development such as loss of hormone dependency. Mammary carcinomas induced by a single carcinogenic insult in pubescent rats was selected as an in vivo model system with direct relevance to human breast cancer. Acquisition of hormone-independent growth in these carcinogen-induced tumors was found to be independent of the activation of ras oncogenes during the early stages of carcinogenesis. In agreement with these observations, introduction of a human ras oncogene into human MCF-7 breast carcinoma cells did not abrogate their hormonal dependency for growth in vivo. These findings suggest that those events responsible for the critical stages of breast cancer development occur independently and in an uncoordinated manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sukumar, S -- Carney, W P -- Barbacid, M -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 22;240(4851):524-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Oncology Section, Basic Research Program, Frederick Cancer Research Facility, MD 21701.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3282307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*physiopathology ; Cell Line ; Estrogens/*physiology ; Gene Expression Regulation ; *Genes, ras ; Humans ; Mammary Neoplasms, Experimental/*physiopathology ; Methylnitrosourea ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Rats ; Receptors, Estrogen/*physiology
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    jun Is bustin' out all over (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-12-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1988 Dec 9;242(4884):1377-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201229" target="_blank"〉PubMed〈/a〉
    Keywords: DNA-Binding Proteins/genetics/metabolism ; Gene Expression Regulation ; *Oncogenes ; Retroviridae Proteins/*genetics
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    Evolution's link to development explored (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-05-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1988 May 13;240(4854):880-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3363370" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Gene Expression Regulation ; *Genes ; *Growth ; Plant Development ; Plants/genetics
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    Activation of developmentally mutated human globin genes by cell fusion (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-18
    Description: Human fetal globin genes are not expressed in hybrid cells produced by the fusion of normal human lymphocytes with mouse erythroleukemia cells. In contrast, when lymphocytes from persons with globin gene developmental mutations (hereditary persistence of fetal hemoglobin) are used for these fusions, fetal globin is expressed in the hybrid cells. Thus, mutations of developmental origin can be reconstituted in vitro by fusing mutant lymphoid cells with differentiated cell lines of the proper lineage. This system can readily be used for analyses, such as globin gene methylation, that normally require large numbers of pure nucleated erythroid cells, which are difficult to obtain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papayannopoulou, T -- Enver, T -- Takegawa, S -- Anagnou, N P -- Stamatoyannopoulos, G -- DK30852/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 18;242(4881):1056-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2461587" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Fusion ; Chromosome Deletion ; Fetal Hemoglobin/*genetics ; Gene Expression Regulation ; Globins/*genetics ; Hemoglobinopathies/*genetics ; Humans ; Leukemia, Erythroblastic, Acute ; Mice ; Mutation ; Promoter Regions, Genetic ; RNA, Messenger/genetics
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    The DNA-binding properties of the major regulatory protein alpha 4 of herpes simplex viruses (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-25
    Description: The transition from the expression of alpha, the first set of five herpes simplex virus genes expressed after infection, to beta and gamma genes, expressed later in infection, requires the participation of infected cell protein 4 (alpha 4), the major viral regulatory protein. The alpha 4 protein is present in complexes formed by proteins extracted from infected cells and viral DNA fragments derived from promoter domains. This report shows that the alpha 4 protein forms specific complexes with DNA fragments derived from 5' transcribed noncoding domains of late (gamma 2) genes whose expression requires viral DNA synthesis as well as functional alpha 4 protein. Some of the DNA fragments to which alpha 4 binds do not contain homologs of the previously reported DNA binding site consensus sequence, suggesting that alpha 4 may recognize and interact with more than one type of DNA binding site. The alpha 4 proteins can bind to DNA directly. A posttranslationally modified form of the alpha 4 protein designated alpha 4c differs from the alpha 4a and alpha 4b forms with respect to its affinity for DNA fragments differing in the nucleotide sequences of the binding sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michael, N -- Spector, D -- Mavromara-Nazos, P -- Kristie, T M -- Roizman, B -- AI124009/AI/NIAID NIH HHS/ -- CA08494/CA/NCI NIH HHS/ -- CA19264/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Mar 25;239(4847):1531-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Marjorie B. Kovler Viral Oncology Laboratories, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2832940" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding Sites ; DNA, Viral/*metabolism ; DNA-Binding Proteins ; Electrophoresis, Polyacrylamide Gel ; Gene Expression Regulation ; Genes, Viral ; *Immediate-Early Proteins ; Immunoassay ; Molecular Sequence Data ; Sequence Homology, Nucleic Acid ; Simplexvirus/*analysis/genetics ; Transcription Factors ; Viral Proteins/*metabolism
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    cDNA expression cloning of the IL-1 receptor, a member of the immunoglobulin superfamily (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-29
    Description: Interleukin-1 alpha and -1 beta (IL-1 alpha and IL-1 beta) are cytokines that participate in the regulation of immune responses, inflammatory reactions, and hematopoiesis. A direct expression strategy was used to clone the receptor for IL-1 from mouse T cells. The product of the cloned complementary DNA binds both IL-1 alpha and IL-1 beta in a manner indistinguishable from that of the native T cell IL-1 receptor. The extracellular, IL-1 binding portion of the receptor is 319 amino acids in length and is composed of three immunoglobulin-like domains. The cytoplasmic portion of the receptor is 217 amino acids long.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sims, J E -- March, C J -- Cosman, D -- Widmer, M B -- MacDonald, H R -- McMahan, C J -- Grubin, C E -- Wignall, J M -- Jackson, J L -- Call, S M -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):585-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Corporation, Seattle, WA 98101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2969618" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Gene Expression Regulation ; Genes, Immunoglobulin ; Interleukin-1/*physiology ; Mice ; Molecular Sequence Data ; *Multigene Family ; Receptors, Immunologic/*genetics ; Receptors, Interleukin-1
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    Developmental expression of PDGF, TGF-alpha, and TGF-beta genes in preimplantation mouse embryos (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-09-30
    Description: Control of growth and differentiation during mammalian embryogenesis may be regulated by growth factors from embryonic or maternal sources. With the use of single-cell messenger RNA phenotyping, the simultaneous expression of growth factor transcripts in single or small numbers of preimplantation mouse embryos was examined. Transcripts for platelet-derived growth factor A chain (PDGF-A), transforming growth factor (TGF)-alpha, and TGF-beta 1, but not for four other growth factors, were found in whole blastocysts. TGF-alpha, TGF-beta 1, and PDGF antigens were detected in blastocysts by immunocytochemistry. Both PDGF-A and TGF-alpha were detected as maternal transcripts in the unfertilized ovulated oocyte, and again in blastocysts. TGF-beta 1 transcripts appeared only after fertilization. The expression of a subset of growth factors in mouse blastocysts suggests a role for these factors in the growth and differentiation of early mammalian embryos.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rappolee, D A -- Brenner, C A -- Schultz, R -- Mark, D -- Werb, Z -- 5T32 ES07106/ES/NIEHS NIH HHS/ -- HD22681/HD/NICHD NIH HHS/ -- HD23539/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 30;241(4874):1823-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Radiobiology and Environmental Health, University of California, San Francisco 94143-0750.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/*physiology ; Cleavage Stage, Ovum/physiology ; Embryonic Development ; Female ; Gene Expression Regulation ; Growth Substances/*genetics ; Mice ; Oocytes/physiology ; Platelet-Derived Growth Factor/*genetics ; Pregnancy ; RNA, Messenger/genetics ; Transcription, Genetic ; Transforming Growth Factors/*genetics
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    The cellular src gene product regulates junctional cell-to-cell communication (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-01-22
    Description: Overexpression of the cellular src gene in NIH 3T3 cells causes reduction of cell-to-cell transmission of molecules in the 400- to 700-dalton range. This down-regulation of gap junctional communication correlates with the activity of the gene product, the protein tyrosine kinase pp60c-src. The down-regulation was enhanced by point mutation of Tyr527 (a site that is phosphorylated in pp60c-src and that inhibits kinase activity) or by substitution of the viral-src for the cellular-src carboxyl-terminal coding region. Mutation of Tyr416 (a site phosphorylated upon Tyr527 mutation) suppresses both the down-regulation of communication by Tyr527 mutation and that by gene overexpression. The regulation of communication by src may be important in the control of embryonic development and cellular growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Azarnia, R -- Reddy, S -- Kmiecik, T E -- Shalloway, D -- Loewenstein, W R -- CA-14464/CA/NCI NIH HHS/ -- CA-32317/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 22;239(4838):398-401.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Miami School of Medicine, FL 33136.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2447651" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Communication ; Cell Line ; Cell Membrane Permeability ; Gene Expression Regulation ; *Intercellular Junctions ; Mice ; Mutation ; Phosphorylation ; Plasmids ; Protein-Tyrosine Kinases/*genetics ; Proto-Oncogene Proteins/genetics/*physiology ; Proto-Oncogene Proteins pp60(c-src) ; Structure-Activity Relationship ; Transcription, Genetic ; Transfection ; Tyrosine/metabolism
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    Cone cell-specific genes expressed in retinoblastoma (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-04-01
    Description: Retinoblastoma, an intraocular tumor that occurs in children, has long been regarded, on the basis of morphological criteria, as a malignancy of the photoreceptor cell lineage. Here it is shown that when this tumor is grown in vitro, the cells express highly specialized photoreceptor cell genes. Transcripts for the transducin alpha subunit, TC alpha, which is specific to the cone cell, as well as transcripts for the red or green cone cell photopigment, were found in seven out of seven low-passage retinoblastoma cell lines. No marker genes specific to rod cell were expressed, suggesting that retinoblastoma has a cone cell lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bogenmann, E -- Lochrie, M A -- Simon, M I -- EY04950/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 1;240(4848):76-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology Oncology, Childrens Hospital of Los Angeles, CA 90027.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2451289" target="_blank"〉PubMed〈/a〉
    Keywords: DNA/genetics ; Gene Expression Regulation ; Humans ; Membrane Proteins/*genetics ; Nucleic Acid Hybridization ; Photoreceptor Cells/*metabolism ; RNA/genetics ; Retinoblastoma/*genetics ; Transcription, Genetic ; Transducin ; Tumor Cells, Cultured
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    One factor recognizes the liver-specific enhancers in alpha 1-antitrypsin and transthyretin genes (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-12
    Description: Four different regulatory sites required for transcriptional stimulation by the enhancers of two unrelated liver-specific genes alpha 1-antitrypsin and transthyretin appear to bind the same nuclear protein that is found mainly in the liver. Such proteins may provide a basis for a coordinated, hepatocyte-specific control of gene transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grayson, D R -- Costa, R H -- Xanthopoulos, K G -- Darnell, J E -- CA 160006-14/CA/NCI NIH HHS/ -- CA 18213-11/CA/NCI NIH HHS/ -- GM 1066-02/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Feb 12;239(4841 Pt 1):786-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3257586" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; *Genes ; Genes, Regulator ; Liver/*metabolism ; Mice ; Mutation ; Nuclear Proteins/*physiology ; Prealbumin/*genetics ; *Transcription, Genetic ; alpha 1-Antitrypsin/*genetics
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    Virus-specific splicing inhibitor in extracts from cells infected with HIV-1 (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-16
    Description: Human immunodeficiency virus type 1 (HIV-1), in contrast with most other retroviruses, encodes trans-regulatory proteins for virus gene expression. It is shown in this study, by means of an in vitro splicing system, that nuclear extracts obtained from cells infected with HIV-1 contain a factor (or factors) that specifically inhibits splicing of a synthetic SP6/HIV pre-messenger RNA (pre-mRNA)-containing donor and acceptor splice sites in the coding region for the envelope protein. It is also shown that the SP6/HIV pre-mRNA is not capable of assembly in a ribonucleoprotein complex, spliceosome, in extracts from infected cells. These findings raise the possibility that specific inhibition of pre-mRNA splicing in the envelope protein coding region by HIV-1 trans-regulatory factors might be one control mechanism for efficient production of structural viral proteins and virion assembly.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gutman, D -- Goldenberg, C J -- AI-24479/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 16;241(4872):1492-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, 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/3047873" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Nucleus/physiology ; Cloning, Molecular ; DNA Mutational Analysis ; Gene Expression Regulation ; HIV/*genetics ; HeLa Cells ; Humans ; RNA Processing, Post-Transcriptional ; *RNA Splicing ; RNA, Viral/*genetics ; Ribonucleoproteins/physiology
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    Hormone-sensitive lipase: sequence, expression, and chromosomal localization to 19 cent-q13.3 (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-16
    Description: Hormone-sensitive lipase, a key enzyme in fatty acid mobilization, overall energy homeostasis, and possibly steroidogenesis, is acutely controlled through reversible phosphorylation by catecholamines and insulin. The 757-amino acid sequence predicted from a cloned rat adipocyte complementary DNA showed no homology with any other known lipase or protein. The activity-controlling phosphorylation site was localized to Ser563 in a markedly hydrophilic domain, and a lipid-binding consensus site was tentatively identified. One or several messenger RNA species (3.3, 3.5, or 3.9 kilobases) were expressed in adipose and steroidogenic tissues and heart and skeletal muscle. The human hormone-sensitive lipase gene mapped to chromosome 19 cent-q13.3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holm, C -- Kirchgessner, T G -- Svenson, K L -- Fredrikson, G -- Nilsson, S -- Miller, C G -- Shively, J E -- Heinzmann, C -- Sparkes, R S -- Mohandas, T -- New York, N.Y. -- Science. 1988 Sep 16;241(4872):1503-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical and Physiological Chemistry, University of Lund, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3420405" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Chromosome Mapping ; *Chromosomes, Human, Pair 19 ; Cloning, Molecular ; DNA/genetics ; Gene Expression Regulation ; Humans ; Molecular Sequence Data ; Rats ; Sterol Esterase/*genetics
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    Molecular characterization of a functional cDNA encoding the serotonin 1c receptor (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-29
    Description: Neurons that release serotonin as a neurotransmitter project to most regions of the central and peripheral nervous system and mediate diverse neural functions. The physiological effects of serotonin are initiated by the activation of multiple, distinct receptor subtypes. Cloning in RNA expression vectors was combined with a sensitive electrophysiological assay in Xenopus oocytes in order to isolate a functional cDNA clone encoding the 5HTlc serotonin receptor. Injection of RNA transcribed in vitro from this clone into Xenopus oocytes elicits serotonin sensitivity. Mouse fibroblasts transformed with this clone bind serotonin agonists and antagonists and exhibit an increase in intracellular Ca2+ concentrations in response to serotonin. The sequence of the 5HTlc receptor reveals that it belongs to the family of G protein-coupled receptors, which are thought to traverse the cytoplasmic membrane seven times. Moreover, in situ hybridization and RNA blot analysis indicate that the 5HTlc receptor is expressed in neurons in many regions of the central nervous system and suggest that this subclass of receptor may mediate many of the central actions of serotonin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Julius, D -- MacDermott, A B -- Axel, R -- Jessell, T M -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):558-64.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3399891" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Fibroblasts/physiology ; Gene Expression Regulation ; Membrane Glycoproteins/genetics ; Molecular Sequence Data ; Oocytes/physiology ; Phosphoproteins/physiology ; Rats ; Receptors, Serotonin/*genetics ; Serotonin/*physiology ; Xenopus laevis
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    Inactivation of the retinoblastoma susceptibility gene in human breast cancers (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-07-08
    Description: Mutational inactivation of the retinoblastoma susceptibility (RB) gene, a recessive cancer gene, has been implicated in the genesis of retinoblastoma and certain other human neoplasms. This gene is now shown to be inactivated in two of nine human breast cancer cell lines examined. The RB gene of one cell line had a homozygous internal duplication of a 5-kilobase region containing exons 5 and 6. The RB messenger RNA transcript was correspondingly lengthened, and its translation was probably terminated prematurely due to a shifted reading frame. The other cell line had a homozygous deletion of the RB gene that removed the entire gene beyond exon 2. The RB gene product, pp110RB, was not detectable in either cell line by immuno-precipitation with specific antibodies. These findings are significant in relation to proposed genetic mechanisms of breast cancer formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, E Y -- To, H -- Shew, J Y -- Bookstein, R -- Scully, P -- Lee, W H -- CA39537/CA/NCI NIH HHS/ -- EY00278/EY/NEI NIH HHS/ -- EY05758/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 8;241(4862):218-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, School 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/3388033" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics ; Chromosomes, Human, Pair 13 ; DNA, Neoplasm/*genetics ; Gene Expression Regulation ; Genes ; Humans ; Retinoblastoma/*genetics ; Tumor Cells, Cultured
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    Heterologous expression of excitability proteins: route to more specific drugs? (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-08-26
    Description: Many clinically important drugs act on the intrinsic membrane proteins (ion channels, receptors, and ion pumps) that control cell excitability. A major goal of pharmacology has been to develop drugs that are more specific for a particular subtype of excitability molecule. DNA cloning has revealed that many excitability proteins are encoded by multigene families and that the diversity of previously recognized pharmacological subtypes is matched, and probably surpassed, by the diversity of messenger RNAs that encode excitability molecules. In general, the diverse subtypes retain their properties when the excitability proteins are expressed in foreign cells such as oocytes and mammalian cell lines. Such heterologous expression may therefore become a tool for testing drugs against specific subtypes. In a systematic research program to exploit this possibility, major considerations include alternative processing of messenger RNA for excitability proteins, coupling to second-messenger systems, and expression of enough protein to provide material for structural studies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lester, H A -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1057-63.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2457947" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Physiological Phenomena ; Cloning, Molecular ; Drug-Related Side Effects and Adverse Reactions ; GTP-Binding Proteins/genetics/physiology ; Gene Expression Regulation ; *Genetic Variation ; Humans ; Ion Channels/drug effects/physiology ; Membrane Proteins/*genetics/physiology ; *Pharmacology ; Receptors, Cell Surface/drug effects/genetics/physiology
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    Distinct cloned class II MHC DNA binding proteins recognize the X box transcription element (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-10-07
    Description: The class II (Ia) major histocompatibility complex (MHC) antigens are a family of integral membrane proteins whose expression is limited to certain cell types. A pair of consensus sequences, X and Y, is found upstream of all class II genes, and deletion of each of these sequences eliminates expression of transfected genes. Furthermore, the absence of a specific X box binding protein in patients with severe combined immunodeficiency disease whose cells lack class II suggests an important role for these proteins in class II regulation. Here, the cloning of two lambda gt11 complementary DNAs encoding DNA binding proteins (murine X box binding proteins lambda mXBP and lambda mXBP-2) is reported. Both phage-encoded fusion proteins bind specifically to the X box of the A alpha, but not to E alpha or E beta class II genes. These two independent isolates do not cross-hybridize. The lambda mXBP complementary DNA hybridizes to two RNA species, 6.2 and 3.0 kilobases in mouse, that are expressed in both Ia positive and Ia negative cells. By means of DNA blot analysis with the lambda mXBP complementary DNA insert and probes generated from each end of this complementary DNA insert, lambda mXBP was found to arise from a multigene family. These data illustrate the high degree of complexity in the transcriptional control of this coordinately regulated gene family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liou, H C -- Boothby, M R -- Glimcher, L H -- New York, N.Y. -- Science. 1988 Oct 7;242(4875):69-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Harvard School of Public Health, Boston, Massachusetts 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3140376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Cloning, Molecular ; DNA-Binding Proteins/*genetics ; Gene Expression Regulation ; *Genes ; *Genes, MHC Class II ; Humans ; Mice ; Molecular Sequence Data ; *Transcription, Genetic ; Transfection
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    Apolipoprotein E: cholesterol transport protein with expanding role in cell biology (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-04-29
    Description: Apolipoprotein E is a plasma protein that serves as a ligand for low density lipoprotein receptors and, through its interaction with these receptors, participates in the transport of cholesterol and other lipids among various cells of the body. A mutant form of apolipoprotein E that is defective in binding to low density lipoprotein receptors is associated with familial type III hyperlipoproteinemia, a genetic disorder characterized by elevated plasma cholesterol levels and accelerated coronary artery disease. Apolipoprotein E is synthesized in various organs, including liver, brain, spleen, and kidney, and is present in high concentrations in interstitial fluid, where it appears to participate in cholesterol redistribution from cells with excess cholesterol to those requiring cholesterol. Apolipo-protein E also appears to be involved in the repair response to tissue injury; for example, markedly increased amounts of apolipoprotein E are found at sites of peripheral nerve injury and regeneration. Other functions of apolipoprotein E, unrelated to lipid transport, are becoming known, including immunoregulation and modulation of cell growth and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mahley, R W -- New York, N.Y. -- Science. 1988 Apr 29;240(4852):622-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Foundation Laboratories for Cardiovascular Disease, University of California, San Francisco 94140-0608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3283935" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Apolipoproteins E/genetics/*physiology ; Biological Transport ; Cholesterol/*metabolism ; Gene Expression Regulation ; Humans ; Hyperlipoproteinemia Type III/genetics/metabolism ; Immunity ; Lipid Metabolism ; Molecular Sequence Data ; Polymorphism, Genetic ; Protein Conformation ; Receptors, LDL/metabolism
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    Research on bacteria in the mainstream of biology (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-06-10
    Description: The study of the genetics, biochemistry, and physiology of bacteria during the last 40 years has provided the concepts and methods for the study of cells of all types at the molecular level. Although much is already known about the mechanisms bacteria use to regulate the expression of their genes, a great deal more remains to be discovered that will have relevance to both prokaryotic and eukaryotic cells. Similarly, the study in bacteria of the transactions of DNA, of the synthesis and function of the cell membrane, of differentiation, and of the interaction with eukaryotic cells will undoubtedly produce results of general importance. The advantages of using bacteria for these studies include their simple noncompartmented structure, the accessibility of their genetic material, and the possibility of correlating the expression of a gene in the intact cell with its expression in a system composed of highly purified components. Finally, the comparative study of a wide variety of microorganisms may result in a better understanding of the evolution of prokaryotes and eukaryotes and lead to a comprehensive theory of cell biology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magasanik, B -- AM-13894/AM/NIADDK NIH HHS/ -- GM-07446/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 10;240(4858):1435-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3287618" target="_blank"〉PubMed〈/a〉
    Keywords: *Bacteria/genetics ; Escherichia coli/genetics ; Gene Expression Regulation ; Models, Biological ; Models, Genetic ; *Research Design
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    Expression and function of the segmentation gene fushi tarazu during Drosophila neurogenesis (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-01-08
    Description: Segmentation genes control cell identities during early pattern formation in Drosophila. One of these genes, fushi tarazu (ftz), is now shown also to control cell fate during neurogenesis. Early in development, ftz is expressed in a striped pattern at the blastoderm stage. Later, it is transiently expressed in a specific subset of neuronal precursor cells, neurons (such as aCC, pCC, RP1, and RP2), and glia in the developing central nervous system (CNS). The function of ftz in the CNS was determined by creating ftz mutant embryos that express ftz in the blastoderm stripes but not in the CNS. In the absence of ftz CNS expression, some neurons appear normal (for example, the aCC, pCC, and RP1), whereas the RP2 neuron extends its growth cone along an abnormal pathway, mimicking its sibling (RP1), suggesting a transformation in neuronal identity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doe, C Q -- Hiromi, Y -- Gehring, W J -- Goodman, C S -- New York, N.Y. -- Science. 1988 Jan 8;239(4836):170-5.〈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/2892267" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Drosophila melanogaster/*embryology/genetics ; Gene Expression Regulation ; Genes, Homeobox ; Morphogenesis ; Nervous System/*embryology ; Neuroglia/cytology/physiology ; Neurons/cytology/physiology
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    Coordinate hormonal and synaptic regulation of vasopressin messenger RNA (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-19
    Description: Previous studies have shown that adrenalectomy augments arginine vasopressin (AVP) messenger RNA levels in the adult paraventricular nucleus. It is now demonstrated that unilateral lesions in the lateral septal nucleus enhance the adrenalectomy-induced expression of AVP mRNA. This effect was entirely ipsilateral to the lesion and most prominent in the rostral paraventricular nucleus and related nuclei. Moreover, AVP and AVP mRNA were found to be colocalized with oxytocin in a few neurons. These results indicate that mRNA expression is modulated by synaptic influences and raise the possibility that synaptically mediated selection of neuronal phenotypes is a dynamic feature of the mature central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baldino, F Jr -- O'Kane, T M -- Fitzpatrick-McElligott, S -- Wolfson, B -- New York, N.Y. -- Science. 1988 Aug 19;241(4868):978-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Products Department, E. I. du Pont de Nemours & Company, Wilmington, DE 19898.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3406747" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenalectomy ; Animals ; Gene Expression Regulation ; Male ; Neurons/analysis/*physiology ; Oxytocin/analysis ; Paraventricular Hypothalamic Nucleus/*physiology ; Phenotype ; RNA, Messenger/analysis/*biosynthesis ; Rats ; Rats, Inbred Strains ; Synapses/*physiology ; Vasopressins/analysis/*genetics
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    Comparison of biological properties and transforming potential of human PDGF-A and PDGF-B chains (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-09-09
    Description: Human platelet-derived growth factor (PDGF) consists of two distinct but related polypeptide chains designated PDGF-A and PDGF-B. The gene encoding PDGF-B has given rise to the v-sis oncogene. In the present study the transforming activities of PDGF-A and PDGF-B genes are compared. The PDGF-A chain gene is markedly less efficient in inducing transformation than the PDGF-B gene under the influence of the same promoter. There are significant differences in the secretory and growth stimulating properties of the two chains. These properties appear to account for the much more potent transforming ability of the PDGF-B gene. These findings provide insights into biologic properties of a growth factor responsible for potent autocrine stimulation of abnormal cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beckmann, M P -- Betsholtz, C -- Heldin, C H -- Westermark, B -- Di Marco, E -- Di Fiore, P P -- Robbins, K C -- Aaronson, S A -- New York, N.Y. -- Science. 1988 Sep 9;241(4871):1346-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2842868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Compartmentation ; Cell Line ; *Cell Transformation, Neoplastic ; Gene Expression Regulation ; Immunologic Techniques ; Mice ; Molecular Weight ; Platelet-Derived Growth Factor/*physiology ; Proto-Oncogene Proteins/*physiology ; Receptors, Cell Surface/*physiology ; Receptors, Platelet-Derived Growth Factor ; Solubility
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    Site-specific oligonucleotide binding represses transcription of the human c-myc gene in vitro (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-07-22
    Description: A 27-base-long DNA oligonucleotide was designed that binds to duplex DNA at a single site within the 5' end of the human c-myc gene, 115 base pairs upstream from the transcription origin P1. On the basis of the physical properties of its bound complex, it was concluded that the oligonucleotide forms a colinear triplex with the duplex binding site. By means of an in vitro assay system, it was possible to show a correlation between triplex formation at -115 base pairs and repression of c-myc transcription. The possibility is discussed that triplex formation (site-specific RNA binding to a DNA duplex) could serve as the basis for an alternative program of gene control in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cooney, M -- Czernuszewicz, G -- Postel, E H -- Flint, S J -- Hogan, M E -- New York, N.Y. -- Science. 1988 Jul 22;241(4864):456-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, NJ 08544.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3293213" target="_blank"〉PubMed〈/a〉
    Keywords: Electrophoresis ; Gene Expression Regulation ; Humans ; In Vitro Techniques ; Nucleic Acid Hybridization ; Oligodeoxyribonucleotides/*pharmacology ; Proto-Oncogene Proteins/*genetics ; *Proto-Oncogenes ; *Transcription, Genetic/drug effects
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    Isotypic exclusion of gamma delta T cell receptors in transgenic mice bearing a rearranged beta-chain gene (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-08-26
    Description: The rearrangement of T cell antigen receptor beta- and gamma-chain gene segments was studied in transgenic mice that bear a functional beta-chain gene. Virtually all CD3-positive T cells derived from transgenic mice express beta chains containing the transgene-encoded V beta 8.2 variable region on their surfaces and do not express endogenous beta-chain variable regions. Expression of endogenous V beta genes is inhibited at the level of somatic recombination during thymic ontogeny. Furthermore, rearrangements of the TCR gamma-chain genes are also markedly inhibited in these transgenic animals. Hence expression of the TCR beta transgene has led to allelic exclusion of alpha beta receptors and isotypic exclusion of gamma delta T cell receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fenton, R G -- Marrack, P -- Kappler, J W -- Kanagawa, O -- Seidman, J G -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1089-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2970670" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Antibodies, Monoclonal ; Bacteriophage lambda/genetics ; Cloning, Molecular ; DNA, Recombinant ; Enhancer Elements, Genetic ; Gene Expression Regulation ; Genes, Immunoglobulin ; Immunoassay ; Immunoglobulin Heavy Chains/genetics ; Liver/analysis ; Mice ; Mice, Transgenic ; Ovalbumin/immunology ; Receptors, Antigen, T-Cell/*genetics ; Recombination, Genetic ; T-Lymphocytes/metabolism ; Thymus Gland/analysis
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    Nef protein of HIV-1 is a transcriptional repressor of HIV-1 LTR (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-16
    Description: In studies of the genetics of human immunodeficiency virus type 1 (HIV-1), the product of the nef gene, formerly known as F, 3'-orf, or B-ORF, was a negative regulator of HIV-1 replication. Proviruses with mutations in the nef gene replicated better than their standard counterparts during transient expression, and the mutant virus maintained its enhanced replication even after serial passages in T lymphocytes. The nef protein trans-suppressed, in a dose-dependent manner, the replication of wild-type and nef mutant proviruses and the expression of reporter genes linked to the HIV-1 long terminal repeat (LTR). The repression induced by the nef protein was mediated by inhibition of transcription from the HIV-1 LTR, which contains a far upstream cis element (previously recognized to be a negative regulatory element) between 340 and 156 nucleotides upstream of the RNA initiation site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ahmad, N -- Venkatesan, S -- New York, N.Y. -- Science. 1988 Sep 16;241(4872):1481-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Microbiology, 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/3262235" target="_blank"〉PubMed〈/a〉
    Keywords: Gene Expression Regulation ; Gene Products, nef ; HIV/*genetics ; Regulatory Sequences, Nucleic Acid ; Repetitive Sequences, Nucleic Acid ; Repressor Proteins/*physiology ; Retroviridae Proteins/*physiology ; Transcription Factors/*physiology ; Transcription, Genetic ; Virus Replication ; nef Gene Products, Human Immunodeficiency Virus
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    The steroid and thyroid hormone receptor superfamily (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-05-13
    Description: Analyses of steroid receptors are important for understanding molecular details of transcriptional control, as well as providing insight as to how an individual transacting factor contributes to cell identity and function. These studies have led to the identification of a superfamily of regulatory proteins that include receptors for thyroid hormone and the vertebrate morphogen retinoic acid. Although animals employ complex and often distinct ways to control their physiology and development, the discovery of receptor-related molecules in a wide range of species suggests that mechanisms underlying morphogenesis and homeostasis may be more ubiquitous than previously expected.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Evans, R M -- New York, N.Y. -- Science. 1988 May 13;240(4854):889-95.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, CA 92138-9216.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3283939" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; DNA/metabolism ; Gene Expression Regulation ; Humans ; Receptors, Steroid/genetics/*physiology ; Receptors, Thyroid Hormone/genetics/*physiology
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    A quantitative bioassay for HIV-1 based on trans-activation (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-01-08
    Description: A bioassay that is based on trans-activation has been developed for the detection and quantitation of the human immunodeficiency virus type 1 (HIV-1). Indicator cell lines were constructed that contain the HIV-1 long terminal repeat ligated to the chloramphenicol acetyltransferase (CAT) gene. Infection of these cells by HIV activates the expression of CAT protein. Isolates of HIV-1 with divergent nucleotide sequences activated the indicator cell lines to a similar extent, approximately 500- to 1000-fold. Human T cell lymphotropic viruses types 1 and 2, equine infectious anemia virus, and herpes simplex virus 1 did not activate the indicator cell lines. Isolates of simian immunodeficiency virus and human T cell lymphotropic virus type 4 activated these cells to a much lesser extent, which suggests that these viruses contain similar, but distinct, trans-activators. This assay can be used for the detection, quantitation, and typing of HIV and for studying the effect of drugs on the replication of HIV in different cellular backgrounds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Felber, B K -- Pavlakis, G N -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 8;239(4836):184-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute, Frederick Cancer Research Facility, Bionetics Research, Inc., MD 21701.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3422113" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Antiviral Agents/pharmacology ; Cell Line ; Chloramphenicol O-Acetyltransferase ; DNA, Recombinant ; Gene Expression Regulation ; Genes, Viral ; HIV/analysis/drug effects/*genetics ; Humans ; Promoter Regions, Genetic ; Repetitive Sequences, Nucleic Acid ; Virus Replication/drug effects
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    Conversion of normal behavior to shiverer by myelin basic protein antisense cDNA in transgenic mice (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-07-29
    Description: Myelin basic proteins (MBPs) are coded by the single gene necessary for myelin formation in the central nervous system of the mouse. An antisense MBP mini-gene was constructed and used to determine the function of antisense DNA in transgenic mice. Several transgenic offspring of a founder transgenic mouse, AS100, were converted from the normal to mutant shiverer phenotype. Antisense MBP messenger RNA was expressed in these mice, and the endogenous MBP messenger RNA, the MBP, and the myelination in the central nervous system were reduced.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Katsuki, M -- Sato, M -- Kimura, M -- Yokoyama, M -- Kobayashi, K -- Nomura, T -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):593-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of DNA Biology, School of Medicine, Tokai University, Isehara, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2456614" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Brain/physiology ; DNA/genetics ; Gene Expression Regulation ; Mice ; Mice, Neurologic Mutants/*physiology ; Mice, Transgenic ; Molecular Sequence Data ; Myelin Basic Protein/genetics/*physiology ; Myelin Sheath/physiology ; Phenotype ; RNA/*genetics ; RNA, Antisense
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    The presence of fibroblast growth factor in the frog egg: its role as a natural mesoderm inducer (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-18
    Description: A complementary DNA clone corresponding to a 4.2-kilobase transcript that is present in the Xenopus oocyte and newly transcribed in the neurula stages of development has been isolated. This messenger RNA encodes a 155-amino acid protein that is 84% identical to the human basic fibroblast growth factor (bFGF). When expressed in Escherichia coli and purified, the Xenopus FGF induced mesoderm in animal cell blastomeres as measured by muscle actin expression. Immunoblots with an antibody to a Xenopus FGF peptide show that the oocyte and early embryo contain a store of the FGF polypeptide at high enough concentrations to induce mesoderm. The presence of FGF in the oocyte, together with the apparent lack of a secretory signal sequence in the protein, suggest that the regulation of mesoderm induction may involve novel mechanisms that occur after the translation of FGF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimelman, D -- Abraham, J A -- Haaparanta, T -- Palisi, T M -- Kirschner, M W -- New York, N.Y. -- Science. 1988 Nov 18;242(4881):1053-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3194757" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/genetics ; Amino Acid Sequence ; Animals ; Blotting, Northern ; Blotting, Western ; Cloning, Molecular ; DNA/genetics ; DNA Probes ; Fibroblast Growth Factors/*physiology ; Gene Expression Regulation ; Mesoderm/*cytology ; Molecular Sequence Data ; Oocytes/physiology ; Xenopus laevis/*embryology
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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)
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    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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    erbB-2 is a potent oncogene when overexpressed in NIH/3T3 cells (1987)
    American Association for the Advancement of Science (AAAS)
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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 80
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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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  • 81
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    Ouabain resistance conferred by expression of the cDNA for a murine Na+, K+-ATPase alpha subunit (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-21
    Description: The molecular basis for the marked difference between primate and rodent cells in sensitivity to the cardiac glycoside ouabain has been established by genetic techniques. A complementary DNA encoding the entire alpha 1 subunit of the mouse Na+- and K+-dependent adenosine triphosphatase (ATPase) was inserted into the expression vector pSV2. This engineered DNA molecule confers resistance against 10(-4) M ouabain to monkey CV-1 cells. Deletion of sequences encoding the carboxyl terminus of the alpha 1 subunit abolish the activity of the complementary DNA. The ability to assay the biological activity of this ATPase in a transfection protocol permits the application of molecular genetic techniques to the analysis of structure-function relationships for the enzyme that establishes the internal Na+/K+ environment of most animal cells. The full-length alpha 1 subunit complementary DNA will also be useful as a dominant selectable marker for somatic cell genetic studies utilizing ouabain-sensitive cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kent, R B -- Emanuel, J R -- Ben Neriah, Y -- Levenson, R -- Housman, D E -- CA-07919/CA/NCI NIH HHS/ -- CA-26712/CA/NCI NIH HHS/ -- CA-38992/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):901-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3039660" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cercopithecus aethiops ; DNA/genetics ; Drug Resistance ; Gene Expression Regulation ; Macromolecular Substances ; Mice ; Ouabain/*pharmacology ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors/*genetics ; Species Specificity ; Structure-Activity Relationship ; Transfection
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  • 82
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    The fos gene as "master switch" (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):854-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3039659" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Gene Expression Regulation ; Growth Substances/pharmacology ; Proto-Oncogene Proteins/*physiology ; *Proto-Oncogenes ; Receptors, GABA-A/physiology
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  • 83
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    Control protein for AIDS virus identified (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1987 Apr 24;236(4800):393.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3494309" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Gene Expression Regulation ; HIV/*genetics ; Humans ; Lymphocyte Activation ; T-Lymphocytes/cytology/*microbiology
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  • 84
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    Mapping patterns of c-fos expression in the central nervous system after seizure (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-10
    Description: A dramatic and specific induction of c-fos was observed in identifiable neuronal populations in vivo after administration of the convulsant Metrazole. This effect was time- and dose-dependent and was abolished by prior treatment with the anticonvulsant drugs diazepam or pentobarbital. About 60 minutes after administration of Metrazole, c-fos messenger RNA reached a maximum and declined to basal levels after 180 minutes. A further decrease below that in normal brain was observed before a return to basal levels after 16 hours. While Metrazole still elicited seizures during this period, reinduction of c-fos was largely refractory. At 90 minutes, c-fos protein was observed in the nuclei of neurons in the dentate gyrus, and in the pyriform and cingulate cortices. Subsequently, c-fos protein appeared throughout the cortex, hippocampus, and limbic system. Thus, seizure activity results in increased c-fos gene expression in particular subsets of neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morgan, J I -- Cohen, D R -- Hempstead, J L -- Curran, T -- New York, N.Y. -- Science. 1987 Jul 10;237(4811):192-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3037702" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry/drug effects ; DNA-Binding Proteins/biosynthesis/genetics ; Diazepam/pharmacology ; Fluorescent Antibody Technique ; Gene Expression Regulation ; Mice ; Mice, Inbred BALB C ; Neurons/metabolism ; Pentobarbital/pharmacology ; Pentylenetetrazole/antagonists & inhibitors/toxicity ; Proto-Oncogene Proteins/*biosynthesis/genetics ; Proto-Oncogene Proteins c-fos ; Receptors, GABA-A/drug effects ; Seizures/chemically induced/*metabolism
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  • 85
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    Allelic exclusion in transgenic mice that express the membrane form of immunoglobulin mu (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-15
    Description: Antibody-producing cells display a special form of regulation whereby each cell produces immunoglobulin from only one of its two sets of antibody genes. This phenomenon, called allelic exclusion, is thought to be mediated by the product of one heavy chain allele restricting the expression of the other. Heavy chains are synthesized in two molecular forms, secreted and membrane bound. In order to determine whether it is specifically the membrane-bound form of the immunoglobulin M (IgM) heavy chain (mu) that mediates this regulation, transgenic mice were created that carry a human mu chain gene altered so that it can only direct the synthesis of the membrane-bound protein. The membrane-bound form of the human mu chain was made by most of the B cells in these animals as measured by assays of messenger RNA and surface immunoglobulins. Further, the many B cells that express the human gene do not express endogenous mouse IgM, and the few B cells that express endogenous mouse mu do not express the transgene. Thus, the membrane-bound form of the mu chain is sufficient to mediate allelic exclusion. In addition, the molecular structures recognized for this purpose are conserved between human and mouse systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nussenzweig, M C -- Shaw, A C -- Sinn, E -- Danner, D B -- Holmes, K L -- Morse, H C 3rd -- Leder, P -- New York, N.Y. -- Science. 1987 May 15;236(4803):816-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107126" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; Antibody-Producing Cells/*immunology ; Gene Expression Regulation ; *Genes ; Humans ; Immunoglobulin M/genetics ; Immunoglobulin mu-Chains/*genetics ; Mice ; Mice, Inbred Strains ; RNA, Messenger/genetics ; Transcription, Genetic
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  • 86
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    The mitochondrial genotype can influence nuclear gene expression in yeast (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-30
    Description: Isochromosomal, respiratory-deficient yeast strains, such as a mit-, a hypersuppressive petite, and a petite lacking mitochondrial DNA, are phenotypically identical in spite of differences in their mitochondrial genomes. Subtractive hybridizations of complementary DNA's to polyadenylated RNA isolated from derepressed cultures of these strains reveal the presence of nuclear-encoded transcripts whose abundance varies not only between them and their respiratory-competent parent, but among the respiratory-deficient strains themselves. Transcripts of some nuclear-encoded mitochondrial proteins, like cytochrome c and the alpha and beta subunits of the mitochondrial adenosine triphosphatase, whose abundance is affected by glucose or heme, do not vary. In the absence of major metabolic variables, yeast cells seem to respond to the quality and quantity of mitochondrial DNA and modulate the levels of nuclear-encoded RNA's, perhaps as a means of intergenomic regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parikh, V S -- Morgan, M M -- Scott, R -- Clements, L S -- Butow, R A -- New York, N.Y. -- Science. 1987 Jan 30;235(4788):576-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3027892" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Nucleus/physiology ; Cytochrome c Group/genetics ; DNA, Fungal/genetics ; DNA, Mitochondrial/genetics ; Electron Transport Complex IV/genetics ; Gene Expression Regulation ; Genes, Fungal ; Genotype ; Mitochondria/*physiology ; Mutation ; RNA, Fungal/genetics ; RNA, Messenger/genetics ; RNA, Ribosomal/genetics ; Saccharomyces cerevisiae/*genetics
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  • 87
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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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  • 88
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    Identification of human uromodulin as the Tamm-Horsfall urinary glycoprotein (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-03
    Description: The primary structure of human uromodulin, a 616-amino acid, 85-kilodalton glycoprotein with in vitro immunosuppressive properties, was determined through isolation and characterization of complementary DNA and genomic clones. The amino acid sequence encoded by one of the exons of the uromodulin gene has homology to the low-density-lipoprotein receptor and the epidermal growth factor precursor. Northern hybridization analyses demonstrate that uromodulin is synthesized by the kidney. Evidence is provided that uromodulin is identical to the previously characterized Tamm-Horsfall glycoprotein, the most abundant protein in normal human urine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennica, D -- Kohr, W J -- Kuang, W J -- Glaister, D -- Aggarwal, B B -- Chen, E Y -- Goeddel, D V -- New York, N.Y. -- Science. 1987 Apr 3;236(4797):83-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3453112" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acids/analysis ; Base Sequence ; Chemistry, Physical ; Cloning, Molecular ; Cysteine ; DNA/genetics ; Gene Expression Regulation ; Genes ; Glycoproteins/*genetics ; Humans ; Mucoproteins/*analysis/*genetics ; Peptide Fragments/analysis ; Physicochemical Phenomena ; RNA, Messenger/genetics ; Uromodulin
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  • 89
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    Redesigning metabolic routes: manipulation of TOL plasmid pathway for catabolism of alkylbenzoates (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-30
    Description: Increasing quantities of man-made organic chemicals are released each year into the biosphere. Some of these compounds are both toxic and relatively resistant to physical, chemical, or biological degradation, and they thus constitute an environmental burden of considerable magnitude. Genetic manipulation of microbial catabolic pathways offers a powerful means by which to accelerate evolution of biodegradative routes through which such compounds might be eliminated from the environment. In the experiments described here, a catabolic pathway for alkylbenzoates specified by the TOL plasmid of Pseudomonas was restructured to produce a pathway capable of processing a new substrate, 4-ethylbenzoate. Analysis of critical steps in the TOL pathway that prevent metabolism of 4-ethylbenzoate revealed that this compound fails to induce synthesis of the catabolic enzymes and that one of its metabolic intermediates inactivates catechol 2,3-dioxygenase (C23O), the enzyme that cleaves the aromatic ring. Consequently, the pathway was sequentially modified by recruitment of genes from mutant bacteria selected for their production of either an altered pathway operon regulator that is activated by 4-ethylbenzoate or an altered C23O that is less sensitive to metabolite inactivation. The redesigned pathway was stably expressed and enabled host bacteria to degrade 4-ethylbenzoate in addition to the normal substrates of the TOL pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramos, J L -- Wasserfallen, A -- Rose, K -- Timmis, K N -- New York, N.Y. -- Science. 1987 Jan 30;235(4788):593-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3468623" target="_blank"〉PubMed〈/a〉
    Keywords: *Benzoates/*metabolism ; Biotransformation ; Catechol 2,3-Dioxygenase ; *Dioxygenases ; Gene Expression Regulation ; Genetic Engineering ; Oxygenases/metabolism ; *Plasmids ; Pseudomonas/enzymology/*genetics/growth & development ; Substrate Specificity
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  • 90
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    Identification of a novel thyroid hormone receptor expressed in the mammalian central nervous system (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-09-25
    Description: A complementary DNA clone derived from rat brain messenger RNA has been isolated on the basis of homology to the human thyroid hormone receptor gene. Expression of this complementary DNA produces a high-affinity binding protein for thyroid hormones. Sequence analysis and the mapping of this gene to a distinct human genetic locus indicate the existence of multiple human thyroid hormone receptors. Messenger RNA from this gene is expressed in a tissue-specific fashion with highest levels in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, C C -- Weinberger, C -- Lebo, R -- Evans, R M -- GM-266444-09/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Sep 25;237(4822):1610-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3629259" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/*physiology ; DNA/genetics ; DNA-Binding Proteins/*genetics ; Gene Expression Regulation ; Genes ; Humans ; RNA, Messenger/genetics ; Rats ; Receptors, Thyroid Hormone/*genetics/metabolism ; Tissue Distribution ; Triiodothyronine/metabolism
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  • 91
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    Assemblage of ortho cleavage route for simultaneous degradation of chloro- and methylaromatics (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-04
    Description: Genetic engineering is a powerful means of accelerating the evolution of new biological activities and has considerable potential for constructing microorganisms that can degrade environmental pollutants. Critical enzymes from five different catabolic pathways of three distinct soil bacteria have been combined in patchwork fashion into a functional ortho cleavage route for the degradation of methylphenols and methylbenzoates. The new bacterium thereby evolved was able to degrade and grow on mixtures of chloro- and methylaromatics that were toxic even for the bacteria that could degrade the individual components of the mixtures. Except for one enzymatic step, the pathway was fully regulated and its component enzymes were only synthesized in response to the presence of pathway substrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rojo, F -- Pieper, D H -- Engesser, K H -- Knackmuss, H J -- Timmis, K N -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1395-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Biochemistry, University of Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3479842" target="_blank"〉PubMed〈/a〉
    Keywords: Alcaligenes/enzymology/genetics ; Bacterial Proteins/genetics/*metabolism ; Benzoates/*metabolism ; *Biodegradation, Environmental ; Chlorobenzoates/*metabolism ; Gene Expression Regulation ; *Genes, Bacterial ; Genetic Engineering ; *Intramolecular Transferases ; Isomerases/genetics/metabolism ; Mixed Function Oxygenases/genetics/metabolism ; Oxidoreductases/genetics/metabolism ; Oxygenases/genetics/metabolism ; Pseudomonas/enzymology/genetics ; Recombinant Proteins/*metabolism
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  • 92
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    Human CSF-1: molecular cloning and expression of 4-kb cDNA encoding the human urinary protein (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-03-20
    Description: A 4-kilobase complementary DNA (cDNA) encoding human macrophage-specific colony-stimulating factor (CSF-1) was isolated. When introduced into mammalian cells, this cDNA directs the expression of CSF-1 that is structurally and functionally indistinguishable from the natural human urinary CSF-1. Direct structural analysis of both the recombinant CSF-1 and the purified human urinary protein revealed that these species contain a sequence of at least 40 amino acids at their carboxyl termini which are not found in the coding region of a 1.6-kilobase CSF-1 cDNA that was previously described. These results demonstrate that the human CSF-1 gene can be expressed to yield at least two different messenger RNA species that encode distinct but related forms of CSF-1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, G G -- Temple, P A -- Leary, A C -- Witek-Giannotti, J S -- Yang, Y C -- Ciarletta, A B -- Chung, M -- Murtha, P -- Kriz, R -- Kaufman, R J -- New York, N.Y. -- Science. 1987 Mar 20;235(4795):1504-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3493529" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cloning, Molecular ; Colony-Stimulating Factors/*genetics/urine ; DNA/genetics ; Gene Expression Regulation ; Humans ; Macrophages/physiology ; Molecular Weight ; Peptide Fragments ; Protein Processing, Post-Translational ; RNA, Messenger/genetics
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  • 93
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    Molecular cloning and expression of a human B-cell growth factor gene in Escherichia coli (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-03-20
    Description: A human B-cell growth factor (BCGF) (12 kilodaltons) supports the clonal proliferation of B lymphocytes. A clone was isolated that contained the proper structural sequence to encode biologically active, 12-kilodalton BCGF in Escherichia coli and to hybridize to a specific messenger RNA, identified by in vitro translation in Xenopus laevis oocytes. A relatively hydrophobic region of 18 amino acids was found at the amino terminal of the 124-amino acid-long polypeptide. The carboxyl terminal is composed of at least 32 amino acids that are derived from nucleotide sequences bearing significant homology to the Alu repeat family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharma, S -- Mehta, S -- Morgan, J -- Maizel, A -- 16672/PHS HHS/ -- CA38499/CA/NCI NIH HHS/ -- CA39798/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 20;235(4795):1489-92.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3547651" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; B-Lymphocytes/*physiology ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Escherichia coli ; Gene Expression Regulation ; Growth Substances/*genetics ; Interleukin-4 ; Lymphokines/*genetics ; Repetitive Sequences, Nucleic Acid ; Sequence Homology, Nucleic Acid
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 94
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    Diurnal expression of transducin mRNA and translocation of transducin in rods of rat retina (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-30
    Description: The messenger RNA (mRNA) that encodes alpha subunit of the guanosine triphosphate-binding protein transducin (T alpha) and T alpha immunoreactivity were localized and measured in the rat retina during the light-dark cycle with in situ hybridization and immunohistochemistry. Both T alpha mRNA and T alpha immunoreactivity were observed only in photoreceptors. Within the photoreceptor T alpha mRNA was present primarily in the inner segments and to a lesser extent in the outer nuclear layer at all times during the day and night. However, the distribution of T alpha immunoreactivity varied profoundly with the light-dark cycle; during the day, T alpha immunoreactivity was highest in the inner segments, and at night the outer segments were more immunoreactive. The amounts of T alpha mRNA and T alpha immunoreactivity also depended on the light-dark cycle. Levels of T alpha mRNA were high immediately before and after lights on; levels were low for the rest of the light-dark cycle. During the day, T alpha immunoreactivity increased in the inner segments following the increase in T alpha mRNA. After the lights were turned off, T alpha immunoreactivity decreased in the inner segments and increased in the outer segments. Thus, it appears that T alpha is synthesized in the inner segments after a morning increase in T alpha mRNA. Newly synthesized T alpha remains in the inner segments until it is transported to the outer segments at night, where it may be involved in the increase in the sensitivity of photoreceptor rods at night.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brann, M R -- Cohen, L V -- New York, N.Y. -- Science. 1987 Jan 30;235(4788):585-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3101175" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Circadian Rhythm ; GTP-Binding Proteins/*genetics/immunology/metabolism ; Gene Expression Regulation ; Immunoenzyme Techniques ; Male ; Membrane Proteins/*genetics/immunology/metabolism ; Photoreceptor Cells/*physiology/ultrastructure ; RNA, Messenger/genetics ; Rats ; Transducin
    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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  • 95
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    Elevated levels of glucose transport and transporter messenger RNA are induced by ras or src oncogenes (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-03-20
    Description: An accelerated rate of glucose transport is among the most characteristic biochemical markers of cellular transformation. To study the molecular mechanism by which transporter activity is altered, cultured rodent fibroblasts transfected with activated myc, ras, or src oncogenes were used. In myc-transfected cells, the rate of 2-deoxy-D-glucose uptake was unchanged. However, in cells transfected with activated ras and src oncogenes, the rate of glucose uptake was markedly increased. The increased transport rate in ras- and src-transfected cells was paralleled by a marked increase in the amount of glucose transporter protein, as assessed by immunoblots, as well as by a markedly increased abundance of glucose transporter messenger RNA. Exposure of control cells to the tumor-promoting phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA) for 18 hours had a similar effect of increasing the rate of glucose transport and the abundance of transporter messenger RNA. For ras, src, and TPA, the predominant mechanism responsible for activation of the transport system is increased expression of the structural gene encoding the glucose transport protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flier, J S -- Mueckler, M M -- Usher, P -- Lodish, H F -- AM00856/AM/NIADDK NIH HHS/ -- AM28082/AM/NIADDK NIH HHS/ -- GM35012/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 20;235(4795):1492-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3103217" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Membrane/physiology ; Cell Transformation, Neoplastic/*physiopathology ; Deoxyglucose/metabolism ; GTP-Binding Proteins/physiology ; Gene Expression Regulation ; Glucose/*metabolism ; Monosaccharide Transport Proteins/*genetics ; *Oncogenes ; Protein-Tyrosine Kinases/physiology ; RNA, Messenger/genetics ; Rats ; Tetradecanoylphorbol Acetate/pharmacology ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
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    Diversity of alpha-fetoprotein gene expression in mice is generated by a combination of separate enhancer elements (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-02
    Description: The 5' flanking region of the mouse alpha-fetoprotein (AFP) gene contains a tissue-specific promoter and three upstream regulatory elements that behave as classical enhancers. At least one of these enhancers is now shown to be required for the tissue-specific expression of the AFP gene when it is introduced into the mouse genome by microinjection of cloned DNA fragments into fertilized eggs. Each enhancer can direct expression in the appropriate tissues, the visceral endoderm of the yolk sac, the fetal liver, and the gastrointestinal tract, but each exerts different influence in these three tissues. These differences may explain the tissue-specific diversity in the levels of expression characteristic of the AFP gene. The postnatal repression of transcription of the AFP gene in both liver and gut, as well as the reinitiation of its transcription during liver regeneration, is mimicked by the introduced gene when it is linked to the enhancer domains together or singly. Thus, the DNA sequence elements responsible for directing the activation of AFP transcription, its repression, and reinduction are contained in a limited segment of DNA within or 5' to the gene (or both) and are operative in the absence of the closely linked albumin gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hammer, R E -- Krumlauf, R -- Camper, S A -- Brinster, R L -- Tilghman, S M -- CA06927/CA/NCI NIH HHS/ -- CA28050/CA/NCI NIH HHS/ -- HD17321/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Jan 2;235(4784):53-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2432657" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; Genes ; *Genes, Regulator ; Intestines/physiology ; Liver/physiology ; Mice ; Promoter Regions, Genetic ; RNA, Messenger/genetics ; Tissue Distribution ; Transcription, Genetic ; Transfection ; Yolk Sac/physiology ; alpha-Fetoproteins/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
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    Cloning of complementary DNA for GAP-43, a neuronal growth-related protein (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-01
    Description: GAP-43 is one of a small subset of cellular proteins selectively transported by a neuron to its terminals. Its enrichment in growth cones and its increased levels in developing or regenerating neurons suggest that it has an important role in neurite growth. A complementary DNA (cDNA) that encodes rat GAP-43 has been isolated to study its structural characteristics and regulation. The predicted molecular size is 24 kilodaltons, although its migration in SDS-polyacrylamide gels is anomalously retarded. Expression of GAP-43 is limited to the nervous system, where its levels are highest during periods of neurite outgrowth. Nerve growth factor or adenosine 3',5'-monophosphate induction of neurites from PC12 cells is accompanied by increased GAP-43 expression. GAP-43 RNA is easily detectable, although at diminished levels, in the adult rat nervous system. This regulation of GAP-43 is concordant with a role in growth-related processes of the neuron, processes that may continue in the mature animal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karns, L R -- Ng, S C -- Freeman, J A -- Fishman, M C -- New York, N.Y. -- Science. 1987 May 1;236(4801):597-600.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2437653" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Axons/physiology ; Bacteriophage lambda/genetics ; Base Sequence ; *Cloning, Molecular ; DNA/*genetics ; Electrophoresis, Polyacrylamide Gel ; GAP-43 Protein ; Ganglia, Spinal/analysis/embryology ; Gene Expression Regulation ; Growth Substances/genetics ; Immunosorbent Techniques ; Membrane Proteins/*genetics ; Nerve Tissue Proteins/*genetics ; Protein Biosynthesis ; RNA/genetics ; RNA, Messenger/genetics ; Rats
    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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  • 98
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    U3 sequences from HTLV-I and -II LTRs confer pX protein response to a murine leukemia virus LTR (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-20
    Description: Human T-cell leukemia virus (HTLV) types I and II are unusual among replication-competent retroviruses in that they contain a fourth gene (chi) necessary for replication. The chi gene product, p chi, transcriptionally transactivates the viral long repeat (LTR), and is thus a positive regulator. To investigate p chi transactivation, sequences from the U3 regions of the LTRs of HTLV-I and -II were inserted into the Moloney murine leukemia virus (M-MuLV) LTR by recombinant DNA techniques. Transient expression assays of the chimeric LTRs indicated that the HTLV sequences conferred to the M-MuLV LTR responsiveness to HTLV p chi protein. M-MuLV enhancers were not required for function of the chimeric LTRs. Infectious recombinant M-MuLVs containing chimeric LTRs were also generated. These viruses showed higher infectivity when assayed in mouse cells expressing HTLV-II p chi protein compared to normal mouse cells. Thus the HTLV sequences were able to confer p chi responsiveness to infectious M-MuLV. The generation of a virus dependent on a transactivating protein for its replication has implications for the evolution of the human T-cell leukemia viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kitado, H -- Chen, I S -- Shah, N P -- Cann, A J -- Shimotohno, K -- Fan, H -- CA32454/CA/NCI NIH HHS/ -- CA32455/CA/NCI NIH HHS/ -- CA38597/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Feb 20;235(4791):901-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3027896" target="_blank"〉PubMed〈/a〉
    Keywords: DNA, Viral/*genetics ; Deltaretrovirus/*genetics ; Enhancer Elements, Genetic ; Gene Expression Regulation ; Moloney murine leukemia virus/*genetics ; Promoter Regions, Genetic ; Repetitive Sequences, Nucleic Acid ; Retroviridae Proteins/*genetics ; Trans-Activators ; Transcription Factors/*genetics ; Transcription, Genetic ; *Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    Oncogene action probed (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1987 Aug 7;237(4815):602-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603042" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Transformation, Neoplastic ; Colonic Neoplasms/genetics ; Fibroblast Growth Factors/genetics ; Gene Expression Regulation ; Humans ; Mutation ; *Oncogenes ; Proto-Oncogenes ; Sarcoma, Kaposi/genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    HTLV x gene mutants exhibit novel transcriptional regulatory phenotypes (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-06
    Description: The human T-cell leukemia viruses, HTLV-I and HTLV-II, contain a gene, termed x, with transcriptional regulatory function. The properties of the x proteins were analyzed by constructing mutant genes containing site-directed deletions and point mutations. The results demonstrate that the amino terminal 17 amino acids of the x protein constitute part of a functional domain that is critical for the transcriptional activating properties of the protein. Within this region, substitution of a leucine residue for a proline residue results in major changes in the trans-activation phenotype of the protein. The mutant HTLV-II x protein, though incapable of activating the HTLV-II long terminal repeat, will block trans-activation of the HTLV-II long terminal repeat by the wild-type protein. The altered phenotype of this mutant suggests a potential negative regulatory function of the x protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wachsman, W -- Cann, A J -- Williams, J L -- Slamon, D J -- Souza, L -- Shah, N P -- Chen, I S -- CA 30388/CA/NCI NIH HHS/ -- CA 32727/CA/NCI NIH HHS/ -- CA 38597/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Feb 6;235(4789):674-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3027894" target="_blank"〉PubMed〈/a〉
    Keywords: Deltaretrovirus/*genetics ; Gene Expression Regulation ; *Genes, Viral ; Mutation ; Transcription Factors/*genetics ; Transcription, Genetic
    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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