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  • Articles  (83)
  • Transfection  (83)
  • American Association for the Advancement of Science (AAAS)  (83)
  • American Chemical Society
  • American Institute of Physics
  • American Institute of Physics (AIP)
  • Periodicals Archive Online (PAO)
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  • Articles  (83)
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  • American Association for the Advancement of Science (AAAS)  (83)
  • American Chemical Society
  • American Institute of Physics
  • American Institute of Physics (AIP)
  • Periodicals Archive Online (PAO)
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  • 1990-1994  (59)
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  • 1
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    Rate and mechanism of nonhomologous recombination during a single cycle of retroviral replication (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-08
    Description: Oncogenes discovered in retroviruses such as Rous sarcoma virus were generated by transduction of cellular proto-oncogenes into the viral genome. Several different kinds of junctions between the viral and proto-oncogene sequences have been found in different viruses. A system of retrovirus vectors and a protocol that mimicked this transduction during a single cycle of retrovirus replication was developed. The transduction involved the formation of a chimeric viral-cellular RNA, strand switching of the reverse transcription growing point from an infectious retrovirus to the chimeric RNA, and often a subsequent deletion during the rest of viral DNA synthesis. A short region of sequence identity was frequently used for the strand switching. The rate of this process was about 0.1 to 1 percent of the rate of homologous retroviral recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Temin, H M -- CA-07175/CA/NCI NIH HHS/ -- CA-22443/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 8;259(5092):234-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McArdle Laboratory for Cancer Research, University of Wisconsin-Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8421784" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Cinnamates ; *DNA Replication ; DNA, Viral/chemistry/genetics ; Drug Resistance/genetics ; Genes, Viral ; Genetic Vectors ; Hygromycin B/analogs & derivatives ; Kinetics ; Mice ; Molecular Sequence Data ; Moloney murine leukemia virus/genetics ; Neomycin ; Plasmids ; *Proto-Oncogenes ; RNA, Viral/analysis/genetics ; *Recombination, Genetic ; Repetitive Sequences, Nucleic Acid ; Retroviridae/*genetics/physiology ; Transfection ; *Virus Replication
    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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    Mutations in the glucose-6-phosphatase gene that cause glycogen storage disease type 1a (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-22
    Description: Glycogen storage disease (GSD) type 1a is caused by the deficiency of D-glucose-6-phosphatase (G6Pase), the key enzyme in glucose homeostasis. Despite both a high incidence and morbidity, the molecular mechanisms underlying this deficiency have eluded characterization. In the present study, the molecular and biochemical characterization of the human G6Pase complementary DNA, its gene, and the expressed protein, which is indistinguishable from human microsomal G6Pase, are reported. Several mutations in the G6Pase gene of affected individuals that completely inactivate the enzyme have been identified. These results establish the molecular basis of this disease and open the way for future gene therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lei, K J -- Shelly, L L -- Pan, C J -- Sidbury, J B -- Chou, J Y -- New York, N.Y. -- Science. 1993 Oct 22;262(5133):580-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211187" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA, Complementary/genetics ; Exons ; Glucose-6-Phosphatase/*genetics/metabolism ; Glycogen Storage Disease Type I/enzymology/*genetics ; Glycosylation ; Humans ; Liver/enzymology ; Mice ; Molecular Sequence Data ; *Mutation ; Protein Conformation ; 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 cloning and signaling properties of the rat glucagon receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-12
    Description: Glucagon and the glucagon receptor are a primary source of control over blood glucose concentrations and are especially important to studies of diabetes in which the loss of control over blood glucose concentrations clinically defines the disease. A complementary DNA clone for the glucagon receptor was isolated by an expression cloning strategy, and the receptor protein was expressed in several kidney cell lines. The cloned receptor bound glucagon and caused an increase in the intracellular concentration of adenosine 3', 5'-monophosphate (cAMP). The cloned glucagon receptor also transduced a signal that led to an increased concentration of intracellular calcium. The glucagon receptor is similar to the calcitonin and parathyroid hormone receptors. It can transduce signals leading to the accumulation of two different second messengers, cAMP and calcium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jelinek, L J -- Lok, S -- Rosenberg, G B -- Smith, R A -- Grant, F J -- Biggs, S -- Bensch, P A -- Kuijper, J L -- Sheppard, P O -- Sprecher, C A -- New York, N.Y. -- Science. 1993 Mar 12;259(5101):1614-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ZymoGenetics Inc., Seattle, WA 98105.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8384375" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/pharmacology ; Cell Line ; Cloning, Molecular ; Cricetinae ; Cyclic AMP/metabolism ; Glucagon/metabolism/*pharmacology ; Kidney ; Kinetics ; Liver/*metabolism ; Molecular Sequence Data ; Rats ; Receptors, Gastrointestinal Hormone/genetics/metabolism/*physiology ; Receptors, Glucagon ; *Signal Transduction ; 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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  • 4
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    Induction of G alpha i2-specific antisense RNA in vivo inhibits neonatal growth (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-14
    Description: Guanosine triphosphate-binding regulatory proteins (G proteins) are key elements in transmembrane signaling and have been implicated as regulators of more complex biological processes such as differentiation and development. The G protein G alpha i2 is capable of mediating the inhibitory control of adenylylcyclase and regulates stem cell differentiation to primitive endoderm. Here an antisense RNA to G alpha i2 was expressed in a hybrid RNA construct whose expression was both tissue-specific and induced at birth. Transgenic mice in which the antisense construct was expressed displayed a lack of normal development in targeted organs that correlated with the absence of G alpha i2. The loss of G alpha i2 expression in adipose tissue of the transgenic mice was correlated with a rise in basal levels of adenosine 3',5'-monophosphate (cAMP) and the loss of receptor-mediated inhibition of adenylylcyclase. These data expand our understanding of G protein function in vivo and demonstrate the necessity for G alpha i2 in the development of liver and fat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moxham, C M -- Hod, Y -- Malbon, C C -- New York, N.Y. -- Science. 1993 May 14;260(5110):991-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Pharmacology, State University of New York (SUNY)/Stony Brook 11794-8651.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493537" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*growth & development/metabolism ; Animals ; Animals, Newborn/growth & development ; Base Sequence ; Body Weight ; GTP-Binding Proteins/biosynthesis/genetics/*physiology ; Growth/drug effects/*physiology ; Kidney/growth & development/metabolism ; Liver/*growth & development/metabolism ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Phosphoenolpyruvate Carboxykinase (GTP)/genetics ; RNA, Antisense/*genetics ; 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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  • 5
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    Uncovering of functional alternative CTLA-4 counter-receptor in B7-deficient mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-05
    Description: B7 delivers a costimulatory signal through CD28, resulting in interleukin-2 secretion and T cell proliferation. Blockade of this pathway results in T cell anergy. The in vivo role of B7 was evaluated with B7-deficient mice. These mice had a 70 percent decrease in costimulation of the response to alloantigen. Despite lacking B7 expression, activated B cells from these mice bound CTLA-4 and GL1 monoclonal antibody, demonstrating that alternative CTLA-4 ligand or ligands exist. These receptors are functionally important because the residual allogenic mixed lymphocyte responses were blocked by CTLA4Ig. Characterization of these CTLA-4 ligands should lead to strategies for manipulating the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freeman, G J -- Borriello, F -- Hodes, R J -- Reiser, H -- Hathcock, K S -- Laszlo, G -- McKnight, A J -- Kim, J -- Du, L -- Lombard, D B -- CA 40216/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Nov 5;262(5135):907-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematologic Malignancies, Dana-Farber Cancer Institute, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7694362" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antigens, CD ; Antigens, CD80/genetics/*immunology/metabolism ; Antigens, Differentiation/immunology/*metabolism ; B-Lymphocytes/*immunology ; Base Sequence ; CTLA-4 Antigen ; Cell Line ; *Immunoconjugates ; Interleukin-2/secretion ; Isoantigens/immunology ; Lymphocyte Activation ; Lymphocyte Culture Test, Mixed ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; T-Lymphocytes/*immunology ; 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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  • 6
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    Selective and ATP-dependent translocation of peptides by the MHC-encoded transporter (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-06
    Description: Major histocompatibility complex (MHC) class I molecules present peptides derived from nuclear and cytosolic proteins to CD8+ T cells. These peptides are translocated into the lumen of the endoplasmic reticulum (ER) to associate with class I molecules. Two MHC-encoded putative transporter proteins, TAP1 and TAP2, are required for efficient assembly of class I molecules and presentation of endogenous peptides. Expression of TAP1 and TAP2 in a mutant cell line resulted in the delivery of an 11-amino acid oligomer model peptide to the ER. Peptide translocation depended on the sequence of the peptide, was adenosine triphosphate (ATP)-dependent, required ATP hydrolysis, and was inhibited in a concentration-dependent manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neefjes, J J -- Momburg, F -- Hammerling, G J -- New York, N.Y. -- Science. 1993 Aug 6;261(5122):769-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Netherlands Cancer Institute, Amsterdam.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8342042" target="_blank"〉PubMed〈/a〉
    Keywords: *ATP-Binding Cassette Transporters ; Adenosine Triphosphate/*metabolism ; Amino Acid Sequence ; Animals ; Biological Transport ; Carrier Proteins/*metabolism ; Cell Line ; Cell Membrane Permeability ; Endoplasmic Reticulum/metabolism ; Glycosylation ; Histocompatibility Antigens Class II/*metabolism ; Molecular Sequence Data ; Oligopeptides/*metabolism ; Rats ; T-Lymphocytes, Cytotoxic/*metabolism ; 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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  • 7
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    IL-6-induced homodimerization of gp130 and associated activation of a tyrosine kinase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-18
    Description: The biological functions of interleukin-6 (IL-6) are mediated through a signal-transducing component of the IL-6 receptor, gp130, which is associated with the ligand-occupied IL-6 receptor (IL-6R) protein. Binding of IL-6 to IL-6R induced disulfide-linked homodimerization of gp130. Tyrosine kinase activity was associated with dimerized but not monomeric gp130 protein. Substitution of serine for proline residues 656 and 658 in the cytoplasmic motif abolished tyrosine kinase activation and cellular responses but not homodimerization of gp130. The IL-6-induced gp130 homodimer appears to be similar in function to the heterodimer formed between the leukemia inhibitory factor (LIF) receptor (LIFR) and gp130 in response to the LIF or ciliary neurotrophic factor (CNTF). Thus, a general first step in IL-6-related cytokine signaling may be the dimerization of signal-transducing molecules and activation of associated tyrosine kinases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murakami, M -- Hibi, M -- Nakagawa, N -- Nakagawa, T -- Yasukawa, K -- Yamanishi, K -- Taga, T -- Kishimoto, T -- New York, N.Y. -- Science. 1993 Jun 18;260(5115):1808-10.〈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/8511589" target="_blank"〉PubMed〈/a〉
    Keywords: *Antigens, CD ; Cytokine Receptor gp130 ; Enzyme Activation ; Haptoglobins/biosynthesis ; Humans ; Interleukin-6/*metabolism/pharmacology ; Macromolecular Substances ; Membrane Glycoproteins/chemistry/*metabolism ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Receptors, Immunologic/*metabolism ; Receptors, Interleukin-6 ; *Signal Transduction ; Transfection ; 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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  • 8
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    Tumor rejection after direct costimulation of CD8+ T cells by B7-transfected melanoma cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-15
    Description: A variety of tumors are potentially immunogenic but do not stimulate an effective anti-tumor immune response in vivo. Tumors may be capable of delivering antigen-specific signals to T cells, but may not deliver the costimulatory signals necessary for full activation of T cells. Expression of the costimulatory ligand B7 on melanoma cells was found to induce the rejection of a murine melanoma in vivo. This rejection was mediated by CD8+ T cells; CD4+ T cells were not required. These results suggest that B7 expression renders tumor cells capable of effective antigen presentation, leading to their eradication in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Townsend, S E -- Allison, J P -- CA57986/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 15;259(5093):368-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7678351" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens, CD80 ; Antigens, Surface/genetics/*immunology ; CD4-Positive T-Lymphocytes/immunology ; Cross Reactions ; Female ; Gene Expression Regulation ; Genetic Vectors ; Ligands ; *Lymphocyte Activation ; Melanoma/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Nude ; T-Lymphocytes, Regulatory/*immunology ; Transfection ; 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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  • 9
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    Primers for mitochondrial DNA replication generated by endonuclease G (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-06
    Description: Endonuclease G (Endo G) is widely distributed among animals and cleaves DNA at double-stranded (dG)n.(dC)n and at single-stranded (dC)n tracts. Endo G is synthesized as a propeptide with an amino-terminal presequence that targets the nuclease to mitochondria. Endo G can also be detected in extranucleolar chromatin. In addition to deoxyribonuclease activities, Endo G also has ribonuclease (RNase) and RNase H activities and specifically cleaves mouse mitochondrial RNA and DNA-RNA substrates containing the origin of heavy-strand DNA replication (OH). The cleavage sites match those found in vivo, indicating that Endo G is capable of generating the RNA primers required by DNA polymerase gamma to initiate replication of mitochondrial DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cote, J -- Ruiz-Carrillo, A -- New York, N.Y. -- Science. 1993 Aug 6;261(5122):765-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Center, Medical School of Laval University, L'Hotel-Dieu de Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7688144" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cell Nucleus/enzymology ; DNA/genetics ; *DNA Replication ; DNA, Mitochondrial/*metabolism ; Endodeoxyribonucleases/chemistry/genetics/*metabolism ; Genetic Vectors ; Mitochondria/enzymology ; Molecular Sequence Data ; RNA/*metabolism ; Ribonuclease H/metabolism ; Ribonucleases/metabolism ; 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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  • 10
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    Interleukin-2 receptor gamma chain: a functional component of the interleukin-4 receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-17
    Description: The interleukin-2 (IL-2) receptor gamma chain (IL-2R gamma) is an essential component of high- and intermediate-affinity IL-2 receptors. IL-2R gamma was demonstrated to be a component of the IL-4 receptor on the basis of chemical cross-linking data, the ability of IL-2R gamma to augment IL-4 binding affinity, and the requirement for IL-2R gamma in IL-4-mediated phosphorylation of insulin receptor substrate-1. The observation that IL-2R gamma is a functional component of the IL-4 receptor, together with the finding that IL-2R gamma associates with the IL-7 receptor, begins to elucidate why deficiency of this common gamma chain (gamma c) has a profound effect on lymphoid function and development, as seen in X-linked severe combined immunodeficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Russell, S M -- Keegan, A D -- Harada, N -- Nakamura, Y -- Noguchi, M -- Leland, P -- Friedmann, M C -- Miyajima, A -- Puri, R K -- Paul, W E -- New York, N.Y. -- Science. 1993 Dec 17;262(5141):1880-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Pulmonary and Molecular Immunology, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266078" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Cell Line, Transformed ; Genetic Linkage ; Humans ; Insulin Receptor Substrate Proteins ; Interleukin-4/metabolism ; L Cells (Cell Line) ; Mice ; Molecular Sequence Data ; Phosphoproteins/metabolism ; Phosphorylation ; Receptors, Interleukin-2/chemistry/genetics/*metabolism ; Receptors, Interleukin-4 ; Receptors, Mitogen/chemistry/genetics/*metabolism ; Severe Combined Immunodeficiency/genetics/immunology ; Signal Transduction ; Transfection ; X Chromosome
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  • 11
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    New test catches drug-resistant TB in the spotlight (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1993 May 7;260(5109):750.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8484114" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Antitubercular Agents/*pharmacology ; Drug Resistance, Microbial ; Luciferases/genetics/metabolism ; *Luminescent Measurements ; Microbial Sensitivity Tests/*methods ; Mycobacterium tuberculosis/*drug effects/genetics/metabolism ; 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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  • 12
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    Naked DNA points way to vaccines (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1691-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456293" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Viral/*genetics/therapeutic use ; Influenza A virus/*genetics/immunology ; Mice ; Nucleoproteins/genetics/immunology ; Orthomyxoviridae Infections/*prevention & control ; *RNA-Binding Proteins ; Transfection ; Viral Core Proteins/genetics/immunology ; Viral Vaccines/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Regulation of V(D)J recombination activator protein RAG-2 by phosphorylation (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-14
    Description: Antigen receptor genes are assembled by site-specific DNA rearrangement. The recombination activator genes RAG-1 and RAG-2 are essential for this process, termed V(D)J rearrangement. The activity and stability of the RAG-2 protein have now been shown to be regulated by phosphorylation. In fibroblasts RAG-2 was phosphorylated predominantly at two serine residues, one of which affected RAG-2 activity in vivo. The threonine at residue 490 was phosphorylated by p34cdc2 kinase in vitro; phosphorylation at this site in vivo was associated with rapid degradation of RAG-2. Instability was transferred to chimeric proteins by a 90-residue portion of RAG-2. Mutation of the p34cdc2 phosphorylation site of the tumor suppressor protein p53 conferred a similar phenotype, suggesting that this association between phosphorylation and degradation is a general mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, W C -- Desiderio, S -- CA16519/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 May 14;260(5110):953-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493533" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; CDC2 Protein Kinase/metabolism ; Cell Line ; *DNA-Binding Proteins ; *Gene Rearrangement ; Humans ; Mice ; Molecular Sequence Data ; Mutation ; Nuclear Proteins ; Phosphorylation ; Proteins/chemistry/genetics/*metabolism ; Receptors, Antigen/*genetics ; Recombinant Fusion Proteins/metabolism ; Transfection ; Tumor Suppressor Protein p53/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Presentation of a viral T cell epitope expressed in the CDR3 region of a self immunoglobulin molecule (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-08
    Description: Synthetic peptides corresponding to microbial epitopes stimulate T cell immunity but their immunogenicity is poor and their half-lives are short. A viral epitope inserted into the complementarity-determining region 3 (CDR3) loop of the heavy chain of a self immunoglobulin (Ig) molecule was generated from the Ig context and was presented by I-Ed class II molecules to virus-specific, CD4+ T cells. Chimeric Ig-peptide was presented 100 to 1000 times more efficiently than free synthetic peptide and was able to prime virus-specific T cells in vivo. These features suggest that antigenized Ig can provide an improved and safe vaccine for the presentation of microbial and other peptides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zaghouani, H -- Steinman, R -- Nonacs, R -- Shah, H -- Gerhard, W -- Bona, C -- AI13013/AI/NIAID NIH HHS/ -- AI18316/AI/NIAID NIH HHS/ -- AI24460/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Jan 8;259(5092):224-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7678469" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigen-Presenting Cells/*immunology ; Antigens, Viral/*immunology ; Arsenic/immunology ; *Arsenicals ; Base Sequence ; CD4-Positive T-Lymphocytes/immunology ; DNA/genetics ; Epitopes/*immunology ; Hemagglutinin Glycoproteins, Influenza Virus ; Hemagglutinins, Viral/genetics/immunology ; Histocompatibility Antigens Class II/immunology ; Immunoglobulin Heavy Chains/genetics/immunology ; Immunoglobulin Variable Region/genetics/immunology ; Immunoglobulins/genetics/*immunology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Mutagenesis ; Receptors, Fc/immunology ; Recombinant Fusion Proteins/immunology ; Transfection
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  • 15
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    Generation of a mouse strain that produces immunoglobulin kappa chains with human constant regions (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-19
    Description: Humanized antibodies are highly efficient as immunotherapeutic reagents and have many advantages over rodent antibodies. A mouse strain was generated by gene targeting to replace the mouse kappa light chain constant (C) region gene with the human C kappa gene. Mice homozygous for the replacement mutation (C kappa R) produced normal concentrations of serum antibodies, most of which carry chimeric kappa light chains, and mounted normal immune responses to hapten-protein conjugates. This technology provides a feasible option for the generation of high-affinity humanized antibodies by means of the powerful somatic hypermutation-selection mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zou, Y R -- Gu, H -- Rajewsky, K -- New York, N.Y. -- Science. 1993 Nov 19;262(5137):1271-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235658" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/*immunology ; Base Sequence ; Gene Rearrangement ; *Genes, Immunoglobulin ; Humans ; Immunoglobulin Constant Regions/*biosynthesis/genetics ; Immunoglobulin Isotypes/biosynthesis ; Immunoglobulin kappa-Chains/*biosynthesis/genetics ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Mutation ; Polymerase Chain Reaction ; Recombinant Fusion Proteins/biosynthesis ; Stem Cells ; Transfection
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  • 16
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    Interleukin-2 receptor gamma chain: a functional component of the interleukin-7 receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-17
    Description: The interleukin-2 receptor gamma chain (IL-2R gamma) is a necessary component of functional IL-2 receptors. IL-2R gamma mutations result in X-linked severe combined immunodeficiency (XSCID) in humans, a disease characterized by the presence of few or no T cells. In contrast, SCID patients with IL-2 deficiency and IL-2-deficient mice have normal numbers of T cells, suggesting that IL-2R gamma is part of more than one cytokine receptor. By using chemical cross-linking, IL-2R gamma was shown to be physically associated with the IL-7 receptor. The presence of IL-2R gamma augmented both IL-7 binding affinity and the efficiency of internalization of IL-7. These findings may help explain the defects of XSCID. Given its role in more than one cytokine receptor system, the common gamma chain (gamma c) is proposed as the designation for IL-2R gamma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noguchi, M -- Nakamura, Y -- Russell, S M -- Ziegler, S F -- Tsang, M -- Cao, X -- Leonard, W J -- New York, N.Y. -- Science. 1993 Dec 17;262(5141):1877-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Pulmonary and Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266077" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Cell Line ; Genetic Linkage ; Interleukin-7/*metabolism ; L Cells (Cell Line) ; Mice ; Receptors, Interleukin/chemistry/genetics/*metabolism ; Receptors, Interleukin-2/chemistry/genetics/*metabolism ; Receptors, Interleukin-7 ; Severe Combined Immunodeficiency/genetics/immunology ; T-Lymphocytes/immunology ; Transfection ; X Chromosome
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  • 17
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    Antagonism of catecholamine receptor signaling by expression of cytoplasmic domains of the receptors (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-05
    Description: The actions of many hormones and neurotransmitters are mediated by the members of a superfamily of receptors coupled to heterotrimeric guanine nucleotide-binding proteins (G proteins). These receptors are characterized by a highly conserved topographical arrangement in which seven transmembrane domains are connected by intracellular and extracellular loops. The interaction between these receptors and G proteins is mediated in large part by the third intracellular loop of the receptor. Coexpression of the third intracellular loop of the alpha 1B-adrenergic receptor with its parent receptor inhibited receptor-mediated activation of phospholipase C. The inhibition extended to the closely related alpha 1C-adrenergic receptor subtype, but not the phospholipase C-coupled M1 muscarinic acetylcholine receptor nor the adenylate cyclase-coupled D1A dopamine receptor. These results suggest that the receptor-G protein interface may represent a target for receptor antagonist drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luttrell, L M -- Ostrowski, J -- Cotecchia, S -- Kendall, H -- Lefkowitz, R J -- HL16037/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1453-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8383880" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Cloning, Molecular ; Cyclic AMP/metabolism ; Cytoplasm/metabolism ; GTP-Binding Proteins/*metabolism ; Globins/genetics ; Glutathione Transferase/genetics/metabolism ; Humans ; Inositol Phosphates/metabolism ; Kinetics ; Molecular Sequence Data ; Muscarinic Antagonists ; Oligodeoxyribonucleotides ; Plasmids ; Protein Structure, Secondary ; Receptors, Adrenergic, alpha/genetics/*metabolism ; Receptors, Dopamine D1/antagonists & inhibitors/genetics/*metabolism ; Receptors, Muscarinic/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Transfection ; Type C Phospholipases/metabolism
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  • 18
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    Inhibition of viral replication by interferon-gamma-induced nitric oxide synthase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: Interferons (IFNs) induce antiviral activity in many cell types. The ability of IFN-gamma to inhibit replication of ectromelia, vaccinia, and herpes simplex-1 viruses in mouse macrophages correlated with the cells' production of nitric oxide (NO). Viral replication was restored in IFN-gamma-treated macrophages exposed to inhibitors of NO synthase. Conversely, epithelial cells with no detectable NO synthesis restricted viral replication when transfected with a complementary DNA encoding inducible NO synthase or treated with organic compounds that generate NO. In mice, an inhibitor of NO synthase converted resolving ectromelia virus infection into fulminant mousepox. Thus, induction of NO synthase can be necessary and sufficient for a substantial antiviral effect of IFN-gamma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karupiah, G -- Xie, Q W -- Buller, R M -- Nathan, C -- Duarte, C -- MacMicking, J D -- CA43610/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1445-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7690156" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/*biosynthesis/metabolism ; Animals ; Arginine/analogs & derivatives/pharmacology ; Cell Line ; Cells, Cultured ; Ectromelia virus/drug effects/*physiology ; Ectromelia, Infectious/microbiology ; Enzyme Induction ; Female ; Humans ; Interferon-gamma/*pharmacology ; Macrophages/*microbiology ; Mice ; Mice, Inbred C57BL ; Nitric Oxide/metabolism/pharmacology ; Nitric Oxide Synthase ; Simplexvirus/drug effects/physiology ; Transfection ; Vaccinia virus/drug effects/physiology ; *Virus Replication/drug effects ; omega-N-Methylarginine
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  • 19
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    Malaria: focus on mosquito genes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aldhous, P -- New York, N.Y. -- Science. 1993 Jul 30;261(5121):546-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8393586" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Anopheles/*genetics/parasitology ; DNA Transposable Elements ; *Genes, Insect ; Genetic Engineering ; Humans ; Insect Vectors/*genetics/parasitology ; Malaria/*prevention & control/transmission ; Plasmodium/*physiology ; Transfection
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  • 20
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    Multiple defects of immune cell function in mice with disrupted interferon-gamma genes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-19
    Description: Interferon-gamma (IFN-gamma) is a pleiotrophic cytokine with immunomodulatory effects on a variety of immune cells. Mice with a targeted disruption of the IFN-gamma gene were generated. These mice developed normally and were healthy in the absence of pathogens. However, mice deficient in IFN-gamma had impaired production of macrophage antimicrobial products and reduced expression of macrophage major histocompatibility complex class II antigens. IFN-gamma-deficient mice were killed by a sublethal dose of the intracellular pathogen Mycobacterium bovis. Splenocytes exhibited uncontrolled proliferation in response to mitogen and alloantigen. After a mixed lymphocyte reaction, T cell cytolytic activity was enhanced against allogeneic target cells. Resting splenic natural killer cell activity was reduced in IFN-gamma-deficient mice. Thus, IFN-gamma is essential for the function of several cell types of the murine immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dalton, D K -- Pitts-Meek, S -- Keshav, S -- Figari, I S -- Bradley, A -- Stewart, T A -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1739-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genentech Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456300" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cytotoxicity, Immunologic ; Histocompatibility Antigens Class II/immunology ; *Immunity ; Interferon-gamma/*genetics/physiology ; Isoantigens/immunology ; Killer Cells, Natural/immunology ; Lymphocyte Culture Test, Mixed ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Mycobacterium bovis ; Nitric Oxide/metabolism ; Spleen/cytology/immunology ; T-Lymphocytes/immunology ; Transfection ; Tuberculosis/immunology
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  • 21
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    Inhibition of transcriptional regulator Yin-Yang-1 by association with c-Myc (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-17
    Description: Yin-Yang-1 (YY1) regulates the transcription of many genes, including the oncogenes c-fos and c-myc. Depending on the context, YY1 acts as a transcriptional repressor, a transcriptional activator, or a transcriptional initiator. The yeast two-hybrid system was used to screen a human complementary DNA (cDNA) library for proteins that associate with YY1, and a c-myc cDNA was isolated. Affinity chromatography confirmed that YY1 associates with c-Myc but not with Max. In cotransfections, c-Myc inhibits both the repressor and the activator functions of YY1, which suggests that one way c-Myc acts is by modulating the activity of YY1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shrivastava, A -- Saleque, S -- Kalpana, G V -- Artandi, S -- Goff, S P -- Calame, K -- CA 38571/CA/NCI NIH HHS/ -- GM29361/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Dec 17;262(5141):1889-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, Columbia University College of Physicians and Surgeons, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266081" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adenovirus E1A Proteins/metabolism ; Animals ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Basic-Leucine Zipper Transcription Factors ; DNA-Binding Proteins/antagonists & inhibitors/genetics/*metabolism/pharmacology ; Erythroid-Specific DNA-Binding Factors ; Helix-Loop-Helix Motifs ; Humans ; Mice ; Proto-Oncogene Proteins c-myc/*metabolism/pharmacology ; Recombinant Fusion Proteins/metabolism ; Transcription Factors/antagonists & inhibitors/genetics/*metabolism/pharmacology ; Transfection ; Tumor Cells, Cultured ; Upstream Stimulatory Factors ; YY1 Transcription Factor ; *Zinc Fingers
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  • 22
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    Heterologous protection against influenza by injection of DNA encoding a viral protein (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-19
    Description: Cytotoxic T lymphocytes (CTLs) specific for conserved viral antigens can respond to different strains of virus, in contrast to antibodies, which are generally strain-specific. The generation of such CTLs in vivo usually requires endogenous expression of the antigen, as occurs in the case of virus infection. To generate a viral antigen for presentation to the immune system without the limitations of direct peptide delivery or viral vectors, plasmid DNA encoding influenza A nucleoprotein was injected into the quadriceps of BALB/c mice. This resulted in the generation of nucleoprotein-specific CTLs and protection from a subsequent challenge with a heterologous strain of influenza A virus, as measured by decreased viral lung titers, inhibition of mass loss, and increased survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ulmer, J B -- Donnelly, J J -- Parker, S E -- Rhodes, G H -- Felgner, P L -- Dwarki, V J -- Gromkowski, S H -- Deck, R R -- DeWitt, C M -- Friedman, A -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1745-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Research, Merck Research Laboratories, West Point, PA 19486.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456302" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA, Viral/*genetics/therapeutic use ; Gene Expression ; Genetic Vectors ; Histocompatibility Antigens Class I/immunology ; Immunization ; Influenza A virus/*genetics/immunology/isolation & purification ; Lung/microbiology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Muscles/metabolism ; Nucleoproteins/*genetics/*immunology ; Orthomyxoviridae Infections/microbiology/*prevention & control ; Plasmids ; *RNA-Binding Proteins ; T-Lymphocytes, Cytotoxic/immunology ; Transfection ; Viral Core Proteins/*genetics/*immunology ; Viral Vaccines/*genetics
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  • 23
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    NF-kappa B activation by ultraviolet light not dependent on a nuclear signal (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: Exposure of mammalian cells to radiation triggers the ultraviolet (UV) response, which includes activation of activator protein-1 (AP-1) and nuclear factor kappa B (NF-kappa B). This was postulated to occur by induction of a nuclear signaling cascade by damaged DNA. Recently, induction of AP-1 by UV was shown to be mediated by a pathway involving Src tyrosine kinases and the Ha-Ras small guanosine triphosphate-binding protein, proteins located at the plasma membrane. It is demonstrated here that the same pathway mediates induction of NF-kappa B by UV. Because inactive NF-kappa B is stored in the cytosol, analysis of its activation directly tests the involvement of a nuclear-initiated signaling cascade. Enucleated cells are fully responsive to UV both in NF-kappa B induction and in activation of another key signaling event. Therefore, the UV response does not require a signal generated in the nucleus and is likely to be initiated at or near the plasma membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Devary, Y -- Rosette, C -- DiDonato, J A -- Karin, M -- CA50528/CA/NCI NIH HHS/ -- ES04151/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1442-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of California at San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8367725" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Catechols/pharmacology ; Cell Nucleus/*physiology ; Cytosol/metabolism ; Genes, ras ; Genes, src ; HeLa Cells ; Humans ; NF-kappa B/*metabolism/radiation effects ; Nitriles/pharmacology ; PC12 Cells ; Phosphatidylcholines/metabolism ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins c-jun/metabolism ; Proto-Oncogene Proteins c-raf ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology ; *Tyrphostins ; *Ultraviolet Rays
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  • 24
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    Determination of type I receptor specificity by the type II receptors for TGF-beta or activin (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-05
    Description: Transforming growth factor-beta (TGF-beta) and activin signal primarily through interaction with type I and type II receptors, which are transmembrane serine-threonine kinases. Tsk 7L is a type I receptor for TGF-beta and requires coexpression of the type II TGF-beta receptor for ligand binding. Tsk 7L also specifically bound activin, when coexpressed with the type IIA activin receptor. Tsk 7L could associate with either type II receptor and the ligand binding specificity of Tsk 7L was conferred by the type II receptor. Tsk 7L can therefore act as type I receptor for both activin and TGF-beta, and possibly other ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ebner, R -- Chen, R H -- Lawler, S -- Zioncheck, T -- Derynck, R -- New York, N.Y. -- Science. 1993 Nov 5;262(5135):900-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Growth and Development, and Anatomy, University of California at San Francisco 94143-0640.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235612" target="_blank"〉PubMed〈/a〉
    Keywords: Activin Receptors ; Activins ; Base Sequence ; DNA Primers ; Growth Substances/metabolism ; Humans ; Inhibins/*metabolism ; Molecular Sequence Data ; Precipitin Tests ; Protein-Serine-Threonine Kinases/*metabolism ; Receptors, Growth Factor/*metabolism ; Receptors, Transforming Growth Factor beta/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transfection ; Transforming Growth Factor beta/*metabolism
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  • 25
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    Reconstitution of T cell receptor zeta-mediated calcium mobilization in nonlymphoid cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-13
    Description: T cell antigen receptor (TCR) activation involves interactions between receptor subunits and nonreceptor protein tyrosine kinases (PTKs). Early steps in signaling through the zeta chain of the TCR were examined in transfected COS-1 cells. Coexpression of the PTK p59fynT, but not p56lck, with zeta or with a homodimeric TCR beta-zeta fusion protein produced tyrosine phosphorylation of both zeta and phospholipase C (PLC)-gamma 1, as well as calcium ion mobilization in response to receptor cross-linking. CD45 coexpression enhanced these effects. No requirement for the PTKZAP-70 was observed. Thus, p59fynT may link zeta directly to the PLC-gamma 1 activation pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hall, C G -- Sancho, J -- Terhorst, C -- AI 15066/AI/NIAID NIH HHS/ -- CA 01486/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Aug 13;261(5123):915-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, Beth Israel Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8346442" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD45/analysis ; Base Sequence ; Calcium/*metabolism ; Cell Line ; Cercopithecus aethiops ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Membrane Proteins/*metabolism ; Molecular Sequence Data ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism/physiology ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-fyn ; Receptors, Antigen, T-Cell/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transfection ; Type C Phospholipases/metabolism ; Tyrosine/metabolism ; ZAP-70 Protein-Tyrosine Kinase
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  • 26
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    Controlling signal transduction with synthetic ligands (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-12
    Description: Dimerization and oligomerization are general biological control mechanisms contributing to the activation of cell membrane receptors, transcription factors, vesicle fusion proteins, and other classes of intra- and extracellular proteins. Cell permeable, synthetic ligands were devised that can be used to control the intracellular oligomerization of specific proteins. To demonstrate their utility, these ligands were used to induce intracellular oligomerization of cell surface receptors that lacked their transmembrane and extracellular regions but contained intracellular signaling domains. Addition of these ligands to cells in culture resulted in signal transmission and specific target gene activation. Monomeric forms of the ligands blocked the pathway. This method of ligand-regulated activation and termination of signaling pathways has the potential to be applied wherever precise control of a signal transduction pathway is desired.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spencer, D M -- Wandless, T J -- Schreiber, S L -- Crabtree, G R -- New York, N.Y. -- Science. 1993 Nov 12;262(5136):1019-24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7694365" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Carrier Proteins/*metabolism ; Cross-Linking Reagents ; Gene Expression Regulation ; Heat-Shock Proteins/*metabolism ; Ligands ; Membrane Proteins/*metabolism ; Models, Biological ; Molecular Sequence Data ; Polymers ; Receptors, Antigen, T-Cell/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; T-Lymphocytes/*metabolism ; Tacrolimus/*analogs & derivatives/chemical synthesis/chemistry/metabolism ; Tacrolimus Binding Proteins ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured
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    Effect of PU.1 phosphorylation on interaction with NF-EM5 and transcriptional activation (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-12
    Description: PU.1 recruits the binding of a second B cell-restricted nuclear factor, NF-EM5, to a DNA site in the immunoglobulin kappa 3' enhancer. DNA binding by NF-EM5 requires a protein-protein interaction with PU.1 and specific DNA contacts. Dephosphorylated PU.1 bound to DNA but did not interact with NF-EM5. Analysis of serine-to-alanine mutations in PU.1 indicated that serine 148 (Ser148) is required for protein-protein interaction. PU.1 produced in bacteria did not interact with NF-EM5. Phosphorylation of bacterially produced PU.1 by purified casein kinase II modified it to a form that interacted with NF-EM5 and that recruited NF-EM5 to bind to DNA. Phosphopeptide analysis of bacterially produced PU.1 suggested that Ser148 is phosphorylated by casein kinase II. This site is also phosphorylated in vivo. Expression of wild-type PU.1 increased expression of a reporter construct containing the PU.1 and NF-EM5 binding sites nearly sixfold, whereas the Ser148 mutant form only weakly activated transcription. These results demonstrate that phosphorylation of PU.1 at Ser148 is necessary for interaction with NF-EM5 and suggest that this phosphorylation can regulate transcriptional activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pongubala, J M -- Van Beveren, C -- Nagulapalli, S -- Klemsz, M J -- McKercher, S R -- Maki, R A -- Atchison, M L -- AI 30656/AI/NIAID NIH HHS/ -- CA 42909/CA/NCI NIH HHS/ -- GM 42415/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 12;259(5101):1622-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Animal Biology, University of Pennsylvania, School of Veterinary Medicine, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456286" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Base Sequence ; Cell Line ; Cell Nucleus/metabolism ; DNA-Binding Proteins/genetics/isolation & purification/*metabolism ; Enhancer Elements, Genetic ; Immunoglobulin kappa-Chains/genetics ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Oligonucleotide Probes ; Phosphorylation ; Plasmacytoma ; Recombinant Proteins/isolation & purification/metabolism ; Retroviridae Proteins, Oncogenic ; Transcription Factors/*metabolism ; *Transcription, Genetic ; Transfection ; Tumor Cells, Cultured
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  • 28
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    A truncated erythropoietin receptor and cell death (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwall, R -- New York, N.Y. -- Science. 1993 Jan 29;259(5095):696.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430322" target="_blank"〉PubMed〈/a〉
    Keywords: Bone Marrow/*physiology ; Cell Death/drug effects/*physiology ; Cell Division/drug effects ; Cell Survival/drug effects ; Erythropoietin/*pharmacology ; Humans ; Receptors, Erythropoietin/*genetics/*physiology ; Transfection
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  • 29
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    Altered growth of human colon cancer cell lines disrupted at activated Ki-ras (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-02
    Description: Point mutations that activate the Ki-ras proto-oncogene are presented in about 50 percent of human colorectal tumors. To study the functional significance of these mutations, the activated Ki-ras genes in two human colon carcinoma cell lines, DLD-1 and HCT 116, were disrupted by homologous recombination. Compared with parental cells, cells disrupted at the activated Ki-ras gene were morphologically altered, lost the capacity for anchorage-independent growth, grew more slowly both in vitro and in nude mice, and showed reduced expression of c-myc. Thus, the activated Ki-ras gene plays a key role in colorectal tumorigenesis through altered cell differentiation and cell growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shirasawa, S -- Furuse, M -- Yokoyama, N -- Sasazuki, T -- New York, N.Y. -- Science. 1993 Apr 2;260(5104):85-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Kyushu University, Fukuoka, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8465203" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Differentiation ; Cell Division ; Codon ; Colonic Neoplasms/*genetics/pathology ; Gene Expression Regulation, Neoplastic ; Genes, myc/genetics ; Genes, ras/*genetics ; Humans ; Infant ; Mice ; Mice, Nude ; Molecular Sequence Data ; Mutagenesis, Insertional ; Nucleic Acid Hybridization ; Plasmids ; *Point Mutation ; Polymerase Chain Reaction ; Restriction Mapping ; Transfection ; Tumor Cells, Cultured
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  • 30
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    A single phosphotyrosine residue of Stat91 required for gene activation by interferon-gamma (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-24
    Description: Interferon-gamma (IFN-gamma) stimulates transcription of specific genes by inducing tyrosine phosphorylation of a 91-kilodalton cytoplasmic protein (termed STAT for signal transducer and activator of transcription). Stat91 was phosphorylated on a single site (Tyr701), and phosphorylation of this site was required for nuclear translocation, DNA binding, and gene activation. Stat84, a differentially spliced product of the same gene that lacks the 38 carboxyl-terminal amino acids of Stat91, did not activate transcription, although it was phosphorylated and translocated to the nucleus and bound DNA. Thus, Stat91 mediates activation of transcription in response to IFN-gamma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shuai, K -- Stark, G R -- Kerr, I M -- Darnell, J E Jr -- AI32489-02/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 24;261(5129):1744-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rockefeller University, Laboratory of Molecular Cell Biology, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7690989" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Line ; Cell Nucleus/metabolism ; DNA-Binding Proteins/chemistry/*metabolism ; *Gene Expression Regulation ; Humans ; Interferon-gamma/*pharmacology ; Molecular Sequence Data ; Peptide Fragments/chemistry/metabolism ; Phosphotyrosine ; *Signal Transduction ; Transcription Factors/chemistry/*metabolism ; Transcriptional Activation ; Transfection ; Tyrosine/analogs & derivatives/chemistry
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    CD40 ligand gene defects responsible for X-linked hyper-IgM syndrome (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-12
    Description: The ligand for CD40 (CD40L) is a membrane glycoprotein on activated T cells that induces B cell proliferation and immunoglobulin secretion. Abnormalities in the CD40L gene were associated with an X-linked immunodeficiency in humans [hyper-IgM (immunoglobulin M) syndrome]. This disease is characterized by elevated concentrations of serum IgM and decreased amounts of all other isotypes. CD40L complementary DNAs from three of four patients with this syndrome contained distinct point mutations. Recombinant expression of two of the mutant CD40L complementary DNAs resulted in proteins incapable of binding to CD40 and unable to induce proliferation or IgE secretion from normal B cells. Activated T cells from the four affected patients failed to express wild-type CD40L, although their B cells responded normally to wild-type CD40L. Thus, these CD40L defects lead to a T cell abnormality that results in the failure of patient B cells to undergo immunoglobulin class switching.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allen, R C -- Armitage, R J -- Conley, M E -- Rosenblatt, H -- Jenkins, N A -- Copeland, N G -- Bedell, M A -- Edelhoff, S -- Disteche, C M -- Simoneaux, D K -- A125129/PHS HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 12;259(5097):990-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7679801" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*metabolism ; Antigens, CD40 ; Antigens, Differentiation, B-Lymphocyte/*metabolism ; Base Sequence ; CD40 Ligand ; DNA/chemistry/genetics ; Humans ; Immunoglobulin M/*blood ; Immunologic Deficiency Syndromes/*genetics/immunology ; Ligands ; Male ; Membrane Glycoproteins/*genetics ; Mice ; Molecular Sequence Data ; *Point Mutation ; Polymerase Chain Reaction ; T-Lymphocytes/*immunology ; Transfection ; *X Chromosome
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  • 32
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    Translocation of TCR alpha chains into the lumen of the endoplasmic reticulum and their degradation (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-03-26
    Description: After synthesis, the alpha chain of the T cell antigen receptor (TCR alpha) can form a complex with other TCR chains and move to the cell surface, or TCR alpha can undergo degradation in the endoplasmic reticulum (ER) if it remains unassembled. The mechanism of translocation and degradation in the ER is unclear. It was found that the putative transmembrane region of TCR alpha (alpha tm) was incompetent on its own to act as a transmembrane region. Molecules that contained alpha tm were translocated into the ER lumen and then underwent either rapid degradation or secretion, depending on the sequence of the cytoplasmic domain. A specific signal for ER degradation within alpha tm does not appear to be present.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shin, J -- Lee, S -- Strominger, J L -- AI20182/AI/NIAID NIH HHS/ -- CA47554/CA/NCI NIH HHS/ -- GM48961/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 26;259(5103):1901-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Tumor Virology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456316" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD4/chemistry/genetics/metabolism ; Cytoplasm/metabolism ; DNA/genetics ; Endoplasmic Reticulum/*metabolism ; Glycosylation ; HeLa Cells/metabolism ; Humans ; Immunosorbent Techniques ; Lipid Bilayers/metabolism ; Macromolecular Substances ; Mice ; Molecular Sequence Data ; Mutagenesis ; Protein Structure, Secondary ; Receptors, Antigen, T-Cell/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Transfection
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    Release of active cytokinin by a beta-glucosidase localized to the maize root meristem (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-12
    Description: A beta-glucoside encoded by a cloned Zea mays complementary DNA (Zm-p60.1) cleaved the biologically inactive hormone conjugates cytokinin-O-glucosides and kinetin-N3-glucoside, releasing active cytokinin. Tobacco protoplasts that transiently expressed Zm-p60.1 could use the inactive cytokinin glucosides to initiate cell division. The ability of protoplasts to sustain growth in response to cytokinin glucosides persisted indefinitely after the likely disappearance of the expression vector. In the roots of maize seedlings, Zm-p60.1 was localized to the meristematic cells and may function in vivo to supply the developing maize embryo with active cytokinin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brzobohaty, B -- Moore, I -- Kristoffersen, P -- Bako, L -- Campos, N -- Schell, J -- Palme, K -- New York, N.Y. -- Science. 1993 Nov 12;262(5136):1051-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck Institut fur Zuchtungsforschung, Koln Federal Republic of Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235622" target="_blank"〉PubMed〈/a〉
    Keywords: Adenine/analogs & derivatives/metabolism ; Amino Acid Sequence ; Base Sequence ; Cell Division ; Cytokinins/*metabolism ; DNA, Complementary/genetics ; Glucosides/metabolism ; Kinetin ; Molecular Sequence Data ; Plants, Toxic ; Protoplasts/cytology/enzymology ; Tobacco/cytology/enzymology ; Transfection ; Zea mays/enzymology/growth & development/*metabolism ; Zeatin/*metabolism ; beta-Glucosidase/genetics/*metabolism
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    Gene replacement in Toxoplasma gondii with chloramphenicol acetyltransferase as selectable marker (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-11-05
    Description: A system for stable transformation of Toxoplasma gondii tachyzoites was developed that exploited the susceptibility of Toxoplasma to chloramphenicol. Introduction of the chloramphenicol acetyltransferase (CAT) gene fused to Toxoplasma flanking sequences followed by chloramphenicol selection resulted in parasites stably expressing CAT. A construct incorporating the tandemly repeated gene, B1, targeted efficiently to its homologous chromosomal locus. Knockout of the single-copy gene, ROP1, was also successful. Stable transformation should permit the identification and analysis of Toxoplasma genes important in the interaction of this opportunistic parasite with its host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, K -- Soldati, D -- Boothroyd, J C -- New York, N.Y. -- Science. 1993 Nov 5;262(5135):911-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Stanford University School of Medicine 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235614" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chloramphenicol/pharmacology ; Chloramphenicol O-Acetyltransferase/*genetics ; Drug Resistance ; *Genes, Protozoan ; Genetic Markers ; Multigene Family ; Plasmids ; Recombination, Genetic ; Toxoplasma/drug effects/*genetics ; Transfection ; *Transformation, Genetic
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  • 35
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    Activation of a phosphotyrosine phosphatase by tyrosine phosphorylation (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-12
    Description: Regulation of cell proliferation, differentiation, and metabolic homeostasis is associated with the phosphorylation and dephosphorylation of specific tyrosine residues of key regulatory proteins. The phosphotyrosine phosphatase 1D (PTP 1D) contains two amino terminally located Src homology 2 (SH2) domains and is similar to the Drosophila corkscrew gene product, which positively regulates the torso tyrosine kinase signal transduction pathway. PTP activity was found to be regulated by physical interaction with a protein tyrosine kinase. PTP 1D did not dephosphorylate receptor tyrosine kinases, despite the fact that it associated with the epidermal growth factor receptor and chimeric receptors containing the extracellular domain of the epidermal growth factor receptor and the cytoplasmic domain of either the HER2-neu, kit-SCF, or platelet-derived growth factor beta (beta PDGF) receptors. PTP 1D was phosphorylated on tyrosine in cells overexpressing the beta PDGF receptor kinase and this tyrosine phosphorylation correlated with an enhancement of its catalytic activity. Thus, protein tyrosine kinases and phosphatases do not simply oppose each other's action; rather, they may work in concert to maintain a fine balance of effector activation needed for the regulation of cell growth and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, W -- Lammers, R -- Huang, J -- Ullrich, A -- New York, N.Y. -- Science. 1993 Mar 12;259(5101):1611-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Max-Planck-Institut fur Biochemie, Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7681217" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Chimera ; Drosophila/genetics ; Enzyme Activation ; Genes, src ; Humans ; Kidney ; Luminescent Measurements ; Mice ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Phosphorylation ; Phosphotyrosine ; Plasmids ; Protein Tyrosine Phosphatases/*metabolism ; Proto-Oncogene Proteins/genetics/metabolism ; Proto-Oncogene Proteins c-kit ; Proto-Oncogenes ; Receptor, Epidermal Growth Factor/genetics/metabolism ; Receptor, ErbB-2 ; Receptors, Platelet-Derived Growth Factor/genetics/metabolism ; Sequence Homology, Amino Acid ; Signal Transduction ; Transfection ; Tyrosine/*analogs & derivatives/metabolism
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  • 36
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    Cloning of a type I TGF-beta receptor and its effect on TGF-beta binding to the type II receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-28
    Description: Transforming growth factor-beta (TGF-beta) affects cellular proliferation, differentiation, and interaction with the extracellular matrix primarily through interaction with the type I and type II TGF-beta receptors. The type II receptors for TGF-beta and activin contain putative serine-threonine kinase domains. A murine serine-threonine kinase receptor, Tsk 7L, was cloned that shared a conserved extracellular domain with the type II TGF-beta receptor. Overexpression of Tsk 7L alone did not increase cell surface binding of TGF-beta, but coexpression with the type II TGF-beta receptor caused TGF-beta to bind to Tsk 7L, which had the size of the type I TGF-beta receptor. Overexpression of Tsk 7L inhibited binding of TGF-beta to the type II receptor in a dominant negative fashion. Combinatorial interactions and stoichiometric ratios between the type I and II receptors may therefore determine the extent of TGF-beta binding and the resulting biological activities.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ebner, R -- Chen, R H -- Shum, L -- Lawler, S -- Zioncheck, T F -- Lee, A -- Lopez, A R -- Derynck, R -- New York, N.Y. -- Science. 1993 May 28;260(5112):1344-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Growth and Development, University of California, San Francisco 94143-0640.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8388127" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cercopithecus aethiops ; Cloning, Molecular ; Humans ; Mice ; Molecular Sequence Data ; Protein-Serine-Threonine Kinases ; Quail ; Receptors, Cell Surface/chemistry/genetics/*metabolism ; Receptors, Transforming Growth Factor beta ; Transfection ; Transforming Growth Factor beta/*metabolism
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    Release of excess amyloid beta protein from a mutant amyloid beta protein precursor (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-01-22
    Description: The 4-kilodalton amyloid beta protein (A beta), which forms fibrillar deposits in Alzheimer's disease (AD), is derived from a large protein referred to as the amyloid beta protein precursor (beta APP). Human neuroblastoma (M17) cells transfected with constructs expressing wild-type beta APP or a mutant, beta APP delta NL, recently linked to familial AD were compared. After continuous metabolic labeling for 8 hours, cells expressing beta APP delta NL had five times more of an A beta-bearing, carboxyl terminal, beta APP derivative than cells expressing wild-type beta APP and they released six times more A beta into the medium. Thus this mutant beta APP may cause AD because its processing is altered in a way that releases increased amounts of A beta.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cai, X D -- Golde, T E -- Younkin, S G -- AG06656/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 22;259(5094):514-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuropathology, Case Western Reserve University, Cleveland, OH 44106.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8424174" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/genetics/metabolism ; Amino Acid Sequence ; Amyloid beta-Peptides/*biosynthesis/genetics ; Amyloid beta-Protein Precursor/*genetics/metabolism ; Base Sequence ; Cloning, Molecular ; Humans ; Molecular Sequence Data ; *Mutagenesis, Site-Directed ; Neuroblastoma ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction/methods ; Transfection ; Tumor Cells, Cultured
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    Anti-oncogenic and oncogenic potentials of interferon regulatory factors-1 and -2 (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-12
    Description: Interferon regulatory factor-1 (IRF-1), a transcriptional activator, and IRF-2, its antagonistic repressor, have been identified as regulators of type I interferon and interferon-inducible genes. The IRF-1 gene is itself interferon-inducible and hence may be one of the target genes critical for interferon action. When the IRF-2 gene was overexpressed in NIH 3T3 cells, the cells became transformed and displayed enhanced tumorigenicity in nude mice. This transformed phenotype was reversed by concomitant overexpression of the IRF-1 gene. Thus, restrained cell growth depends on a balance between these two mutually antagonistic transcription factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harada, H -- Kitagawa, M -- Tanaka, N -- Yamamoto, H -- Harada, K -- Ishihara, M -- Taniguchi, T -- New York, N.Y. -- Science. 1993 Feb 12;259(5097):971-4.〈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/8438157" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells/metabolism ; Animals ; Blotting, Northern ; Cell Transformation, Neoplastic/*genetics ; Chromosome Mapping ; Chromosomes, Human, Pair 5 ; DNA/biosynthesis ; DNA-Binding Proteins/*genetics ; *Gene Expression ; Humans ; Immunosorbent Techniques ; Interferon Regulatory Factor-1 ; Interferon Regulatory Factor-2 ; Mice ; Mice, Nude ; Phenotype ; Phosphoproteins/*genetics ; Promoter Regions, Genetic ; RNA, Messenger/genetics ; *Repressor Proteins ; *Transcription Factors ; Transfection
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    Induction of apoptosis by the low-affinity NGF receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-16
    Description: Nerve growth factor (NGF) binding to cellular receptors is required for the survival of some neural cells. In contrast to TrkA, the high-affinity NGF receptor that transduces NGF signals for survival and differentiation, the function of the low-affinity NGF receptor, p75NGFR, remains uncertain. Expression of p75NGFR induced neural cell death constitutively when p75NGFR was unbound; binding by NGF or monoclonal antibody, however, inhibited cell death induced by p75NGFR. Thus, expression of p75NGFR may explain the dependence of some neural cells on NGF for survival. These findings also suggest that p75NGFR has some functional similarities to other members of a superfamily of receptors that include tumor necrosis factor receptors, Fas (Apo-1), and CD40.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rabizadeh, S -- Oh, J -- Zhong, L T -- Yang, J -- Bitler, C M -- Butcher, L L -- Bredesen, D E -- AG10671/AG/NIA NIH HHS/ -- NS10928/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 16;261(5119):345-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8332899" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis/drug effects ; Cell Line ; Cell Survival/drug effects ; Culture Media, Serum-Free ; Nerve Growth Factors/*metabolism/pharmacology ; Neurons/*cytology/drug effects/metabolism ; PC12 Cells ; Receptors, Nerve Growth Factor/metabolism/*physiology ; Transfection
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    Regulation of heat shock factor trimer formation: role of a conserved leucine zipper (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-08
    Description: The human and Drosophila heat shock transcription factors (HSFs) are multi-zipper proteins with high-affinity binding to DNA that is regulated by heat shock-induced trimerization. Formation of HSF trimers is dependent on hydrophobic heptad repeats located in the amino-terminal region of the protein. Two subregions at the carboxyl-terminal end of human HSF1 were identified that maintain the monomeric form of the protein under normal conditions. One of these contains a leucine zipper motif that is conserved between vertebrate and insect HSFs. These results suggest that the carboxyl-terminal zipper may suppress formation of trimers by the amino-terminal HSF zipper elements by means of intramolecular coiled-coil interactions that are sensitive to heat shock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rabindran, S K -- Haroun, R I -- Clos, J -- Wisniewski, J -- Wu, C -- New York, N.Y. -- Science. 1993 Jan 8;259(5092):230-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8421783" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Cell Line ; DNA/metabolism ; Drosophila/chemistry ; Heat-Shock Proteins/*chemistry/genetics/metabolism ; Hot Temperature ; Humans ; *Leucine Zippers ; Macromolecular Substances ; Molecular Sequence Data ; Mutagenesis ; Structure-Activity Relationship ; Transfection
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    Cyclin-dependent regulation of G1 in mammalian fibroblasts (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-26
    Description: Eukaryotic cells become committed to proliferate during the G1 phase of the cell cycle. In budding yeast, commitment occurs when the catalytic subunit of a protein kinase, encoded by the CDC28 gene (the homolog of the fission yeast cdc2+ gene), binds to a positively acting regulatory subunit, a cyclin. Related kinases are also required for progression through the G1 phase in higher eukaryotes. The role of cyclins in controlling G1 progression in mammalian cells was tested by construction of fibroblasts that constitutively overexpress human cyclin E. This was found to shorten the duration of G1, decrease cell size, and diminish the serum requirement for the transition from G1 to S phase. These observations show that cyclin levels can be rate-limiting for G1 progression in mammalian cells and suggest that cyclin synthesis may be the target of physiological signals that control cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ohtsubo, M -- Roberts, J M -- New York, N.Y. -- Science. 1993 Mar 26;259(5103):1908-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8384376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/physiology ; Cell Line ; Cloning, Molecular ; Cyclins/genetics/*physiology ; Fibroblasts/*cytology/metabolism ; Flow Cytometry ; G1 Phase/*physiology ; Gene Expression ; Genetic Vectors ; Humans ; Kanamycin Kinase ; Male ; Phosphotransferases/genetics ; Rats ; Recombinant Fusion Proteins/metabolism ; Retroviridae/genetics ; S Phase/physiology ; Time Factors ; Transfection
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    HLA-A11 epitope loss isolates of Epstein-Barr virus from a highly A11+ population (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-04-02
    Description: Cytotoxic T lymphocytes (CTLs) control viral infections by recognizing viral peptides presented by major histocompatibility complex (MHC) class I molecules. Human leukocyte antigen (HLA)-A11-restricted CTLs that recognize peptide residues 416 to 424 of the Epstein-Barr virus (EBV) nuclear antigen-4 frequently dominate EBV-induced responses in A11+ Caucasian donors. This epitope is conserved in type A EBV strains from Caucasians and central African populations, where A11 is relatively infrequent. However, strains from highly A11+ populations in New Guinea carry a lysine-to-threonine mutation at residue 424 that abrogates CTL recognition and binding of the peptide to nascent A11 molecules. The results suggest that evolution of a widespread and genetically stable virus such as EBV is influenced by pressure from MHC-restricted CTL responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Campos-Lima, P O -- Gavioli, R -- Zhang, Q J -- Wallace, L E -- Dolcetti, R -- Rowe, M -- Rickinson, A B -- Masucci, M G -- 2RO1 CA30264/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 2;260(5104):98-100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7682013" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Antigens, Viral/genetics/*immunology ; Cell Line, Transformed ; Cell Nucleus/*immunology ; Cell Transformation, Viral ; DNA-Binding Proteins/genetics/*immunology ; Epitopes/genetics/immunology ; Epstein-Barr Virus Nuclear Antigens ; European Continental Ancestry Group ; Gene Frequency ; HLA-A Antigens/genetics/*immunology ; HLA-A11 Antigen ; Herpesvirus 4, Human/*immunology ; Humans ; New Guinea ; Point Mutation ; T-Lymphocytes, Cytotoxic/*immunology ; Transfection
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    Mineralocorticoid and glucocorticoid receptor activities distinguished by nonreceptor factors at a composite response element (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-02-19
    Description: Mineralocorticoid and glucocorticoid hormones elicit distinct physiologic responses, yet the mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) bind to and activate transcription similarly from a consensus simple hormone response element (HRE). The activities of GR and MR at plfG, a 25-base pair composite response element to which both the steroid receptors and transcription factor AP1 can bind, are analyzed here. Under conditions in which GR represses AP1-stimulated transcription from plfG, MR was inactive. With the use of MR-GR chimeras, a segment of the NH2-terminal region of GR (amino acids 105 to 440) was shown to be required for this repression. Thus, the distinct physiologic effects mediated by MR and GR may be determined by differential interactions of nonreceptor factors with specific receptor domains at composite response elements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pearce, D -- Yamamoto, K R -- New York, N.Y. -- Science. 1993 Feb 19;259(5098):1161-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco 94143-0448.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8382376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chloramphenicol O-Acetyltransferase/genetics/metabolism ; Corticosterone/*pharmacology ; DNA/*metabolism ; DNA-Binding Proteins/*metabolism ; HeLa Cells ; Humans ; Hydrocortisone/*pharmacology ; Mineralocorticoids/*metabolism ; Plasmids ; Proto-Oncogene Proteins c-jun/*metabolism ; Receptors, Glucocorticoid/genetics/*metabolism ; Receptors, Mineralocorticoid ; Receptors, Steroid/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; *Transcription, Genetic/drug effects ; Transfection ; Zinc Fingers/genetics/physiology
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    A link between cyclin A expression and adhesion-dependent cell cycle progression (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-12-03
    Description: Cell adhesion has an essential role in regulating proliferation during the G1 phase of the cell cycle, and loss of this adhesion requirement is a classic feature of oncogenic transformation. The appearance of cyclin A messenger RNA and protein in late G1 was dependent on cell adhesion in both NRK and NIH 3T3 fibroblasts. In contrast, the expression of Cdc2, Cdk2, cyclin D1, and cyclin E was independent of adhesion in both cell lines. Transfection of NRK cells with a cyclin A complementary DNA resulted in adhesion-independent accumulation of cyclin A protein and cyclin A-associated kinase activity. These transfected cells also entered S phase and complete multiple rounds of cell division in the absence of cell adhesion. Thus, cyclin A is a target of the adhesion-dependent signals that control cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guadagno, T M -- Ohtsubo, M -- Roberts, J M -- Assoian, R K -- GM48224/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Dec 3;262(5139):1572-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8248807" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; CDC2 Protein Kinase/biosynthesis ; *CDC2-CDC28 Kinases ; Cell Adhesion/*physiology ; Cell Cycle/*physiology ; Cell Line ; Cyclin-Dependent Kinase 2 ; *Cyclin-Dependent Kinases ; Cyclins/*biosynthesis ; Fibroblasts/cytology/metabolism ; Gene Expression Regulation ; Humans ; Mice ; Protein Kinases/biosynthesis ; *Protein-Serine-Threonine Kinases ; Rats ; Transfection
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    IRS-1: essential for insulin- and IL-4-stimulated mitogenesis in hematopoietic cells (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-09-17
    Description: Although several interleukin-3 (IL-3)-dependent cell lines proliferate in response to IL-4 or insulin, the 32D line does not. Insulin and IL-4 sensitivity was restored to 32D cells by expression of IRS-1, the principal substrate of the insulin receptor. Although 32D cells possessed receptors for both factors, they lacked the IRS-1--related protein, 4PS, which becomes phosphorylated by tyrosine in insulin- or IL-4--responsive lines after stimulation. These results indicate that factors that bind unrelated receptors can use similar mitogenic signaling pathways in hematopoietic cells and that 4PS and IRS-1 are functionally similar proteins that are essential for insulin- and IL-4--induced proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, L M -- Myers, M G Jr -- Sun, X J -- Aaronson, S A -- White, M -- Pierce, J H -- DK-43808/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 17;261(5128):1591-4.〈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/8372354" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/drug effects ; Cell Line ; Hematopoietic Stem Cells/*cytology/drug effects ; Insulin/*pharmacology ; Insulin Receptor Substrate Proteins ; Interleukin-4/*pharmacology ; Phosphoproteins/*metabolism ; Phosphorylation ; Receptor, Insulin/metabolism ; Receptors, Interleukin-4 ; Receptors, Mitogen/metabolism ; Transfection ; Tyrosine/metabolism
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    Inactivation of the type II receptor reveals two receptor pathways for the diverse TGF-beta activities (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-05-28
    Description: Transforming growth factor-beta (TGF-beta) is a multifunctional protein that regulates cell proliferation and differentiation and extracellular matrix production. Although two receptor types, the type I and type II receptors, have been implicated in TGF-beta-induced signaling, it is unclear how the many activities of TGF-beta are mediated through these receptors. With the use of cells overexpressing truncated type II receptors as dominant negative mutants to selectively block type II receptor signaling, the existence of two receptor pathways was shown. The type II receptors, possibly in conjunction with type I receptors, mediate the induction of growth inhibition and hypophosphorylation of the retinoblastoma gene product pRB. The type I receptors are responsible for effects on extracellular matrix, such as the induction of fibronectin and plasminogen activator inhibitor I, and for increased JunB expression. Selective inactivation of the type II receptors alters the TGF-beta response in a similar manner to the functional inactivation of pRB, suggesting a role for pRB in the type II, but not the type I, receptor pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, R H -- Ebner, R -- Derynck, R -- New York, N.Y. -- Science. 1993 May 28;260(5112):1335-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Growth and Development, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8388126" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/drug effects ; Cell Line ; DNA/biosynthesis ; Down-Regulation ; Fibronectins/biosynthesis ; Plasminogen Activator Inhibitor 1/biosynthesis ; Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins c-jun/genetics ; Receptors, Cell Surface/genetics/*physiology ; *Receptors, Transforming Growth Factor beta ; Retinoblastoma Protein/metabolism ; Signal Transduction ; Transfection ; Transforming Growth Factor beta/*pharmacology/physiology
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    SH2-containing phosphotyrosine phosphatase as a target of protein-tyrosine kinases (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-03-12
    Description: A mouse phosphotyrosine phosphatase containing two Src homology 2 (SH2) domains, Syp, was identified. Syp bound to autophosphorylated epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) receptors through its SH2 domains and was rapidly phosphorylated on tyrosine in PDGF- and EGF-stimulated cells. Furthermore, Syp was constitutively phosphorylated on tyrosine in cells transformed by v-src. This mammalian phosphatase is most closely related, especially in its SH2 domains, to the corkscrew (csw) gene product of Drosophila, which is required for signal transduction downstream of the Torso receptor tyrosine kinase. The Syp gene is widely expressed throughout embryonic mouse development and in adult tissues. Thus, Syp may function in mammalian embryonic development and as a common target of both receptor and nonreceptor tyrosine kinases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng, G S -- Hui, C C -- Pawson, T -- New York, N.Y. -- Science. 1993 Mar 12;259(5101):1607-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular and Developmental Biology, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8096088" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line, Transformed ; Cell Transformation, Neoplastic ; Embryo, Mammalian ; Embryonic and Fetal Development ; Epidermal Growth Factor/pharmacology ; *Genes, src ; Humans ; Intracellular Signaling Peptides and Proteins ; Kinetics ; Mice ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Phosphorylation ; Platelet-Derived Growth Factor/pharmacology ; Poly A/isolation & purification/metabolism ; Polymerase Chain Reaction ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 ; Protein Tyrosine Phosphatases/genetics/*metabolism ; Protein-Tyrosine Kinases/*metabolism ; RNA, Messenger/isolation & purification/metabolism ; Rats ; Receptor, Epidermal Growth Factor/metabolism ; Receptors, Platelet-Derived Growth Factor/genetics/metabolism ; Sequence Homology, Amino Acid ; Transfection
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    Germ line transmission of a yeast artificial chromosome spanning the murine alpha 1(I) collagen locus (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-03-26
    Description: Molecular complementation of mutant phenotypes by transgenic technology is a potentially important tool for gene identification. A technology was developed that allows the transfer of a physically intact yeast artificial chromosome (YAC) into the germ line of the mouse. A purified 150-kilobase YAC encompassing the murine gene Col1a1 was efficiently introduced into embryonic stem (ES) cells via lipofection. Chimeric founder mice were derived from two transfected ES cell clones. These chimeras transmitted the full length transgene through the germ line, generating two transgenic mouse strains. Transgene expression was visualized as nascent transcripts in interphase nuclei and quantitated by ribonuclease protection analysis. Both assays indicated that the transgene was expressed at levels comparable to the endogenous collagen gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strauss, W M -- Dausman, J -- Beard, C -- Johnson, C -- Lawrence, J B -- Jaenisch, R -- 5 F32 GM13756-02/GM/NIGMS NIH HHS/ -- 5 R35 CA44339-05/CA/NCI NIH HHS/ -- HG00198-01/HG/NHGRI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Mar 26;259(5103):1904-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8096090" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/metabolism ; Blotting, Southern ; Chromosomes, Fungal ; Collagen/*genetics ; *Gene Expression ; Gene Library ; In Situ Hybridization ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutagenesis, Insertional ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Transfection
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    NF-kappa B controls expression of inhibitor I kappa B alpha: evidence for an inducible autoregulatory pathway (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-03-26
    Description: The eukaryotic transcription factor nuclear factor-kappa B (NF-kappa B) participates in many parts of the genetic program mediating T lymphocyte activation and growth. Nuclear expression of NF-kappa B occurs after its induced dissociation from its cytoplasmic inhibitor I kappa B alpha. Phorbol ester and tumor necrosis factor-alpha induction of nuclear NF-kappa B is associated with both the degradation of performed I kappa B alpha and the activation of I kappa B alpha gene expression. Transfection studies indicate that the I kappa B alpha gene is specifically induced by the 65-kilodalton transactivating subunit of NF-kappa B. Association of the newly synthesized I kappa B alpha with p65 restores intracellular inhibition of NF-kappa B DNA binding activity and prolongs the survival of this labile inhibitor. Together, these results show that NF-kappa B controls the expression of I kappa B alpha by means of an inducible autoregulatory pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, S C -- Ganchi, P A -- Ballard, D W -- Greene, W C -- 5T32CA09111/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 26;259(5103):1912-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Virology and Immunology, University of California, San Francisco.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8096091" target="_blank"〉PubMed〈/a〉
    Keywords: CD4-Positive T-Lymphocytes/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Cycloheximide/pharmacology ; Cytoplasm/metabolism ; DNA/metabolism ; DNA-Binding Proteins/*genetics ; *Gene Expression Regulation ; Humans ; *I-kappa B Proteins ; Immunoblotting ; Kinetics ; Molecular Weight ; Mutagenesis ; NF-kappa B/*antagonists & inhibitors/genetics/*physiology ; RNA, Messenger/biosynthesis ; Tetradecanoylphorbol Acetate/pharmacology ; Trans-Activators/pharmacology ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology
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    The effect of posttranslational modifications on the interaction of Ras2 with adenylyl cyclase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-29
    Description: Ras proteins undergo a series of posttranslational modifications that are critical for their cellular function. These modifications are necessary to anchor Ras proteins to the membrane. Yeast Ras2 proteins were purified with various degrees of modification and examined for their ability to activate their effector, adenylyl cyclase. The farnesylated intermediate form of Ras2 had more than 100 times higher affinity for adenylyl cyclase than for the unprocessed form. The subsequent palmitoylation reaction had little effect. In contrast, palmitoylation was required for efficient membrane localization of the Ras2 protein. These results indicate the importance of farnesylation in the interaction of Ras2 with its effector.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuroda, Y -- Suzuki, N -- Kataoka, T -- New York, N.Y. -- Science. 1993 Jan 29;259(5095):683-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Kobe University School of Medicine, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430318" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/genetics/isolation & purification/*metabolism ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cell Membrane/enzymology ; Electrophoresis, Polyacrylamide Gel ; Enzyme Activation ; Fungal Proteins/genetics/isolation & purification/*metabolism ; GTP-Binding Proteins/genetics/*metabolism ; Genes, Fungal ; Guanosine 5'-O-(3-Thiotriphosphate)/metabolism ; Insects ; Kinetics ; Molecular Sequence Data ; Molecular Weight ; Oligodeoxyribonucleotides ; Palmitic Acid ; Palmitic Acids/metabolism ; Protein Binding ; *Protein Processing, Post-Translational ; Recombinant Fusion Proteins/isolation & purification/metabolism ; Saccharomyces cerevisiae/genetics/*metabolism ; *Saccharomyces cerevisiae Proteins ; Transfection ; *ras Proteins
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    Deficiency in rhabdomyosarcomas of a factor required for MyoD activity and myogenesis (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-05
    Description: Rhabdomyosarcoma cells express the myogenic helix-loop-helix proteins of the MyoD family but do not differentiate into skeletal muscle cells. Gel shift and transient transfection assays revealed that MyoD in the rhabdomyosarcoma cells was capable of binding DNA but was relatively nonfunctional as a transcriptional activator. Heterokaryon formation with fibroblasts resulted in the restoration of transcriptional activation by MyoD and the differentiation of the rhabdomyosarcoma cells into skeletal muscle cells. These results suggest that rhabdomyosarcomas are deficient in a factor required for MyoD activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tapscott, S J -- Thayer, M J -- Weintraub, H -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1450-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center, Seattle, WA 98104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8383879" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cell Differentiation ; Cell Nucleus/metabolism/ultrastructure ; Chloramphenicol O-Acetyltransferase/genetics/metabolism ; Humans ; Mice ; Muscle Proteins/genetics/*metabolism ; Muscles/pathology ; MyoD Protein ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/metabolism ; Rhabdomyosarcoma/genetics/*metabolism/pathology ; Transcription Factors/*metabolism ; Transcription, Genetic ; 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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    Regulation of gene expression in hippocampal neurons by distinct calcium signaling pathways (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-09
    Description: Calcium ions (Ca2+) act as an intracellular second messenger and can enter neurons through various ion channels. Influx of Ca2+ through distinct types of Ca2+ channels may differentially activate biochemical processes. N-Methyl-D-aspartate (NMDA) receptors and L-type Ca2+ channels, two major sites of Ca2+ entry into hippocampal neurons, were found to transmit signals to the nucleus and regulated gene transcription through two distinct Ca2+ signaling pathways. Activation of the multifunctional Ca(2+)-calmodulin-dependent protein kinase (CaM kinase) was evoked by stimulation of either NMDA receptors or L-type Ca2+ channels; however, activation of CaM kinase appeared to be critical only for propagating the L-type Ca2+ channel signal to the nucleus. Also, the NMDA receptor and L-type Ca2+ channel pathways activated transcription by means of different cis-acting regulatory elements in the c-fos promoter. These results indicate that Ca2+, depending on its mode of entry into neurons, can activate two distinct signaling pathways. Differential signal processing may provide a mechanism by which Ca2+ controls diverse cellular functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bading, H -- Ginty, D D -- Greenberg, M E -- 2F32 NS 08764/NS/NINDS NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 9;260(5105):181-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8097060" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/metabolism ; Calcium-Calmodulin-Dependent Protein Kinases ; Cells, Cultured ; DNA-Binding Proteins/genetics ; *Gene Expression Regulation ; Genes, fos ; Glutamates/pharmacology ; Glutamic Acid ; Hippocampus/*metabolism ; Neurons/*metabolism ; Nuclear Proteins/genetics ; Protein Kinases/metabolism ; Rats ; Receptors, N-Methyl-D-Aspartate/metabolism ; Regulatory Sequences, Nucleic Acid ; Second Messenger Systems ; Serum Response Factor ; *Signal Transduction ; Transcription Factors/genetics ; Transfection
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    Rescue of signaling by a chimeric protein containing the cytoplasmic domain of CD45 (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-23
    Description: Surface expression of the CD45 tyrosine phosphatase is essential for the T cell antigen receptor (TCR) to couple optimally with its second messenger pathways. CD45 may be required to dephosphorylate a TCR-activated protein tyrosine kinase, which then transduces an activation signal from the TCR. A chimeric molecule that contained extracellular and transmembrane sequences from an allele of a major histocompatibility class I molecule and cytoplasmic sequences of CD45 restored TCR signaling in a CD45-deficient mutant T cell line. Thus, expression of the complex extracellular domain of CD45 is not required for the TCR to couple to its signaling machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hovis, R R -- Donovan, J A -- Musci, M A -- Motto, D G -- Goldman, F D -- Ross, S E -- Koretzky, G A -- CA56050-01/CA/NCI NIH HHS/ -- CA56843-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 23;260(5107):544-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8475387" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD45/genetics/*metabolism ; Base Sequence ; Cell Line ; Cell Membrane/metabolism ; Cytoplasm/metabolism ; Enzyme Activation ; Humans ; Inositol Phosphates/metabolism ; Membrane Proteins/metabolism ; Molecular Sequence Data ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Recombinant Fusion Proteins/metabolism ; Second Messenger Systems ; *Signal Transduction ; T-Lymphocytes/*metabolism ; Transfection ; Tyrosine/metabolism
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    Signal sequence trap: a cloning strategy for secreted proteins and type I membrane proteins (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-30
    Description: A method was developed to clone, without the use of specific functional assays, complementary DNAs (cDNAs) that carry specific amino-terminal signal sequences, such as those encoding intercellular signal-transducing molecules and receptors. The vector used in this system directed the cell surface expression of interleukin-2 receptor fusion proteins when inserts with signal sequences were cloned in-frame with the correct orientation. An expression cDNA library was constructed from a bone marrow stromal cell line, which contained 5' portion-enriched cDNAs (the average size was 400 base pairs). Two cDNAs that encoded putative cytokine molecules, stromal cell-derived factor-1 alpha (SDF-1 alpha) and SDF-1 beta, which belong to the intercrine-macrophage inflammatory protein superfamily, were cloned.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tashiro, K -- Tada, H -- Heilker, R -- Shirozu, M -- Nakano, T -- Honjo, T -- New York, N.Y. -- Science. 1993 Jul 30;261(5121):600-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Kyoto University Faculty of Medicine, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8342023" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Chemokine CXCL12 ; *Chemokines, CXC ; Cloning, Molecular/*methods ; Cytokines/chemistry/*genetics ; Genetic Vectors ; Molecular Sequence Data ; Open Reading Frames ; Protein Sorting Signals/chemistry/*genetics/metabolism ; Receptors, Interleukin-2/genetics ; Recombinant Fusion Proteins/biosynthesis ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Repression of MHC class I gene promoter activity by two-exon Tat of HIV (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-28
    Description: Major histocompatibility complex (MHC) class I molecules are the major receptors for viral peptides and serve as targets for specific cytotoxic T lymphocytes. Human immunodeficiency virus-type 1 (HIV-1) specifically decreased activity of an MHC class I gene promoter up to 12-fold. Repression was effected by the HIV-1 Tat protein derived from a spliced viral transcript (two-exon Tat). These studies define an activity for two-exon Tat distinct from that of one-exon Tat and suggest a mechanism whereby HIV-1-infected cells might be able to avoid immune surveillance, allowing the virus to persist in the infected host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Howcroft, T K -- Strebel, K -- Martin, M A -- Singer, D S -- New York, N.Y. -- Science. 1993 May 28;260(5112):1320-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493575" target="_blank"〉PubMed〈/a〉
    Keywords: Exons ; *Gene Expression Regulation ; Gene Products, tat/*genetics/physiology ; Genes, MHC Class I/*genetics ; Genes, tat ; HIV-1/*genetics ; HeLa Cells ; Humans ; *Promoter Regions, Genetic ; Regulatory Sequences, Nucleic Acid ; Transfection ; tat Gene Products, Human Immunodeficiency Virus
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    PAC-1: a mitogen-induced nuclear protein tyrosine phosphatase (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-03-19
    Description: Tyrosine phosphorylation of proteins is required for signal transduction in cells and for growth regulation. A mitogen-induced gene (PAC-1) has been cloned from human T cells and encodes a 32-kilodalton protein that contains a sequence that defines the enzymatic site of known protein phosphotyrosine phosphatases (PTPases). Other than this sequence, PAC-1 is different from several other known related PTPases exemplified by PTP-1b. PAC-1 is similar to a phosphatase induced by mitogens or heat shock in fibroblasts, a yeast gene, and a vaccinia virus-encoded serine-tyrosine phosphatase (VH1). PAC-1 was predominantly expressed in hematopoietic tissues and localized to the nucleus in transfected COS-7 cells and in mitogen-stimulated T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rohan, P J -- Davis, P -- Moskaluk, C A -- Kearns, M -- Krutzsch, H -- Siebenlist, U -- Kelly, K -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1763-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Pathology, National Cancer Institute, NIH, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7681221" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Cell Line ; Cell Nucleus/enzymology ; Conserved Sequence ; Cytoplasm/enzymology ; Dual Specificity Phosphatase 2 ; Fluorescent Antibody Technique ; Humans ; Immunosorbent Techniques ; Mice ; Mitogens/*pharmacology ; Molecular Sequence Data ; Organ Specificity ; Protein Phosphatase 2 ; Protein Tyrosine Phosphatases/chemistry/*genetics ; RNA/analysis ; Sequence Homology, Amino Acid ; Signal Transduction/physiology ; T-Lymphocytes/enzymology ; Transfection
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  • 57
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    G protein-coupled signal transduction pathways for interleukin-8 (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-07-02
    Description: Interleukin-8 (IL-8) is one of the major mediators of the inflammatory response. The pathways by which IL-8 activates inositide-specific phospholipase C (PLC) were investigated by co-expression of different components of the guanosine triphosphate binding protein (G protein) pathway in COS-7 cells. Two distinct IL-8 receptors reconstituted ligand-dependent activation of endogenous PLC when transfected together with the G protein alpha subunits G alpha 14, G alpha 15, or G alpha 16. However, reconstitution was not observed with cells that overexpressed G alpha q or G alpha 11. Furthermore, IL-8 receptors interacted with endogenous pertussis toxin-sensitive G proteins or with the recombinant G protein Gi to release free beta gamma subunits that could then specifically activate the beta 2 isoform of PLC. These findings suggest that IL-8 acts through signal-transducing pathways that are limited to specific heterotrimeric G proteins and effectors. These may provide suitable targets for the development of anti-inflammatory agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, D -- LaRosa, G J -- Simon, M I -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):101-3.〈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/8316840" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Enzyme Activation ; GTP-Binding Proteins/genetics/*metabolism ; Interleukin-8/*metabolism/pharmacology ; Pertussis Toxin ; Receptors, Immunologic/genetics/*metabolism ; Receptors, Interleukin-8A ; Recombinant Proteins/metabolism ; *Signal Transduction ; Transfection ; Type C Phospholipases/metabolism ; Virulence Factors, Bordetella/pharmacology
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    Binding of the Ras activator son of sevenless to insulin receptor substrate-1 signaling complexes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-25
    Description: Signal transmission by insulin involves tyrosine phosphorylation of a major insulin receptor substrate (IRS-1) and exchange of Ras-bound guanosine diphosphate for guanosine triphosphate. Proteins containing Src homology 2 and 3 (SH2 and SH3) domains, such as the p85 regulatory subunit of phosphatidylinositol-3 kinase and growth factor receptor-bound protein 2 (GRB2), bind tyrosine phosphate sites on IRS-1 through their SH2 regions. Such complexes in COS cells were found to contain the heterologously expressed putative guanine nucleotide exchange factor encoded by the Drosophila son of sevenless gene (dSos). Thus, GRB2, p85, or other proteins with SH2-SH3 adapter sequences may link Sos proteins to IRS-1 signaling complexes as part of the mechanism by which insulin activates Ras.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baltensperger, K -- Kozma, L M -- Cherniack, A D -- Klarlund, J K -- Chawla, A -- Banerjee, U -- Czech, M P -- DK 30648/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1950-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular Medicine, University of Massachusetts Medical Center, Worcester 01605.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8391166" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Cell Line ; GRB2 Adaptor Protein ; Guanosine Triphosphate/metabolism ; Insulin/pharmacology ; Insulin Receptor Substrate Proteins ; Membrane Proteins/*metabolism ; Phosphatidylinositol 3-Kinases ; Phosphoproteins/*metabolism ; Phosphorylation ; Phosphotransferases/metabolism ; Proteins/metabolism ; Proto-Oncogene Proteins p21(ras)/*metabolism ; Receptor, Insulin/*metabolism ; Signal Transduction ; Son of Sevenless Proteins ; Transfection ; Tyrosine/metabolism
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    Skepticism greets HIV coreceptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, M -- New York, N.Y. -- Science. 1993 Nov 5;262(5135):843-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7901911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/genetics/metabolism ; Antigens, Differentiation, T-Lymphocyte/genetics/*metabolism ; Dipeptidyl Peptidase 4 ; HIV/*metabolism/physiology ; Humans ; Mice ; Receptors, HIV/*metabolism ; Transfection ; Virus Replication
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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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    Primary structure and biochemical properties of an M2 muscarinic receptor (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-01
    Description: A partial amino acid sequence obtained for porcine atrial muscarinic acetylcholine receptor was used to isolate complementary DNA clones containing the complete receptor coding region. The deduced 466-amino acid polypeptide exhibits extensive structural and sequence homology with other receptors coupled to guanine nucleotide binding (G) proteins (for example, the beta-adrenergic receptor and rhodopsins); this similarity predicts a structure of seven membrane-spanning regions distinguished by the disposition of a large cytoplasmic domain. Stable transfection of the Chinese hamster ovary cell line with the atrial receptor complementary DNA leads to the binding of muscarinic antagonists in these cells with affinities characteristic of the M2 receptor subtype. The atrial muscarinic receptor is encoded by a unique gene consisting of a single coding exon and multiple, alternatively spliced 5' noncoding regions. The atrial receptor is distinct from the cerebral muscarinic receptor gene product, sharing only 38% overall amino acid homology and possessing a completely nonhomologous large cytoplasmic domain, suggesting a role for the latter region in differential effector coupling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peralta, E G -- Winslow, J W -- Peterson, G L -- Smith, D H -- Ashkenazi, A -- Ramachandran, J -- Schimerlik, M I -- Capon, D J -- CA16417/CA/NCI NIH HHS/ -- HL23632/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 May 1;236(4801):600-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107123" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA/genetics ; Exons ; GTP-Binding Proteins/metabolism ; Heart Atria/analysis ; Immunosorbent Techniques ; Membrane Proteins ; Molecular Weight ; Nucleic Acid Hybridization ; Peptide Fragments/metabolism ; Quinuclidinyl Benzilate/metabolism ; Receptors, Muscarinic/*genetics/metabolism ; Sequence Homology, Nucleic Acid ; Swine ; Transfection
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  • 62
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    Identification of a family of muscarinic acetylcholine receptor genes (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-31
    Description: Complementary DNAs for three different muscarinic acetylcholine receptors were isolated from a rat cerebral cortex library, and the cloned receptors were expressed in mammalian cells. Analysis of human and rat genomic clones indicates that there are at least four functional muscarinic receptor genes and that these genes lack introns in the coding sequence. This gene family provides a new basis for evaluating the diversity of muscarinic mechanisms in the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonner, T I -- Buckley, N J -- Young, A C -- Brann, M R -- New York, N.Y. -- Science. 1987 Jul 31;237(4814):527-32.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3037705" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/metabolism ; Cloning, Molecular ; Codon ; Dna ; DNA Restriction Enzymes ; *Genes ; Genetic Code ; Humans ; Models, Molecular ; Nucleic Acid Hybridization ; Rats ; Receptors, Muscarinic/classification/*genetics ; Swine ; Transfection
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    Mitogens and oncogenes can block the induction of specific voltage-gated ion channels (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-01
    Description: The mechanisms underlying the ontogeny of voltage-gated ion channels in muscle are unknown. Whether expression of voltage-gated channels is dependent on mitogen withdrawal and growth arrest, as is generally true for the induction of muscle-specific gene products, was investigated in the BC3H1 muscle cell line by patch-clamp techniques. Differentiated BC3H1 myocytes expressed functional Ca2+ and Na+ channels that correspond to those found in T tubules of skeletal muscle. However, Ca2+ and Na+ channels were first detected after about 5 days of mitogen withdrawal. In order to test whether cellular oncogenes, as surrogates for exogenous growth factors, could prevent the expression of ion channels whose induction was contingent on mitogen withdrawal, BC3H1 cells were modified by stable transfection with oncogene expression vectors. Expression vectors containing v-erbB, or c-myc under the control of the SV40 promoter, delayed but did not prevent the appearance of functional Ca2+ and Na+ channels. In contrast, transfection with a Val12 c-H-ras vector, or cotransfection of c-myc together with v-erbB, suppressed the formation of functional Ca2+ and Na+ channels for greater than or equal to 4 weeks. Potassium channels were affected neither by mitogenic medium nor by transfected oncogenes. Thus, the selective effects of certain oncogenes on ion channel induction corresponded to the suppressive effects of mitogenic medium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caffrey, J M -- Brown, A M -- Schneider, M D -- HL36475/HL/NHLBI NIH HHS/ -- HL37044/HL/NHLBI NIH HHS/ -- RR-05425/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 May 1;236(4801):570-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2437651" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium/metabolism ; Cell Line ; Electric Conductivity ; Growth Substances/physiology ; Ion Channels/*physiology ; Mitogens/*pharmacology ; Muscles/*physiology ; *Oncogenes ; Potassium/metabolism ; Sodium/metabolism ; Transfection
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    The CML-specific P210 bcr/abl protein, unlike v-abl, does not transform NIH/3T3 fibroblasts (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-31
    Description: The v-abl oncogene of the Abelson murine leukemia virus (A-MuLV) is known to efficiently transform NIH/3T3 fibroblasts in vitro and to cause an acute lymphosarcoma in susceptible murine hosts. The role of its relative, the bcr/abl gene product, in the etiology of human chronic myelogenous leukemia (CML) remains speculative. To assess the transforming properties of the bcr/abl gene product, complementary DNA clones encoding the CML-specific P210 bcr/abl protein were expressed in NIH/3T3 fibroblasts. In contrast to the v-abl oncogene product P160, the P210 bcr/abl gene product did not transform NIH/3T3 cells. Cell lines were isolated that expressed high levels of the P210 bcr/abl protein but were morphologically normal. During the course of these experiments, a transforming recombinant of bcr/abl was isolated which fuses gag determinants derived from helper virus to the NH2-terminus of the bcr/abl protein. This suggests that a property of viral gag sequences, probably myristylation-dependent membrane localization, must be provided to bcr/abl for it to transform fibroblasts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daley, G Q -- McLaughlin, J -- Witte, O N -- Baltimore, D -- 2T 32 GM07753-07/GM/NIGMS NIH HHS/ -- CA27507/CA/NCI NIH HHS/ -- CA38497/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 31;237(4814):532-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2440107" target="_blank"〉PubMed〈/a〉
    Keywords: Abelson murine leukemia virus/physiology ; Animals ; Cell Line ; *Cell Transformation, Neoplastic ; Cell Transformation, Viral ; Epitopes ; Fibroblasts/pathology ; Fusion Proteins, bcr-abl ; Gene Products, gag ; Leukemia, Myeloid/*genetics ; Neoplasm Proteins/*genetics/physiology ; Oncogene Proteins, Viral/*physiology ; Recombinant Fusion Proteins/*genetics/physiology ; Recombinant Proteins/*genetics ; Retroviridae Proteins/physiology ; Transfection ; Viral Proteins/*physiology
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    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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    Recombinant fragment of protein kinase inhibitor blocks cyclic AMP-dependent gene transcription (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-23
    Description: Transcriptional regulation by cyclic adenosine monophosphate (cAMP) in mammalian cells could be mediated by a phosphoprotein substrate of the cAMP-dependent protein kinase or, as in prokaryotes, by a cAMP-binding protein. Two synthetic genes that code for an active fragment of the protein inhibitor of this kinase and a mutant inactive fragment were constructed and used to distinguish these alternatives. Transient expression of the active peptide product specifically inhibited the cAMP-stimulated expression of a cotransfected reporter gene by more than 90 percent, whereas the expression of the inactive peptide did not alter cAMP-stimulated gene expression. The results indicate that an active kinase catalytic subunit is a necessary intermediate in the cAMP stimulation of gene transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grove, J R -- Price, D J -- Goodman, H M -- Avruch, J -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):530-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821622" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Carrier Proteins/*pharmacology ; Chloramphenicol O-Acetyltransferase ; Cyanogen Bromide ; Cyclic AMP/*pharmacology ; DNA, Recombinant ; Escherichia coli/genetics ; *Intracellular Signaling Peptides and Proteins ; Nucleic Acid Hybridization ; Peptide Fragments/*pharmacology ; Phosphorylation ; Plasmids ; Protein Kinase Inhibitors ; Protein Kinases/metabolism ; RNA, Messenger/genetics ; Recombinant Proteins/*pharmacology ; Transcription, Genetic/*drug effects ; Transfection
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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)
    Details
    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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    Glucocorticoid receptor mutants that define a small region sufficient for enhancer activation (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-24
    Description: Transcriptional enhancement is a general mechanism for regulation of gene expression in which particular proteins bound to specific DNA sequences stimulate the efficiency of initiation from linked promoters. One such protein, the glucocorticoid receptor, mediates enhancement in a glucocorticoid hormone-dependent manner. In this study, a region of the 795-amino acid rat glucocorticoid receptor that is active in transcriptional enhancement was identified. The active region was defined by expressing various receptor deletion mutants in stably and transiently transfected cells and examining the regulated transcription of hormone-responsive genes. Mutant receptors lacking as many as 439 amino-terminal amino acids retained activity, as did those with as many as 270 carboxyl-terminal amino acids deleted. This suggests that the 86-amino acid segment between the most extensive terminal deletions, which also includes sequences required for specific DNA binding in vitro, is sufficient for enhancer activation. In fact, a 150-amino acid receptor fragment that encompasses this segment mediates constitutive enhancement.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miesfeld, R -- Godowski, P J -- Maler, B A -- Yamamoto, K R -- New York, N.Y. -- Science. 1987 Apr 24;236(4800):423-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563519" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; DNA-Binding Proteins/*genetics ; *Enhancer Elements, Genetic ; *Genes, Regulator ; Mutation ; Rats ; Receptors, Glucocorticoid/*genetics ; Structure-Activity Relationship ; Transfection
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    Rapid identification of nonessential genes of herpes simplex virus type 1 by Tn5 mutagenesis (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-01
    Description: The large genome of herpes simplex virus type of (HSV-1) encodes at least 80 polypeptides, the majority of which have no recognized function. A subgroup of these gene products appears to be nonessential for virus replication in cell culture, but contributes to the complex life cycle of the virus in the host. To identify such functions, a simple insertional mutagenesis method has been used for selective inactivation of individual HSV-1 genes. The bacterial transposon Tn5 was allowed to insert randomly into cloned restriction fragments representing the entire short unique (US) region of the HSV-1 genome. Of the 12 open reading frames that were mutagenized with Tn5, mutant derivatives of US2, US4, and US5 were recombined into the virus. These three genes proved to be nonessential for HSV-1 replication in Vero (African Green monkey kidney) cells and the US4 gene appeared to be involved in viral pathogenesis in the central nervous system of mice. This rapid mutagenesis procedure should prove useful in exploring the entire HSV-1 genome as well as the genomes of other complex animal viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weber, P C -- Levine, M -- Glorioso, J C -- AI18228/AI/NIAID NIH HHS/ -- GM34534/GM/NIGMS NIH HHS/ -- RR00200/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 May 1;236(4801):576-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3033824" target="_blank"〉PubMed〈/a〉
    Keywords: DNA Restriction Enzymes ; *DNA Transposable Elements ; DNA, Recombinant ; DNA, Viral/genetics ; Escherichia coli/genetics ; *Genes, Viral ; *Mutation ; Plasmids ; Simplexvirus/*genetics/growth & development ; Transfection ; Virus Replication
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    Implantation of genetically engineered fibroblasts into mice: implications for gene therapy (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-08
    Description: In a variety of human genetic diseases, replacement of the absent or defective protein provides significant therapeutic benefits. As a model for a somatic cell gene therapy system, cultured murine fibroblasts were transfected with a human growth hormone (hGH) fusion gene and cells from one of the resulting clonal lines were subsequently implanted into various locations in mice. Such implants synthesized and secreted hGH, which was detectable in the serum. The function of the implants depended on their location and size, and on the histocompatibility of the donor cells with their recipients. The expression of hGH could be modified by addition of regulatory effectors, and, with appropriate immunosuppression, the implants survived for more than 3 months. This approach to gene therapy, here termed "transkaryotic implantation," is potentially applicable to many genetic diseases in that the transfected cell line can be extensively characterized prior to implantation, several anatomical sites are suitable for implantation, and regulated expression of the gene of therapeutic interest can be obtained.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selden, R F -- Skoskiewicz, M J -- Howie, K B -- Russell, P S -- Goodman, H M -- AM-07055/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 May 8;236(4802):714-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3472348" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; DNA, Recombinant ; Fibroblasts/immunology/*transplantation ; *Genetic Engineering ; Graft Survival ; Growth Hormone/biosynthesis/*genetics ; Humans ; Immunosuppression ; Kidney ; Kinetics ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Plasmids ; Therapeutics ; Transfection
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    In situ detection of beta-galactosidase in lenses of transgenic mice with a gamma-crystallin/lacZ gene (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-23
    Description: Transgenic mice carrying the gamma 2-crystallin promoter fused to the coding region of the bacterial lacZ gene were generated. The offspring of three founder mice expressed high levels of the enzyme solely in the central nuclear fiber cells of the lens as measured by an in situ assay for the detection of beta-galactosidase activity. These results suggest that gamma 2-crystallin sequences between -759 to +45 contain essential information required for appropriate tissue-specific and temporal regulation of the mouse gamma 2-crystallin gene. In a broader context, this study also demonstrates the utility of beta-galactosidase hybrid gene constructs for monitoring the activity of gene regulatory elements in transgenic mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goring, D R -- Rossant, J -- Clapoff, S -- Breitman, M L -- Tsui, L C -- New York, N.Y. -- Science. 1987 Jan 23;235(4787):456-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3099390" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cataract/enzymology ; Crystallins/*genetics ; Galactosidases/*genetics ; Gene Expression Regulation ; *Lac Operon ; Lens, Crystalline/*physiology ; Mice ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/*genetics ; Recombinant Proteins/*genetics ; Tissue Distribution ; Transfection ; beta-Galactosidase/*genetics/metabolism
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    Construction of a novel oncogene based on synthetic sequences encoding epidermal growth factor (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-16
    Description: The autocrine model postulates that constitutive release of a mitogenic growth factor can lead to uncontrolled proliferation and cell transformation. A synthetic polynucleotide encoding epidermal growth factor conferred a tumorigenic phenotype on cells. These cells were transformed through the action of an autocrine circuit having an extracellular component.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stern, D F -- Hare, D L -- Cecchini, M A -- Weinberg, R A -- CA07285-03/CA/NCI NIH HHS/ -- R01CA39964/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 16;235(4786):321-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3492043" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Cell Division ; *Cell Transformation, Neoplastic/pathology ; DNA, Recombinant ; Epidermal Growth Factor/antagonists & inhibitors/*genetics/immunology ; Gene Expression Regulation ; Mice ; Neoplasms, Experimental/genetics/pathology ; *Oncogenes ; Rats ; Transfection
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    Signal for attachment of a phospholipid membrane anchor in decay accelerating factor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-27
    Description: Decay accelerating factor (DAF) belongs to a novel group of membrane proteins anchored to the cell surface by a glycophospholipid membrane anchor that is covalently attached to the carboxyl terminus of the protein. The last 37 amino acids of membrane DAF, when fused to the carboxyl terminus of a secreted protein, are sufficient to target the fusion protein to the plasma membrane by means of a glycophospholipid anchor. This approach provides a novel means of targeting proteins to the cell-surface membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caras, I W -- Weddell, G N -- Davitz, M A -- Nussenzweig, V -- Martin, D W Jr -- AI-08499/AI/NIAID NIH HHS/ -- AI-23276/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 27;238(4831):1280-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genentech, Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2446389" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD55 ; Cell Line ; Cell Membrane/physiology ; DNA/metabolism ; Membrane Lipids/*metabolism ; Membrane Proteins/genetics/*metabolism ; Phospholipids/*metabolism ; Transfection
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    The role of individual cysteine residues in the structure and function of the v-sis gene product (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-06-05
    Description: The v-sis oncogene encodes a platelet-derived growth factor (PDGF)-related product whose transforming activity is mediated by its functional interaction with the PDGF receptor. PDGF, as well as processed forms of the v-sis gene product, is a disulfide-linked dimer with eight conserved cysteine residues in the minimum region necessary for biologic activity. Site-directed mutagenesis of the v-sis gene revealed that each conserved cysteine residue was required directly or indirectly for disulfide-linked dimer formation. However, substitution of serine for cysteine codons at any of four positions had no detrimental effect on transforming activity of the encoded v-sis protein. These results establish that interchain disulfide bonds are not essential in order for this protein to act as a functional ligand for the PDGF receptor. The remaining four substitutions of serine for cysteine each inactivated transforming function of the molecule. In each case this was associated with loss of a conformation shown to involve intramolecular disulfide bonds. These studies provide insight into the role of individual cysteine residues in determining the structure of the sis/PDGF molecule critical for biological activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giese, N A -- Robbins, K C -- Aaronson, S A -- New York, N.Y. -- Science. 1987 Jun 5;236(4806):1315-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3035718" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Polyomavirus Transforming ; Antigens, Viral, Tumor/analysis/*physiology ; Cell Transformation, Viral ; Cross Reactions ; Cysteine ; *Genes, Viral ; Mutation ; Oncogene Proteins, Viral/analysis/*physiology ; *Oncogenes ; Platelet-Derived Growth Factor/analysis/physiology ; Protein Conformation ; Protein Processing, Post-Translational ; Receptors, Cell Surface/metabolism ; Receptors, Platelet-Derived Growth Factor ; Retroviridae/*genetics ; Sarcoma Virus, Woolly Monkey/*genetics ; Serine ; Transfection
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    Identification by cell fusion of gene sequences that interact with positive trans-acting factors (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-17
    Description: Cell fusion experiments have implicated positive or negative regulatory factors in the cell type--specific expression of specialized endogenous genes. The inability to readily manipulate such genes has prevented characterization of the cis-acting DNA sequences that interact with these factors. A transfection-fusion technique, which combined stable gene transfer and formation of transient heterokaryons, was used to study this class of factors and their DNA binding sites. Messenger RNA directed by a quiescent, rat prolactin promoter region stably transferred into mouse fibroblasts was detected only after fusion to rat pituitary cells, implying that pituitary cells contain a positive cell type--specific factor or factors. Nuclear run-on assays showed that fusion activation is transcriptional. Fusion did not activate either a stably transferred rat growth hormone gene promoter or expression of the endogenous silent fibroblast prolactin or growth hormone genes. Analysis by 5'-deletion mutation identified a 30-base pair DNA sequence required for cell fusion activation of the rat prolactin promoter region. Comparison with previous results from direct cellular transfer of this region implies that transfection-fusion identifies novel regulatory DNA sequences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lufkin, T -- Bancroft, C -- GM36847/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):283-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3474782" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Animals ; Cell Fusion ; Chloramphenicol O-Acetyltransferase ; Gene Expression Regulation ; Growth Hormone/genetics ; Pituitary Gland/*physiology ; Prolactin/*genetics ; *Promoter Regions, Genetic ; Rats ; Transcription Factors/*genetics ; Transcription, Genetic ; Transfection
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    Retroviral vector-mediated gene transfer into human hematopoietic progenitor cells (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-11-29
    Description: The transfer of the human gene for hypoxanthine phosphoribosyltransferase (HPRT) into human bone marrow cells was accomplished by use of a retroviral vector. The cells were infected in vitro with a replication-incompetent murine retroviral vector that carried and expressed a mutant HPRT complementary DNA. The infected cells were superinfected with a helper virus and maintained in long-term culture. The production of progeny HPRT virus by the bone marrow cells was demonstrated with a colony formation assay on cultured HPRT-deficient, ouabain-resistant murine fibroblasts. Hematopoietic progenitor cells able to form colonies of granulocytes or macrophages (or both) in semisolid medium in the presence of colony stimulating factor were present in the nonadherent cell population. Colony forming units cloned in agar and subsequently cultured in liquid medium produced progeny HPRT virus, indicating infection of this class of hematopoietic progenitor cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gruber, H E -- Finley, K D -- Hershberg, R M -- Katzman, S S -- Laikind, P K -- Seegmiller, J E -- Friedmann, T -- Yee, J K -- Jolly, D J -- AM 13622/AM/NIADDK NIH HHS/ -- GM 28223/GM/NIGMS NIH HHS/ -- HD20034/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Nov 29;230(4729):1057-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3864246" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Gene Expression Regulation ; *Genetic Engineering ; Genetic Vectors ; Hematopoietic Stem Cells/*physiology ; Humans ; Hypoxanthine Phosphoribosyltransferase/*genetics ; Mice ; Retroviridae/*genetics ; Transfection
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    Trans-acting transcriptional regulation of human T-cell leukemia virus type III long terminal repeat (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-11
    Description: Human T-cell leukemia virus type III (HTLV-III) was recently identified as the probable etiologic agent of the acquired immune deficiency syndrome (AIDS). Here it is shown that, in human T-cell lines infected with HTLV-III, gene expression directed by the long terminal repeat sequence of this virus is stimulated by more than two orders of magnitude compared to matched uninfected cells. The rate of transcription of the HTLV-III long terminal repeat is more than 1000 times that of the SV40 early promoter in one infected cell line. Thus, HTLV-III, like HTLV-I, HTLV-II, and the bovine leukemia virus, is characterized by trans-activation of transcription in infected cells. The efficiency of trans-activation in the case of HTLV-III may account, at least in part, for the virulent nature of HTLV-III infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sodroski, J -- Rosen, C -- Wong-Staal, F -- Salahuddin, S Z -- Popovic, M -- Arya, S -- Gallo, R C -- Haseltine, W A -- CA07094/CA/NCI NIH HHS/ -- CA07580/CA/NCI NIH HHS/ -- CA36974/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jan 11;227(4683):171-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2981427" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics/metabolism ; Cell Line ; Chloramphenicol O-Acetyltransferase ; DNA, Recombinant ; Deltaretrovirus/*genetics ; *Gene Expression Regulation ; Humans ; Operon ; Plasmids ; Transcription, Genetic ; 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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  • 78
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    Malignant transformation of erythroid cells in vivo by introduction of a nonreplicating retrovirus vector (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-06-28
    Description: DNA from a replication-defective spleen focus-forming virus (SFFV) was reconstructed and transfected into psi-2 cells containing a packaging-defective mutant of Moloney murine leukemia virus. Replication-incompetent retrovirus particles (helper virus-free containing genomes that express the transforming envelope gene of SFFV (gp52) transformed bone marrow cells in vitro and, after direct intravenous introduction of the vector, induced malignant erythroid disease in vivo. Disease induction was dependent on prior treatment of mice with phenylhydrazine, which probably increased the availability of erythroid target cells. Since there was no evidence of virus particle expression in mice with malignant disease, this study demonstrates the acute oncogenic potential of a limited number of erythroid cells expressing SFFV gp52. Direct inoculation of animals with nonreplicating retroviral vectors containing transforming genes may be useful in study the oncogenic effects of such genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolff, L -- Ruscetti, S -- New York, N.Y. -- Science. 1985 Jun 28;228(4707):1549-52.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990034" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/analysis ; *Cell Transformation, Neoplastic ; DNA Restriction Enzymes/metabolism ; DNA, Viral/metabolism ; Erythroblasts/*cytology ; Gene Expression Regulation ; Mice ; Oncogenes ; Phenotype ; Retroviridae/*genetics ; Spleen/microbiology ; Transfection ; Viral Envelope Proteins/genetics ; Virion/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 79
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    Human GM-CSF: molecular cloning of the complementary DNA and purification of the natural and recombinant proteins (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-17
    Description: Clones of complementary DNA encoding the human lymphokine known as granulocyte-macrophage colony-stimulating factor (GM-CSF) were isolated by means of a mammalian cell (monkey COS cell) expression screening system. One of these clones was used to produce recombinant GM-CSF in mammalian cells. The recombinant hematopoietin was similar to the natural product that was purified to apparent homogeneity from medium conditioned by a human T-cell line. The human T-cell GM-CSF was found to be 60 percent homologous with the GM-CSF recently cloned from murine lung messenger RNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, G G -- Witek, J S -- Temple, P A -- Wilkens, K M -- Leary, A C -- Luxenberg, D P -- Jones, S S -- Brown, E L -- Kay, R M -- Orr, E C -- New York, N.Y. -- Science. 1985 May 17;228(4701):810-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3923623" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; *Cloning, Molecular ; Colony-Stimulating Factors/biosynthesis/*genetics/isolation & purification ; *Dna ; DNA, Recombinant ; *Granulocytes ; Haplorhini ; Humans ; *Macrophages ; RNA, Messenger/genetics ; T-Lymphocytes ; 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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  • 80
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    cis- and trans-acting transcriptional regulation of visna virus (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-08-02
    Description: Visna virus is a pathogenic lentivirus of sheep that is related to human T-cell lymphotropic virus type III (HTLV-III), the probable etiologic agent of the acquired immune deficiency syndrome (AIDS). The transcriptional activity of visna virus promoter and enhancer sequences was studied by means of an assay based on the transient expression of the bacterial gene chloramphenicol acetyltransferase (CAT). The results suggest that the high level of expression of visna virus is due in part to cis-acting enhancer sequences that give the viral promoter a high level of transcriptional activity. In addition, the rate of transcription from the visna virus promoter situated in a plasmid expressing the CAT gene was much greater in infected than uninfected cells. This phenomenon of trans-acting transcriptional activation may involve either virally or cellularly encoded factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hess, J L -- Clements, J E -- Narayan, O -- NS-15721/NS/NINDS NIH HHS/ -- NS-16145/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Aug 2;229(4712):482-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990051" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Animals ; Base Sequence ; Cell Line ; Chloramphenicol O-Acetyltransferase ; Choroid Plexus ; Chromosome Mapping ; Enhancer Elements, Genetic ; *Genes, Regulator ; Goats ; Humans ; L Cells (Cell Line) ; Macrophages ; Mice ; Plasmids ; Promoter Regions, Genetic ; Sheep ; Synovial Membrane ; T-Lymphocytes ; *Transcription, Genetic ; Transfection ; Visna-maedi virus/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 81
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    Control of cytochrome P1-450 gene expression by dioxin (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-22
    Description: The environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) may produce its effects by altering gene expression in susceptible cells. In mouse hepatoma cells, TCDD induces the transcription of the cytochrome P1-450 gene, whose product, aryl hydrocarbon hydroxylase, contributes both to the detoxification and to the metabolic activation of carcinogenic polycyclic aromatic hydrocarbons. A DNA fragment containing sequences flanking the 5' end of the cytochrome P1-450 gene was isolated and analyzed. This DNA fragment contains a cis-acting control element with at least three functional domains: a putative promoter, an inhibitory domain upstream from the promoter that blocks its function, and a TCDD-responsive domain still farther (1265 to 1535 base pairs) upstream of the promoter. These findings, together with results from earlier studies, imply that transcription of the cytochrome P1-450 gene is under both positive and negative control by at least two trans-acting regulatory factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, P B -- Galeazzi, D R -- Fisher, J M -- Whitlock, J P Jr -- CA09302/CA/NCI NIH HHS/ -- CA32786/CA/NCI NIH HHS/ -- GM07149/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1499-502.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3856321" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/biosynthesis/genetics ; Animals ; Cell Line ; Chloramphenicol O-Acetyltransferase ; Cytochrome P-450 Enzyme System/*genetics ; DNA, Recombinant ; Dioxins/*pharmacology ; Enzyme Induction ; Gene Expression Regulation/*drug effects ; *Genes, Regulator ; Liver Neoplasms, Experimental ; Mice ; *Promoter Regions, Genetic ; Tetrachlorodibenzodioxin/*pharmacology ; Transcription Factors/metabolism ; Transcription, Genetic/drug effects ; 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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  • 82
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    Pathways of protein secretion in eukaryotes (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-04
    Description: Protein secretion from cells can take several forms. Secretion is constitutive if proteins are secreted as fast as they are synthesized. In regulated secretion newly synthesized proteins destined for secretion are stored at high concentration in secretory vesicles until the cell receives an appropriate stimulus. When both constitutive and regulated protein secretion can take place in the same cell a mechanism must exist for sorting the correct secretory protein into the correct secretory vesicle. The secretory vesicle must then be delivered to the appropriate region of plasma membrane. Transfection of DNA encoding foreign secretory proteins into regulated secretory cells has provided insight into the specificity of sorting into secretory vesicles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelly, R B -- New York, N.Y. -- Science. 1985 Oct 4;230(4721):25-32.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2994224" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/secretion ; Animals ; Calcium/metabolism ; Calmodulin/metabolism ; Carrier Proteins/physiology ; Cell Compartmentation ; Cell Fusion ; Cell Line ; Cells/*secretion ; Cytoplasmic Granules/metabolism ; Eukaryotic Cells/cytology/*secretion ; Exocytosis ; Golgi Apparatus/ultrastructure ; Half-Life ; Leukemia Virus, Murine/genetics ; Lysosomes/enzymology ; Membrane Proteins/genetics/metabolism ; Microscopy, Electron ; Models, Biological ; Peptide Hydrolases/metabolism ; Pituitary Gland/cytology ; Pro-Opiomelanocortin/secretion ; Proteins/*secretion ; 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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  • 83
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    Functional relation between HTLV-II x and adenovirus E1A proteins in transcriptional activation (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-11-01
    Description: The mechanism of cellular transformation by the human T-cell leukemia viruses (HTLV) is thought to involve a novel gene known as the x gene. This gene is essential for HTLV replication and acts by enhancing transcription from the HTLV long terminal repeat. The HTLV x gene product may also cause aberrant transcription of normal cellular genes, resulting in transformation of the infected cells. Although there is no evidence as yet for such a mechanism, it was shown that the HTLV-II x gene product can activate transcription from adenovirus E1A-dependent early promoters and therefore has the potential to activate cellular genes. It was also shown that the adenovirus and herpes pseudorabies immediate early proteins activate expression from the HTLV-I and HTLV-II long terminal repeats, though at lower levels than with the x gene product. These findings indicate possible common mechanisms of action for transcription-regulatory genes of distinct viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, I S -- Cann, A J -- Shah, N P -- Gaynor, R B -- CA 16042/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- CA 38597/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Nov 1;230(4725):570-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2996140" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/*genetics ; Cell Transformation, Viral ; Deltaretrovirus/*genetics ; Endonucleases/metabolism ; HeLa Cells ; Herpesvirus 4, Human ; Humans ; Operon ; Repetitive Sequences, Nucleic Acid ; Single-Strand Specific DNA and RNA Endonucleases ; Transcription, Genetic/*drug effects ; Transfection ; Viral Proteins/*pharmacology
    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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