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  • Transfection  (133)
  • American Association for the Advancement of Science (AAAS)  (133)
  • American Institute of Physics (AIP)
  • Oxford University Press
  • 1995-1999
  • 1990-1994  (133)
  • 1993  (59)
  • 1992  (74)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (133)
  • American Institute of Physics (AIP)
  • Oxford University Press
  • Springer  (1)
Years
  • 1995-1999
  • 1990-1994  (133)
Year
  • 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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  • 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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  • 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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  • 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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  • 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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  • 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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  • 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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  • 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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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    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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    G protein-coupled signal transduction pathways for interleukin-8 (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Regulation of plasma membrane recycling by CFTR (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-04-24
    Description: The gene that encodes the cystic fibrosis transmembrane conductance regulator (CFTR) is defective in patients with cystic fibrosis. Although the protein product of the CFTR gene has been proposed to function as a chloride ion channel, certain aspects of its function remain unclear. The role of CFTR in the adenosine 3',5'-monophosphate (cAMP)-dependent regulation of plasma membrane recycling was examined. Adenosine 3',5'-monophosphate is known to regulate endocytosis and exocytosis in chloride-secreting epithelial cells that express CFTR. However, mutant epithelial cells derived from a patient with cystic fibrosis exhibited no cAMP-dependent regulation of endocytosis and exocytosis until they were transfected with complementary DNA encoding wild-type CFTR. Thus, CFTR is critical for cAMP-dependent regulation of membrane recycling in epithelial tissues, and this function of CFTR could explain in part the pleiotropic nature of cystic fibrosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bradbury, N A -- Jilling, T -- Berta, G -- Sorscher, E J -- Bridges, R J -- Kirk, K L -- New York, N.Y. -- Science. 1992 Apr 24;256(5056):530-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Alabama, Birmingham 35294.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1373908" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Membrane/*physiology ; Chlorides/metabolism ; Colforsin/pharmacology ; Cyclic AMP/pharmacology ; Cystic Fibrosis/*physiopathology ; Cystic Fibrosis Transmembrane Conductance Regulator ; DNA/genetics ; Endocytosis/drug effects/physiology ; Epithelium/secretion ; Exocytosis/drug effects/physiology ; Gene Expression ; Horseradish Peroxidase/metabolism ; Humans ; Membrane Proteins/genetics/*physiology ; Molecular Sequence Data ; Pancreatic Neoplasms ; Transfection ; Tumor Cells, Cultured ; Wheat Germ Agglutinins/metabolism
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    Repression of the insulin-like growth factor II gene by the Wilms tumor suppressor WT1 (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-07-31
    Description: The Wilms tumor suppressor gene wt1 encodes a zinc finger DNA binding protein, WT1, that functions as a transcriptional repressor. The fetal mitogen insulin-like growth factor II (IGF-II) is overexpressed in Wilms tumors and may have autocrine effects in tumor progression. The major fetal IGF-II promoter was defined in transient transfection assays as a region spanning from nucleotides -295 to +135, relative to the transcription start site. WT1 bound to multiple sites in this region and functioned as a potent repressor of IGF-II transcription in vivo. Maximal repression was dependent on the presence of WT1 binding sites on each side of the transcriptional initiation site. These findings provide a molecular basis for overexpression of IGF-II in Wilms tumors and suggest that WT1 negatively regulates blastemal cell proliferation by limiting the production of a fetal growth factor in the developing vertebrate kidney.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drummond, I A -- Madden, S L -- Rohwer-Nutter, P -- Bell, G I -- Sukhatme, V P -- Rauscher, F J 3rd -- CA 10817/CA/NCI NIH HHS/ -- CA 47983/CA/NCI NIH HHS/ -- CA 52009/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 31;257(5070):674-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1323141" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Blotting, Northern ; DNA/chemistry/metabolism ; DNA-Binding Proteins/*metabolism ; Deoxyribonuclease I/metabolism ; *Gene Expression Regulation, Neoplastic ; Genes, Wilms Tumor/*physiology ; Humans ; Insulin-Like Growth Factor II/*genetics ; Kidney/embryology/metabolism ; Mice ; Molecular Sequence Data ; Promoter Regions, Genetic ; Rats ; Sequence Homology, Nucleic Acid ; Transfection ; WT1 Proteins ; Wilms Tumor/genetics/metabolism ; Zinc Fingers
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    The fms-like tyrosine kinase, a receptor for vascular endothelial growth factor (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-02-21
    Description: The fms-like tyrosine kinase (Flt) is a transmembrane receptor in the tyrosine kinase family. Expression of flt complementary DNA in COS cells conferred specific, high-affinity binding of vascular endothelial growth factor, also known as vascular permeability factor (VEGF-VPF), a factor that induces vascular permeability when injected in the guinea pig skin and stimulates endothelial cell proliferation. Expression of Flt in Xenopus laevis oocytes caused the oocytes to release calcium in response to VEGF-VPF. These findings show that flt encodes a receptor for VEGF-VPF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Vries, C -- Escobedo, J A -- Ueno, H -- Houck, K -- Ferrara, N -- Williams, L T -- P01 HL-43821/HL/NHLBI NIH HHS/ -- R01 HL-32898/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Feb 21;255(5047):989-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1312256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; Cross-Linking Reagents ; Endothelial Growth Factors/*physiology ; Enzyme Activation ; Humans ; In Vitro Techniques ; Lymphokines/*physiology ; Proto-Oncogene Proteins/genetics/*physiology ; Receptors, Cell Surface/*genetics ; Signal Transduction ; Transfection ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factor Receptor-1 ; Vascular Endothelial Growth Factors ; Xenopus laevis
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    Acetylcholine receptor channel structure probed in cysteine-substitution mutants (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-09
    Description: In order to understand the structural bases of ion conduction, ion selectivity, and gating in the nicotinic acetylcholine receptor, mutagenesis and covalent modification were combined to identify the amino acid residues that line the channel. The side chains of alternate residues--Ser248, Leu250, Ser252, and Thr254--in M2, a membrane-spanning segment of the alpha subunit, are exposed in the closed channel. Thus alpha 248-254 probably forms a beta strand, and the gate is closer to the cytoplasmic end of the channel than any of these residues. On channel opening, Leu251 is also exposed. These results lead to a revised view of the closed and open channel structures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akabas, M H -- Stauffer, D A -- Xu, M -- Karlin, A -- NS07065/NS/NINDS NIH HHS/ -- NS07258/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Oct 9;258(5080):307-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1384130" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/metabolism/pharmacology ; Amino Acid Sequence ; Animals ; Cysteine/*chemistry ; Gene Expression ; Ion Channel Gating ; Ion Channels/*chemistry/physiology ; Mice ; Molecular Sequence Data ; Muscles/chemistry ; *Mutagenesis ; Oocytes/metabolism ; Receptors, Cholinergic/*chemistry/genetics ; Structure-Activity Relationship ; Sulfhydryl Reagents/pharmacology ; Thermodynamics ; Transfection ; Xenopus
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    Targeted degradation of c-Fos, but not v-Fos, by a phosphorylation-dependent signal on c-Jun (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-12-18
    Description: The proto-oncogene products c-Fos and c-Jun heterodimerize through their leucine zippers to form the AP-1 transcription factor. The transcriptional activity of the heterodimer is regulated by signal-dependent phosphorylation and dephosphorylation events. The stability of c-Fos was found to also be controlled by intracellular signal transduction. In transient expression and in vitro degradation experiments, the stability of c-Fos was decreased when the protein was dimerized with phosphorylated c-Jun. c-Jun protein isolated from phorbol ester-induced cells did not target c-Fos for degradation, which suggests that c-Fos is transiently stabilized after stimulation of cell growth. v-Fos protein, the retroviral counterpart of c-Fos, was not susceptible to degradation targeted by c-Jun.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papavassiliou, A G -- Treier, M -- Chavrier, C -- Bohmann, D -- New York, N.Y. -- Science. 1992 Dec 18;258(5090):1941-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Molecular Biology Laboratory, Differentiation Program, Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1470918" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Codon/genetics ; HeLa Cells ; Humans ; Macromolecular Substances ; Molecular Sequence Data ; Oncogene Proteins v-fos/genetics/*metabolism ; Phosphorylation ; Protein Biosynthesis ; Proto-Oncogene Proteins c-fos/genetics/*metabolism ; Proto-Oncogene Proteins c-jun/genetics/*metabolism ; Rabbits ; Recombinant Proteins/metabolism ; Reticulocytes/metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription, Genetic ; Transfection
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    The Autographa californica baculovirus genome: evidence for multiple replication origins (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-09-04
    Description: The Autographa californica multinucleocapsid nuclear polyhedrosis virus (AcMNPV), which is used for the overexpression of eukaryotic genes and is being engineered for possible use as a viral insecticide, has a circular, supercoiled genome of approximately 128 kilobases. Despite its widespread use, little is known about the mechanism by which AcMNPV replicates. Evidence is presented in this report that AcMNPV origins of DNA replication are repeated sequences each containing several closely related imperfect palindromes that are present in six regions distributed around the genome. Although AcMNPV infection-dependent plasmid replication was initiated by a single complete palindrome, the amount of replication was substantially increased in plasmids containing six or eight palindromes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pearson, M -- Bjornson, R -- Pearson, G -- Rohrmann, G -- AI21973/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 Sep 4;257(5075):1382-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Agricultural Chemistry, Oregon State University, Corvallis 97331.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1529337" target="_blank"〉PubMed〈/a〉
    Keywords: Baculoviridae/*genetics ; Base Sequence ; *DNA Replication ; DNA, Superhelical/chemistry/*genetics ; DNA, Viral/chemistry/*genetics ; Genes, Viral/*genetics ; Molecular Sequence Data ; Mutagenesis ; Nucleic Acid Hybridization ; Plasmids ; Repetitive Sequences, Nucleic Acid ; Transfection ; *Virus Replication
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    Dual-target inhibition of HIV-1 in vitro by means of an adeno-associated virus antisense vector (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-12-07
    Description: An adeno-associated virus vector encoding an antisense RNA was used to transduce stable intracellular resistance to human immunodeficiency virus-1 (HIV-1) in human hemopoietic and non-hemopoietic cell lines. The antisense targets are present in all HIV-1 transcripts and include the TAR sequence, which is critical for transcription and virus replication, and the polyadenylation signal. Cell lines expressing antisense RNA showed up to 95 percent inhibition of gene expression directed by the HIV-1 long terminal repeat and greater than 99 percent reduction in infectious HIV-1 production, with no detectable cellular toxicity. Because of their efficient transcription and inability to recombine with HIV-1, adeno-associated virus vectors represent a promising form of anti-retroviral gene therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chatterjee, S -- Johnson, P R -- Wong, K K Jr -- New York, N.Y. -- Science. 1992 Nov 27;258(5087):1485-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health, Rockville, MD 20852.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1359646" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; CD4-Positive T-Lymphocytes/microbiology ; Cell Line ; Chloramphenicol O-Acetyltransferase/genetics ; Dependovirus/*genetics ; Drug Resistance, Microbial/genetics ; Gene Products, tat/genetics ; Genetic Vectors/*genetics ; HIV Long Terminal Repeat/genetics ; HIV-1/*genetics/physiology ; Humans ; Molecular Sequence Data ; Neomycin/pharmacology ; RNA, Antisense/*genetics ; RNA, Messenger/genetics ; RNA, Viral/genetics ; Transfection ; Virus Replication/genetics ; tat Gene Products, Human Immunodeficiency Virus
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    Appearance of water channels in Xenopus oocytes expressing red cell CHIP28 protein (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-04-17
    Description: Water rapidly crosses the plasma membrane of red blood cells (RBCs) and renal tubules through specialized channels. Although selective for water, the molecular structure of these channels is unknown. The CHIP28 protein is an abundant integral membrane protein in mammalian RBCs and renal proximal tubules and belongs to a family of membrane proteins with unknown functions. Oocytes from Xenopus laevis microinjected with in vitro-transcribed CHIP28 RNA exhibited increased osmotic water permeability; this was reversibly inhibited by mercuric chloride, a known inhibitor of water channels. Therefore it is likely that CHIP28 is a functional unit of membrane water channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Preston, G M -- Carroll, T P -- Guggino, W B -- Agre, P -- DK32753/DK/NIDDK NIH HHS/ -- HL33991/HL/NHLBI NIH HHS/ -- HL48268/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Apr 17;256(5055):385-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, 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/1373524" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aquaporin 1 ; *Aquaporins ; Cell Membrane Permeability ; Electric Conductivity ; Erythrocyte Membrane/*metabolism ; Immunoblotting ; Membrane Proteins/chemistry/genetics/*physiology ; Mercuric Chloride/pharmacology ; Molecular Structure ; Oocytes/*metabolism ; Osmolar Concentration ; RNA/genetics ; Thermodynamics ; Transfection ; Water/*metabolism ; Xenopus laevis
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    Cytoplasmic domain heterogeneity and functions of IgG Fc receptors in B lymphocytes (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-26
    Description: B lymphocytes and macrophages express closely related immunoglobulin G (IgG) Fc receptors (Fc gamma RII) that differ only in the structures of their cytoplasmic domains. Because of cell type-specific alternative messenger RNA splicing, B-cell Fc gamma RII contains an insertion of 47 amino acids that participates in determining receptor function in these cells. Transfection of an Fc gamma RII-negative B-cell line with complementary DNA's encoding the two splice products and various receptor mutants indicated that the insertion was responsible for preventing both Fc gamma RII-mediated endocytosis and Fc gamma RII-mediated antigen presentation. The insertion was not required for Fc gamma RII to modulate surface immunoglobulin-triggered B-cell activation. Instead, regulation of activation involved a region of the cytoplasmic domain common to both the lymphocyte and macrophage receptor isoforms. In contrast, the insertion did contribute to the formation of caps in response to receptor cross-linking, consistent with suggestions that the lymphocyte but not macrophage form of the receptor can associate with the detergent-insoluble cytoskeleton.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amigorena, S -- Bonnerot, C -- Drake, J R -- Choquet, D -- Hunziker, W -- Guillet, J G -- Webster, P -- Sautes, C -- Mellman, I -- Fridman, W H -- New York, N.Y. -- Science. 1992 Jun 26;256(5065):1808-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire d'Immunologie Cellulaire et Clinique, INSERM U 255, Institut Curie, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1535455" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antigen-Antibody Complex/metabolism ; Antigen-Antibody Reactions/genetics/immunology ; Antigens, CD/genetics/*immunology ; Antigens, Differentiation/genetics/*immunology ; B-Lymphocytes/*immunology ; Calcium/metabolism ; *DNA-Binding Proteins ; Dose-Response Relationship, Immunologic ; Endocytosis/genetics/immunology ; Humans ; Immunohistochemistry ; Lymphocyte Activation/immunology ; Microscopy, Electron ; Molecular Sequence Data ; Receptors, Fc/genetics/*immunology ; Receptors, IgG ; Repressor Proteins/pharmacology ; Transcription Factors/pharmacology ; Transfection ; Viral Proteins ; Viral Regulatory and Accessory Proteins
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    Molecular cloning of the interleukin-1 beta converting enzyme (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-04-03
    Description: Interleukin-1 beta (IL-1 beta) mediates a wide range of immune and inflammatory responses. The active cytokine is generated by proteolytic cleavage of an inactive precursor. A complementary DNA encoding a protease that carries out this cleavage has been cloned. Recombinant expression in COS-7 cells enabled the cells to process precursor IL-1 beta to the mature form. Sequence analysis indicated that the enzyme itself may undergo proteolytic processing. The gene encoding the protease was mapped to chromosomal band 11q23, a site frequently involved in rearrangement in human cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cerretti, D P -- Kozlosky, C J -- Mosley, B -- Nelson, N -- Van Ness, K -- Greenstreet, T A -- March, C J -- Kronheim, S R -- Druck, T -- Cannizzaro, L A -- New York, N.Y. -- Science. 1992 Apr 3;256(5053):97-100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Corporation, Seattle, WA 98101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1373520" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Caspase 1 ; Cell Line ; Chromosome Banding ; *Chromosomes, Human, Pair 11 ; Cloning, Molecular ; Enzyme Precursors/biosynthesis/*genetics/isolation & purification ; Humans ; Metalloendopeptidases/biosynthesis/*genetics/isolation & purification ; Molecular Sequence Data ; Neutrophils/enzymology ; Oligodeoxyribonucleotides ; Poly A/genetics/isolation & purification ; Polymerase Chain Reaction/methods ; RNA/genetics/isolation & purification ; RNA, Messenger/genetics ; Recombinant Proteins/biosynthesis/isolation & purification ; Transfection
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    Regulatory elements that control the lineage-specific expression of myoD (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-04
    Description: The molecular basis of skeletal muscle lineage determination was investigated by analyzing DNA control elements that regulate the myogenic determination gene myoD. A distal enhancer was identified that positively regulates expression of the human myoD gene. The myoD enhancer and promoter were active in myogenic and several nonmyogenic cell lines. In transgenic mouse embryos, however, the myoD enhancer and promoter together directed expression of a lacZ transgene specifically to the skeletal muscle lineage. These data suggest that during development myoD is regulated by mechanisms that restrict accessibility of myoD control elements to positive trans-acting factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldhamer, D J -- Faerman, A -- Shani, M -- Emerson, C P Jr -- CA-06927/CA/NCI NIH HHS/ -- HD-07796/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1992 Apr 24;256(5056):538-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Research, Fox Chase Cancer Center, Philadelphia, PA 19111.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1315077" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Chloramphenicol O-Acetyltransferase/genetics ; Cloning, Molecular ; Enhancer Elements, Genetic ; *Gene Expression Regulation ; Humans ; Mice ; Mice, Transgenic ; Muscle Proteins/*genetics ; Muscles/embryology/metabolism ; MyoD Protein ; Promoter Regions, Genetic ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured ; beta-Galactosidase/genetics
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    Interaction cloning: identification of a helix-loop-helix zipper protein that interacts with c-Fos (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-15
    Description: A facile method for isolating genes that encode interacting proteins has been developed with a polypeptide probe that contains an amino-terminal extension with recognition sites for a monoclonal antibody, a specific endopeptidase, and a site-specific protein kinase. This probe, containing the basic region-leucine zipper dimerization motif of c-Fos, was used to screen a complementary DNA library. A complementary DNA that encoded a member of the basic-helix-loop-helix-zipper (bHLH-Zip) family of proteins was isolated. The complementary DNA-encoded polypeptide FIP (Fos interacting protein) bound to oligonucleotide probes that contained DNA binding motifs for other HLH proteins. When cotransfected with c-Fos, FIP stimulated transcription of an AP-1-responsive promoter.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blanar, M A -- Rutter, W J -- DK-21344/DK/NIDDK NIH HHS/ -- DK-41822/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1992 May 15;256(5059):1014-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hormone Research Institute, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1589769" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; *Cloning, Molecular ; DNA/isolation & purification ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; *Genes, fos/genetics ; HeLa Cells ; Humans ; Leucine Zippers/*genetics ; Macromolecular Substances ; Molecular Sequence Data ; Oligonucleotide Probes/chemistry/metabolism ; Protein Conformation ; Proto-Oncogene Proteins c-fos/chemistry/metabolism ; Proto-Oncogene Proteins c-jun/chemistry/metabolism ; Sequence Homology, Nucleic Acid ; Transfection
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    A human gene responsible for Zellweger syndrome that affects peroxisome assembly (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-02-28
    Description: The primary defect arising from Zellweger syndrome appears to be linked to impaired assembly of peroxisomes. A human complementary DNA has been cloned that complements the disease's symptoms (including defective peroxisome assembly) in fibroblasts from a patient with Zellweger syndrome. The cause of the syndrome in this patient was a point mutation that resulted in the premature termination of peroxisome assembly factor-1. The homozygous patient apparently inherited the mutation from her parents, each of whom was heterozygous for that mutation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shimozawa, N -- Tsukamoto, T -- Suzuki, Y -- Orii, T -- Shirayoshi, Y -- Mori, T -- Fujiki, Y -- New York, N.Y. -- Science. 1992 Feb 28;255(5048):1132-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Gifu University School of Medicine, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1546315" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cricetinae ; DNA Mutational Analysis ; Genes ; Genetic Complementation Test ; Humans ; Membrane Proteins/*genetics ; Microbodies/*ultrastructure ; Molecular Sequence Data ; Oligodeoxyribonucleotides/chemistry ; Pedigree ; Polymerase Chain Reaction ; Transfection ; Zellweger Syndrome/*genetics
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    Human and Drosophila homeodomain proteins that enhance the DNA-binding activity of serum response factor (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-21
    Description: Cells with distinct developmental histories can respond differentially to identical signals, suggesting that signals are interpreted in a fashion that reflects a cell's identity. How this might occur is suggested by the observation that proteins of the homeodomain family, including a newly identified human protein, enhance the DNA-binding activity of serum response factor, a protein required for the induction of genes by growth and differentiation factors. Interaction with proteins of the serum response factor family may allow homeodomain proteins to specify the transcriptional response to inductive signals. Moreover, because the ability to enhance the binding of serum response factor to DNA residues within the homeodomain but is independent of homeodomain DNA-binding activity, this additional activity of the homeodomain may account for some of specificity of action of homeodomain proteins in development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grueneberg, D A -- Natesan, S -- Alexandre, C -- Gilman, M Z -- CA08968/CA/NCI NIH HHS/ -- CA45642/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 21;257(5073):1089-95.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, NY 11724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1509260" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; DNA/genetics/*metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism/*pharmacology ; Drosophila/genetics ; *Drosophila Proteins ; Fungal Proteins/chemistry/pharmacology ; *Homeodomain Proteins ; Humans ; Minichromosome Maintenance 1 Protein ; Molecular Sequence Data ; Nuclear Proteins/*metabolism ; Saccharomyces cerevisiae/genetics ; Serum Response Factor ; Transcription Factors/chemistry/*metabolism/pharmacology ; Transfection
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    NF-kappa B subunit regulation in nontransformed CD4+ T lymphocytes (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-05
    Description: Regulation of interleukin-2 (IL-2) gene expression by the p50 and p65 subunits of the DNA binding protein NF-kappa B was studied in nontransformed CD4+ T lymphocyte clones. A homodimeric complex of the NF-kappa B p50 subunit was found in resting T cells. The amount of p50-p50 complex decreased after full antigenic stimulation, whereas the amount of the NF-kappa B p50-p65 heterodimer was increased. Increased expression of the IL-2 gene and activity of the IL-2 kappa B DNA binding site correlated with a decrease in the p50-p50 complex. Overexpression of p50 repressed IL-2 promoter expression. The switch from p50-p50 to p50-p65 complexes depended on a protein that caused sequestration of the p50-p50 complex in the nucleus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, S M -- Tran, A C -- Grilli, M -- Lenardo, M J -- New York, N.Y. -- Science. 1992 Jun 5;256(5062):1452-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute for 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/1604322" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/*immunology ; Base Sequence ; Binding Sites ; Cell Line ; Cell Nucleus/physiology ; Chloramphenicol O-Acetyltransferase/genetics/metabolism ; Clone Cells ; Columbidae ; DNA/genetics ; *Gene Expression Regulation ; Interleukin-2/*genetics ; Macromolecular Substances ; Mice ; Molecular Sequence Data ; NF-kappa B/*metabolism ; Oligonucleotide Probes ; Promoter Regions, Genetic ; RNA, Messenger/metabolism ; Recombinant Fusion Proteins/metabolism ; T-Lymphocyte Subsets/*immunology ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology
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    Structure and functional expression of an omega-conotoxin-sensitive human N-type calcium channel (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-17
    Description: N-type calcium channels are omega-conotoxin (omega-CgTx)-sensitive, voltage-dependent ion channels involved in the control of neurotransmitter release from neurons. Multiple subtypes of voltage-dependent calcium channel complexes exist, and it is the alpha 1 subunit of the complex that forms the pore through which calcium enters the cell. The primary structures of human neuronal calcium channel alpha 1B subunits were deduced by the characterization of overlapping complementary DNAs. Two forms (alpha 1B-1 and alpha 1B-2) were identified in human neuroblastoma (IMR32) cells and in the central nervous system, but not in skeletal muscle or aorta tissues. The alpha 1B-1 subunit directs the recombinant expression of N-type calcium channel activity when it is transiently co-expressed with human neuronal beta 2 and alpha 2b subunits in mammalian HEK293 cells. The recombinant channel was irreversibly blocked by omega-CgTx but was insensitive to dihydropyridines. The alpha 1B-1 alpha 2b beta 2-transfected cells displayed a single class of saturable, high-affinity (dissociation constant = 55 pM) omega-CgTx binding sites. Co-expression of the beta 2 subunit was necessary for N-type channel activity, whereas the alpha 2b subunit appeared to modulate the expression of the channel. The heterogeneity of alpha 1B subunits, along with the heterogeneity of alpha 2 and beta subunits, is consistent with multiple, biophysically distinct N-type calcium channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, M E -- Brust, P F -- Feldman, D H -- Patthi, S -- Simerson, S -- Maroufi, A -- McCue, A F -- Velicelebi, G -- Ellis, S B -- Harpold, M M -- New York, N.Y. -- Science. 1992 Jul 17;257(5068):389-95.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉SIBIA, Inc., La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1321501" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Calcium/metabolism ; Calcium Channels/*drug effects/*genetics/*metabolism ; Cell Line ; Female ; Humans ; Male ; Membrane Potentials ; Molecular Sequence Data ; Neuroblastoma/metabolism ; Peptides, Cyclic/*pharmacology ; Sequence Alignment ; Sequence Homology, Nucleic Acid ; Transfection ; omega-Conotoxin GVIA
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    Oncogenic forms of p53 inhibit p53-regulated gene expression (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-08
    Description: Mutant forms of the gene encoding the tumor suppressor p53 are found in numerous human malignancies, but the physiologic function of p53 and the effects of mutations on this function are unknown. The p53 protein binds DNA in a sequence-specific manner and thus may regulate gene transcription. Cotransfection experiments showed that wild-type p53 activated the expression of genes adjacent to a p53 DNA binding site. The level of activation correlated with DNA binding in vitro. Oncogenic forms of p53 lost this activity. Moreover, all mutants inhibited the activity of coexpressed wild-type p53, providing a basis for the selection of such mutants during tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kern, S E -- Pietenpol, J A -- Thiagalingam, S -- Seymour, A -- Kinzler, K W -- Vogelstein, B -- CA06973/CA/NCI NIH HHS/ -- CA09243/CA/NCI NIH HHS/ -- CA35494/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 May 8;256(5058):827-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1589764" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Line ; Chloramphenicol O-Acetyltransferase/genetics/metabolism ; DNA-Binding Proteins/*genetics/*metabolism ; Exons ; *Gene Expression Regulation, Neoplastic ; *Genes, p53 ; Genetic Vectors ; Humans ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction/methods ; Recombinant Fusion Proteins/metabolism ; Repetitive Sequences, Nucleic Acid ; Saccharomyces cerevisiae/genetics/growth & development ; *Transcription, Genetic ; Transfection ; Tumor Suppressor Protein p53/*genetics/*metabolism ; beta-Galactosidase/genetics/metabolism
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  • 77
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    Calcium-dependent transmitter secretion reconstituted in Xenopus oocytes: requirement for synaptophysin (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-07-31
    Description: Calcium-dependent glutamate secretion was reconstituted in Xenopus oocytes by injecting the oocyte with total rat cerebellar messenger RNA (mRNA). Co-injection of total mRNA with antisense oligonucleotides to synaptophysin message decreased the expression of synaptophysin in the oocyte and reduced the calcium-dependent secretion. A similar effect on secretion was observed for oocytes injected with total mRNA together with an antibody to rat synaptophysin. These results indicate that synaptophysin is necessary for transmitter secretion and that the oocyte expression system may be useful for dissecting the molecular events associated with the secretory process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alder, J -- Lu, B -- Valtorta, F -- Greengard, P -- Poo, M M -- MH 39327/MH/NIMH NIH HHS/ -- NS 22764/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 31;257(5070):657-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Columbia University, New York, NY 10027.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1353905" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Blotting, Western ; Calcimycin/pharmacology ; Calcium/*pharmacology ; Cerebellum/chemistry ; Fluorescent Antibody Technique ; Gene Expression ; Glutamates/*secretion ; Glutamic Acid ; Kinetics ; Liver/chemistry ; Microscopy, Immunoelectron ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacology ; Oocytes/*physiology ; RNA, Messenger/genetics ; Rats ; Synaptophysin/genetics/*physiology ; Transfection ; Xenopus
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  • 78
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    Gz-mediated hormonal inhibition of cyclic AMP accumulation (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-17
    Description: Hormones inhibit synthesis of adenosine 3',5'-monophosphate (cAMP) in most cells via receptors coupled to pertussis toxin (PTX)-sensitive guanine nucleotide-binding (G) proteins. Mutationally activated alpha subunits of Gi2 (alpha i2) constitutively inhibit cAMP accumulation when transfected into cells. Cells have now been transfected with mutant alpha subunits of four other G proteins--Gz, a PTX-insensitive G protein of unknown function, and Gi1, Gi3, and G(o), which are PTX-sensitive. Mutant alpha z, alpha i1, and alpha i3 inhibited cAMP accumulation but alpha o did not. Moreover, expression of wild-type alpha z produced cells in which PTX did not block hormonal inhibition of cAMP accumulation. Thus, Gz can trigger an effector pathway in response to hormone receptors that ordinarily interact with PTX-sensitive Gi proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, Y H -- Conklin, B R -- Bourne, H R -- New York, N.Y. -- Science. 1992 Jan 17;255(5042):339-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1347957" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic alpha-Agonists/pharmacology ; Animals ; Brimonidine Tartrate ; Chorionic Gonadotropin/pharmacology ; Colforsin/pharmacology ; Cyclic AMP/*biosynthesis ; Dinoprostone/pharmacology ; Dopamine/pharmacology ; GTP-Binding Proteins/*physiology ; Gene Expression Regulation/*physiology ; Hormones/*physiology ; In Vitro Techniques ; Lysophospholipids/pharmacology ; Pertussis Toxin ; Quinoxalines/pharmacology ; Rats ; Signal Transduction/physiology ; Transfection ; Virulence Factors, Bordetella/pharmacology
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  • 79
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    Participation of non-zinc finger residues in DNA binding by two nuclear orphan receptors (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-04-03
    Description: Steroid-thyroid hormone receptors typically bind as dimers to DNA sequences that contain repeated elements termed half-sites. NGFI-B, an early response protein and orphan member of this receptor superfamily, binds to a DNA sequence that contains only one half-site (5'-AAAGGTCA-3'). A domain separate from the NGFI-B zinc fingers, termed the A box, was identified and is required for recognition of the two adenine-thymidine (A-T) base pairs at the 5' end of the NGFI-B DNA binding element. In addition, a domain downstream of the zinc fingers of the orphan receptor H-2 region II binding protein, termed the T box, determined binding to tandem repeats of the estrogen receptor half-site (5'-AGGTCA-3').〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, T E -- Paulsen, R E -- Padgett, K A -- Milbrandt, J -- NS01018/NS/NINDS NIH HHS/ -- P01 CA49712/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Apr 3;256(5053):107-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1314418" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; CHO Cells ; Cell Nucleus/*physiology ; Cricetinae ; DNA/*metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Kinetics ; Mice ; Molecular Sequence Data ; Nuclear Receptor Subfamily 4, Group A, Member 1 ; Oligodeoxyribonucleotides/metabolism ; Polymerase Chain Reaction ; Receptors, Cell Surface/*metabolism ; Receptors, Cytoplasmic and Nuclear ; Receptors, Steroid ; Recombinant Fusion Proteins/metabolism ; Sequence Homology, Nucleic Acid ; Substrate Specificity ; Transcription Factors/genetics/*metabolism ; Transfection ; Zinc Fingers/genetics
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  • 80
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    High-efficiency expression and solubilization of functional T cell antigen receptor heterodimers (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-29
    Description: The T cell receptor (TCR) zeta chain was attached to the TCR alpha and beta extracellular domains to induce efficient expression of alpha beta heterodimers that can recognize complexes of antigen with major histocompatibility complex (MHC) molecules. Chimeric constructs expressed in RBL-2H3 cells were efficiently transported to the cell surface uniquely as disulfide-linked heterodimers. Transfectants were activated by specific antigen-MHC complexes, which demonstrated that the expressed alpha beta was functional and that CD3 was not required for antigen-MHC binding. Constructs with thrombin cleavage sites were efficiently cleaved to soluble disulfide-linked heterodimers. Thus, attachment of TCR zeta domains and protease cleavage sites to TCR alpha and beta induces expression of demonstrably functional heterodimers that can be solubilized.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Engel, I -- Ottenhoff, T H -- Klausner, R D -- New York, N.Y. -- Science. 1992 May 29;256(5061):1318-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism 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/1598575" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cell Membrane/immunology ; Disulfides ; Flow Cytometry ; Histocompatibility Antigens/metabolism ; Kinetics ; Macromolecular Substances ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction ; Receptors, Antigen, T-Cell/genetics/isolation & purification/*metabolism ; Solubility ; Transfection
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  • 81
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    Mutation of the POU-specific domain of Pit-1 and hypopituitarism without pituitary hypoplasia (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-08-21
    Description: A point mutation in the POU-specific portion of the human gene that encodes the tissue-specific POU-domain transcription factor, Pit-1, results in hypopituitarism, with deficiencies of growth hormone, prolactin, and thyroid-stimulating hormone. In two unrelated Dutch families, a mutation in Pit-1 that altered an alanine in the first putative alpha helix of the POU-specific domain to proline was observed. This mutation generated a protein capable of binding to DNA response elements but unable to effectively activate its known target genes, growth hormone and prolactin. The phenotype of the affected individuals suggests that the mutant Pit-1 protein is competent to initiate other programs of gene activation required for normal proliferation of somatotrope, lactotrope, and thyrotrope cell types. Thus, a mutation in the POU-specific domain of Pit-1 has a selective effect on a subset of Pit-1 target genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfaffle, R W -- DiMattia, G E -- Parks, J S -- Brown, M R -- Wit, J M -- Jansen, M -- Van der Nat, H -- Van den Brande, J L -- Rosenfeld, M G -- Ingraham, H A -- HD24960/HD/NICHD NIH HHS/ -- HD2697/HD/NICHD NIH HHS/ -- NIDDK 18477/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 21;257(5073):1118-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Emory University School of Medicine, Atlanta, GA 30322.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1509263" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Blotting, Northern ; DNA/chemistry/metabolism ; DNA-Binding Proteins/*genetics/metabolism ; Growth Hormone/deficiency ; Humans ; Hypopituitarism/*genetics/pathology ; Mice ; Molecular Sequence Data ; *Mutation ; Nucleic Acid Hybridization ; Pituitary Gland, Anterior/*pathology ; Pituitary Hormones/*deficiency ; Polymerase Chain Reaction ; Prolactin/deficiency ; Rats ; Sequence Homology, Nucleic Acid ; Thyrotropin/deficiency ; Transcription Factor Pit-1 ; Transcription Factors/*genetics/metabolism ; Transfection
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  • 82
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    Control by asparagine residues of calcium permeability and magnesium blockade in the NMDA receptor (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-09-04
    Description: The N-methyl-D-aspartate (NMDA) receptor forms a cation-selective channel with a high calcium permeability and sensitivity to channel block by extracellular magnesium. These properties, which are believed to be important for the induction of long-term changes in synaptic strength, are imparted by asparagine residues in a putative channel-forming segment of the protein, transmembrane 2 (TM2). In the NR1 subunit, replacement of this asparagine by a glutamine residue decreases calcium permeability of the channel and slightly reduces magnesium block. The same substitution in NR2 subunits strongly reduces magnesium block and increases the magnesium permeability but barely affects calcium permeability. These asparagines are in a position homologous to the site in the TM2 region (Q/R site) of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors that is occupied by either glutamine (Q) or arginine (R) and that controls divalent cation permeability of the AMPA receptor channel. Hence AMPA and NMDA receptor channels contain common structural motifs in their TM2 segments that are responsible for some of their ion selectivity and conductance properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burnashev, N -- Schoepfer, R -- Monyer, H -- Ruppersberg, J P -- Gunther, W -- Seeburg, P H -- Sakmann, B -- New York, N.Y. -- Science. 1992 Sep 4;257(5075):1415-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abteilung Zellphysiologie, Max-Planck-Institut fur Medizinische Forschung, Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1382314" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Asparagine/*chemistry ; Binding Sites ; Calcium/*metabolism/pharmacology ; Cell Line ; Electric Conductivity ; Glutamates/pharmacology ; Glutamic Acid ; Ion Channels/chemistry/*physiology ; Magnesium/metabolism/*pharmacology ; Mice ; Molecular Sequence Data ; Mutagenesis ; Oocytes/metabolism ; Permeability ; Rats ; Receptors, N-Methyl-D-Aspartate/chemistry/genetics/*physiology ; Structure-Activity Relationship ; Transfection ; Xenopus
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  • 83
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    Potentially amyloidogenic, carboxyl-terminal derivatives of the amyloid protein precursor (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-02-07
    Description: The 39- to 43-amino acid amyloid beta protein (beta AP), which is deposited as amyloid in Alzheimer's disease, is encoded as an internal peptide that begins 99 residues from the carboxyl terminus of a 695- to 770-amino acid glycoprotein referred to as the amyloid beta protein precursor (beta APP). To clarify the processing that produces amyloid, carboxyl-terminal derivatives of the beta APP were analyzed. This analysis showed that the beta APP is normally processed into a complex set of 8- to 12-kilodalton carboxyl-terminal derivatives. The two largest derivatives in human brain have the entire beta AP at or near their amino terminus and are likely to be intermediates in the pathway leading to amyloid deposition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Estus, S -- Golde, T E -- Kunishita, T -- Blades, D -- Lowery, D -- Eisen, M -- Usiak, M -- Qu, X M -- Tabira, T -- Greenberg, B D -- AG06656/AG/NIA NIH HHS/ -- AG08012/AG/NIA NIH HHS/ -- AG08992/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1992 Feb 7;255(5045):726-8.〈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/1738846" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid/*biosynthesis ; Amyloid beta-Protein Precursor/chemistry/genetics/*metabolism ; Cell Line ; Cell Membrane/chemistry ; Cerebral Cortex/chemistry ; Glycosylation ; Humans ; Immunoblotting ; Immunosorbent Techniques ; Molecular Weight ; Peptide Fragments/chemistry/isolation & purification/*metabolism ; Transfection
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  • 84
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    Cloning of a delta opioid receptor by functional expression (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-12-28
    Description: Opiate drugs have potent analgesic and addictive properties. These drugs interact with receptors that also mediate the response to endogenous opioid peptide ligands. However, the receptors for opioids have eluded definitive molecular characterization. By transient expression in COS cells and screening with an iodinated analog of the opioid peptide enkephalin, a complementary DNA clone encoding a functional delta opioid receptor has been identified. The sequence shows homology to G protein-coupled receptors, in particular the receptors for somatostatin, angiotensin, and interleukin-8.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Evans, C J -- Keith, D E Jr -- Morrison, H -- Magendzo, K -- Edwards, R H -- DA05010/DA/NIDA NIH HHS/ -- P50 DA005010/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1992 Dec 18;258(5090):1952-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, University of California, School of Medicine, Los Angeles 90024-1759.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1335167" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding, Competitive ; Blotting, Northern ; Blotting, Southern ; Cell Line ; Cyclic AMP/metabolism ; Diprenorphine/metabolism ; Enkephalin, D-Penicillamine (2,5)- ; Enkephalins/pharmacology ; Etorphine/pharmacology ; Gene Expression ; Humans ; Kinetics ; Models, Structural ; Molecular Sequence Data ; Naloxone/pharmacology ; Narcotics/pharmacology ; Protein Structure, Secondary ; Receptors, Opioid, delta/chemistry/*genetics/*metabolism ; Sequence Homology, Amino Acid ; Transfection ; Tumor Cells, Cultured
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  • 85
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    Gene therapy for CF advances (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1992 Jan 17;255(5042):289.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1549773" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Animals ; Cystic Fibrosis/*therapy ; Genetic Therapy/*methods ; Genetic Vectors ; Rats ; Transfection
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  • 86
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    Thermal stability comparison of purified empty and peptide-filled forms of a class I MHC molecule (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-12-04
    Description: A secreted form of a class I major histocompatibility complex (MHC) molecule was denatured and renatured in vitro in the absence of peptide. The resulting empty class I heterodimer was immunologically reactive and structurally similar to a heterodimer renatured in the presence of an appropriate restricted peptide. Thermal stability profiles indicated that the two forms of heterodimer differed in their resistance to denaturation by heat but that a significant portion of the empty class I heterodimers had a native conformation at physiological temperatures. Free energies calculated from these data gave a direct measure of the stabilization of the class I MHC molecule that resulted from peptide binding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fahnestock, M L -- Tamir, I -- Narhi, L -- Bjorkman, P J -- AI28931/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 Dec 4;258(5088):1658-62.〈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/1360705" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CHO Cells ; Circular Dichroism ; Cricetinae ; Drug Stability ; Enzyme-Linked Immunosorbent Assay ; Glutamate-Ammonia Ligase/genetics/metabolism ; Histocompatibility Antigens Class I/*chemistry/genetics ; Hot Temperature ; Humans ; Macromolecular Substances ; *Protein Conformation ; Protein Folding ; Thermodynamics ; Transfection
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  • 87
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    Calmodulin trapping by calcium-calmodulin-dependent protein kinase (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-05-22
    Description: Multifunctional calcium-calmodulin-dependent protein kinase (CaM kinase) transduces transient elevations in intracellular calcium into changes in the phosphorylation state and activity of target proteins. By fluorescence emission anisotropy, the affinity of CaM kinase for dansylated calmodulin was measured and found to increase 1000 times after autophosphorylation of the threonine at position 286 of the protein. Autophosphorylation markedly slowed the release of bound calcium-calmodulin; the release time increased from less than a second to several hundred seconds. In essence, calmodulin is trapped by autophosphorylation. The shift in affinity does not occur in a site-directed mutant in which threonine at position 286 has been replaced by a non-phosphorylatable amino acid. These experiments demonstrate the existence of a new state in which calmodulin is bound to CaM kinase even though the concentration of calcium is basal. Calmodulin trapping provides for molecular potentiation of calcium transients and may enable detection of their frequency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, T -- Hanson, P I -- Stryer, L -- Schulman, H -- GM 40600/GM/NIGMS NIH HHS/ -- GM24032/GM/NIGMS NIH HHS/ -- MH45324/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 May 22;256(5060):1199-202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1317063" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Binding, Competitive ; Calcium/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinases ; Calmodulin/*metabolism ; Cell Line ; Egtazic Acid/pharmacology ; Kinetics ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Phosphorylation ; Protein Binding ; Protein Kinases/genetics/*metabolism ; Recombinant Proteins/metabolism ; Spectrometry, Fluorescence ; Threonine ; Time Factors ; Transfection
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  • 88
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    A functional connection between the pores of distantly related ion channels as revealed by mutant K+ channels (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-13
    Description: The overall sequence similarity between the voltage-activated K+ channels and cyclic nucleotide-gated ion channels from retinal and olfactory neurons suggests that they arose from a common ancestor. On the basis of sequence comparisons, mutations were introduced into the pore of a voltage-activated K+ channel. These mutations confer the essential features of ion conduction in the cyclic nucleotide-gated ion channels; the mutant K+ channels display little selectivity among monovalent cations and are blocked by divalent cations. The property of K+ selectivity is related to the presence of two amino acids that are absent from the pore-forming region of the cyclic nucleotide-gated channels. These data demonstrate that very small differences in the primary structure of an ion channel can account for extreme functional diversity, and they suggest a possible connection between the pore-forming regions of K+, Ca2+, and cyclic nucleotide-gated ion channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heginbotham, L -- Abramson, T -- MacKinnon, R -- GM43949/GM/NIGMS NIH HHS/ -- GM47400/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Nov 13;258(5085):1152-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1279807" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/pharmacology ; Cattle ; Cyclic AMP/pharmacology ; Cyclic GMP/pharmacology ; Drosophila ; Electric Conductivity ; Ion Channel Gating/drug effects ; Ion Channels/drug effects/*physiology ; Magnesium/pharmacology ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Oocytes/physiology ; Plants ; Potassium Channels/chemistry/*genetics/*physiology ; Retina/ultrastructure ; Transfection ; Xenopus laevis
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  • 89
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    Malignant transformation by a mutant of the IFN-inducible dsRNA-dependent protein kinase (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-09-18
    Description: The double-stranded RNA-dependent protein kinase (dsRNA-PK) is thought to be a key mediator of the antiviral and antiproliferative effects of interferons (IFNs). Studies examining the physiological function of the kinase suggest that it participates in cell growth and differentiation by regulating protein synthesis. Autophosphorylation and consequent activation of dsRNA-PK in vitro and in vivo result in phosphorylation of the alpha subunit of eukaryotic initiation factor-2 (eIF-2) and inhibition of protein synthesis. Expression of a functionally defective mutant of human dsRNA-PK in NIH 3T3 cells resulted in malignant transformation, suggesting that dsRNA-PK may function as a suppressor of cell proliferation and tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koromilas, A E -- Roy, S -- Barber, G N -- Katze, M G -- Sonenberg, N -- AI22646/AI/NIAID NIH HHS/ -- RR00166/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1992 Sep 18;257(5077):1685-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Faculty of Medicine, McGill University, Montreal, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1382315" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; Cell Division ; Cell Line ; *Cell Transformation, Neoplastic ; Cloning, Molecular ; DNA/genetics ; Enzyme Induction ; Gene Expression ; Humans ; Immunoblotting ; Interferons/*pharmacology ; Mice ; Molecular Sequence Data ; *Mutation ; Phosphorylation ; Protein Kinases/chemistry/*genetics/physiology ; Transfection ; eIF-2 Kinase
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 90
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    Implication of GAP in Ras-dependent transactivation of a polyoma enhancer sequence (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-08
    Description: Controversy exists as to whether the interaction of a guanosine triphosphatase activating protein (GAP) with Ras proteins functions both to initiate and to terminate Ras-dependent signaling events or only to terminate them. GAP-C, a carboxyl-terminal fragment of GAP that is sufficient to stimulate GTPase activity, inhibited the stimulation of transcription produced by some oncoproteins (v-Src, polyoma middle T, wild-type Ras, and oncogenic Ras) but not that produced by v-Mos. Wild-type GAP did not affect transcription induced by oncogenic Ras but reversed the inhibitory effect of GAP-C on transcription induced by oncogenic Ras. These results indicate that GAP is a negative regulator of wild-type Ras and elicits a downstream signal by interacting with Ras-GTP (guanosine triphosphate).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schweighoffer, F -- Barlat, I -- Chevallier-Multon, M C -- Tocque, B -- New York, N.Y. -- Science. 1992 May 8;256(5058):825-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rhone-Poulenc Rorer, Centre de Recherche de Vitry-Alfortville, Vitry Sur Seine.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1317056" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Antigens, Polyomavirus Transforming/genetics ; CHO Cells ; *Cell Cycle Proteins ; *Cell Transformation, Neoplastic ; Chloramphenicol O-Acetyltransferase/genetics/metabolism ; Cricetinae ; *Enhancer Elements, Genetic ; Fungal Proteins/genetics/metabolism ; GTPase-Activating Proteins ; *Genes, ras ; Humans ; Mice ; Oncogene Proteins v-mos ; Oncogenes ; Polyomavirus/*genetics ; Promoter Regions, Genetic ; Protein-Tyrosine Kinases/genetics ; Proteins/*metabolism ; Retroviridae Proteins, Oncogenic/genetics ; Signal Transduction ; Simian virus 40/genetics ; Transcription, Genetic ; *Transcriptional Activation ; Transfection ; ras GTPase-Activating Proteins ; *ras-GRF1
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  • 91
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    Brain tumor treatment: significant contributions (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blaese, R M -- Culver, K W -- Ishii, H -- Oldfield, E H -- Ram, Z -- Wallbridge, S -- New York, N.Y. -- Science. 1992 Dec 18;258(5090):1960.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1470923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Neoplasms/*therapy ; *Genetic Therapy ; Glioma ; Mice ; Retroviridae/genetics ; Thymidine Kinase/genetics ; Transfection ; Tumor Cells, Cultured ; beta-Galactosidase/genetics/metabolism
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  • 92
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    Initiation of deregulated growth of multipotent progenitor cells by bcr-abl in vitro (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-08
    Description: Expression of the bcr-abl oncogene in multipotent progenitor cells (MPPCs) is implicated as a key event in the development of chronic myelogenous leukemia. Bone marrow enriched for MPPCs was infected with a retrovirus that carried bcr-abl. The mixed-lineage colonies that resulted were responsive to growth factors and could differentiate. These cells later became growth factor-independent but, when injected into severe combined immunodeficient mice, were not leukemogenic. Thus, the presence of bcr-abl alone does not cause growth factor independence, although it initiates a stepwise process. This system may prove useful in the study of other oncogenes that cause leukemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gishizky, M L -- Witte, O N -- New York, N.Y. -- Science. 1992 May 8;256(5058):836-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1375394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/drug effects ; Bone Marrow Cells ; Cell Differentiation/drug effects ; Cell Division/drug effects ; Cells, Cultured ; Clone Cells ; Drug Resistance, Microbial/genetics ; Fluorouracil/pharmacology ; Fusion Proteins, bcr-abl/*genetics ; Hematopoietic Cell Growth Factors/pharmacology ; Hematopoietic Stem Cells/*cytology/drug effects/physiology ; Humans ; Interleukin-3/pharmacology ; Macrophages/cytology/drug effects ; Mast Cells/cytology/drug effects ; Mice ; Rats ; Retroviridae/genetics ; Stem Cell Factor ; Transfection
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  • 93
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    Production of the Alzheimer amyloid beta protein by normal proteolytic processing (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-02
    Description: The 4-kilodalton (39 to 43 amino acids) amyloid beta protein (beta AP), which is deposited as amyloid in the brains of patients with Alzheimer's diseases, is derived from a large protein, the amyloid beta protein precursor (beta APP). Human mononuclear leukemic (K562) cells expressing a beta AP-bearing, carboxyl-terminal beta APP derivative released significant amounts of a soluble 4-kilodalton beta APP derivative essentially identical to the beta AP deposited in Alzheimer's disease. Human neuroblastoma (M17) cells transfected with constructs expressing full-length beta APP and M17 cells expressing only endogenous beta APP also released soluble 4-kilodalton beta AP, and a similar, if not identical, fragment was readily detected in cerebrospinal fluid from individuals with Alzheimer's disease and normal individuals. Thus cells normally produce and release soluble 4-kilodalton beta AP that is essentially identical to the 4-kilodalton beta AP deposited as insoluble amyloid fibrils in Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shoji, M -- Golde, T E -- Ghiso, J -- Cheung, T T -- Estus, S -- Shaffer, L M -- Cai, X D -- McKay, D M -- Tintner, R -- Frangione, B -- AG05891/AG/NIA NIH HHS/ -- AG06656/AG/NIA NIH HHS/ -- AR02594/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Oct 2;258(5079):126-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Gunma University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439760" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*cerebrospinal fluid ; Amino Acid Sequence ; Amyloid beta-Peptides/*biosynthesis ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Base Sequence ; Cell Line ; Immunoblotting ; Leukemia, Myeloid/*metabolism ; Molecular Sequence Data ; Neuroblastoma/*metabolism ; Transfection
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  • 94
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    Calcium-regulated phosphorylation within the leucine zipper of C/EBP beta (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-04-17
    Description: Alterations in intracellular calcium levels activate several signal transduction pathways resulting in distinct patterns of gene expression. Here, a pathway for calcium-mediated signals is demonstrated that involves C/EBP beta, a member of the bZip family of transcription factors. In pituitary cells C/EBP beta was phosphorylated in response to increased intracellular calcium concentrations as a consequence of the activation of a calcium-calmodulin-dependent protein kinase. Phosphorylation of serine at position 276 within the leucine zipper of C/EBP beta appeared to confer calcium-regulated transcriptional stimulation of a promoter that contained binding sites for C/EBP beta.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wegner, M -- Cao, Z -- Rosenfeld, M G -- New York, N.Y. -- Science. 1992 Apr 17;256(5055):370-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California, San Diego, La Jolla 92093-0648.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1314426" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Binding Sites ; CCAAT-Enhancer-Binding Proteins ; Calcimycin/pharmacology ; Calcium/*pharmacology ; Calcium-Calmodulin-Dependent Protein Kinases ; Cell Line ; DNA/chemistry/genetics/metabolism ; DNA-Binding Proteins/chemistry/*metabolism ; Enzyme Activation/drug effects ; *Leucine Zippers ; Molecular Sequence Data ; Nuclear Proteins/chemistry/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Pituitary Gland/metabolism ; Protein Kinases/metabolism ; Signal Transduction/drug effects ; Transcription Factors/chemistry/*metabolism ; Transcription, Genetic/drug effects ; Transfection
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  • 95
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    Transactivation by AP-1 is a molecular target of T cell clonal anergy (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-21
    Description: Anergy is a mechanism of T lymphocyte tolerance induced by antigen receptor stimulation in the absence of co-stimulation. Anergic T cells were shown to have a defect in antigen-induced transcription of the interleukin-2 gene. Analysis of the promoter indicated that the transcription factor AP-1 and its corresponding cis element were specifically down-regulated. Exposure of anergic T cells to interleukin-2 restored both antigen responsiveness and activity of the AP-1 element.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, S M -- Beverly, B -- Tran, A C -- Brorson, K -- Schwartz, R H -- Lenardo, M J -- New York, N.Y. -- Science. 1992 Aug 21;257(5073):1134-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, 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/1509265" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens/*immunology ; Base Sequence ; Binding Sites ; Blotting, Northern ; Cell Line ; Concanavalin A/pharmacology ; *Gene Expression Regulation ; *Immune Tolerance ; Interleukin-2/*genetics/pharmacology ; Mice ; Molecular Sequence Data ; Mutation ; Promoter Regions, Genetic/genetics ; Proto-Oncogene Proteins c-jun/*physiology ; RNA, Messenger/metabolism ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/*immunology ; Transcription, Genetic ; Transfection
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  • 96
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    Deficient hippocampal long-term potentiation in alpha-calcium-calmodulin kinase II mutant mice (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-10
    Description: As a first step in a program to use genetically altered mice in the study of memory mechanisms, mutant mice were produced that do not express the alpha-calcium-calmodulin-dependent kinase II (alpha-CaMKII). The alpha-CaMKII is highly enriched in postsynaptic densities of hippocampus and neocortex and may be involved in the regulation of long-term potentiation (LTP). Such mutant mice exhibited mostly normal behaviors and presented no obvious neuroanatomical defects. Whole cell recordings reveal that postsynaptic mechanisms, including N-methyl-D-aspartate (NMDA) receptor function, are intact. Despite normal postsynaptic mechanisms, these mice are deficient in their ability to produce LTP and are therefore a suitable model for studying the relation between LTP and learning processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Silva, A J -- Stevens, C F -- Tonegawa, S -- Wang, Y -- 5 R01 NS 12961-17/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 10;257(5067):201-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Center for Cancer Research, Cambridge, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1378648" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/physiology ; Blotting, Northern ; Blotting, Southern ; Calcium-Calmodulin-Dependent Protein Kinases ; Chromosome Mapping ; DNA/analysis ; Electrophysiology ; Female ; Hippocampus/*physiology ; Learning/physiology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Mutant Strains/*genetics ; Mutagenesis, Site-Directed ; Plasmids ; Protein Kinases/*deficiency/*physiology ; RNA/analysis ; Receptors, N-Methyl-D-Aspartate ; Synapses/physiology ; Transfection
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  • 97
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    Identification of the Ah receptor nuclear translocator protein (Arnt) as a component of the DNA binding form of the Ah receptor (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-22
    Description: The Ah (dioxin) receptor binds a number of widely disseminated environmental pollutants, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polycyclic aromatic hydrocarbons, and mediates their carcinogenic effects. The ligand-bound receptor activates Cyp 1a1 gene transcription through interaction with specific DNA sequences, termed xenobiotic responsive elements (XREs). The Ah receptor nuclear translocator protein (Arnt) is required for Ah receptor function. Arnt is now shown to be a structural component of the XRE binding form of the Ah receptor. Furthermore, Arnt and the ligand-binding subunit of the receptor were extracted as a complex from the nuclei of cells treated with ligand. Arnt contains a basic helix-loop-helix motif, which may be responsible for interacting with both the XRE and the ligand-binding subunit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reyes, H -- Reisz-Porszasz, S -- Hankinson, O -- CA 28868/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 May 22;256(5060):1193-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1317062" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Aryl Hydrocarbon Receptor Nuclear Translocator ; Base Sequence ; Cell Line ; Cells, Cultured ; Cytochrome P-450 Enzyme System/genetics ; DNA/genetics/metabolism ; DNA-Binding Proteins/genetics/isolation & purification/*metabolism ; Humans ; Hydrocarbons/metabolism ; Mice ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Proteins/genetics/isolation & purification/*metabolism ; Receptors, Aryl Hydrocarbon ; Receptors, Drug/genetics/isolation & purification/*metabolism ; Recombinant Proteins/isolation & purification/metabolism ; Tetrachlorodibenzodioxin/metabolism ; *Transcription Factors ; Transcription, Genetic ; Transfection
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  • 98
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    Participation of tyrosine phosphorylation in the cytopathic effect of human immunodeficiency virus-1 (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-04-24
    Description: Protein tyrosine phosphorylation is a common mechanism of signaling in pathways that regulate T cell receptor-mediated cell activation, cell proliferation, and the cell cycle. Because human immunodeficiency virus (HIV) is though to affect normal cell signaling, tyrosine phosphorylation may be associated with HIV cytopathicity. In both HIV-infected cells and transfected cells that stably express HIV envelope glycoproteins undergoing HIVgp41-induced cell fusion, a 30-kilodalton protein was phosphorylated on tyrosine with kinetics similar to those of syncytium formation and cell death. When tyrosine phosphorylation was inhibited by the protein tyrosine kinase inhibitor herbimycin A, envelope-mediated syncytium formation was coordinately reduced. These studies show that specific intracellular signals, which apparently participate in cytopathicity, are generated by HIV and suggest strategies by which the fusion process might be interrupted.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, D I -- Tani, Y -- Tian, H -- Boone, E -- Samelson, L E -- Lane, H C -- New York, N.Y. -- Science. 1992 Apr 24;256(5056):542-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunoregulation, 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/1570514" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD4/physiology ; Benzoquinones ; Cell Line ; Cytopathogenic Effect, Viral/*physiology ; HIV Envelope Protein gp41/genetics/physiology ; HIV-1/*physiology ; Humans ; Lactams, Macrocyclic ; Phosphoproteins/*metabolism ; Phosphorylation ; Protein-Tyrosine Kinases/antagonists & inhibitors/metabolism ; Quinones/pharmacology ; Receptors, Antigen, T-Cell/physiology ; Rifabutin/analogs & derivatives ; Signal Transduction/*physiology ; T-Lymphocytes/microbiology/*physiology ; Transfection ; Tyrosine/*metabolism ; Viral Envelope Proteins/genetics/physiology
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  • 99
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    Processing of the amyloid protein precursor to potentially amyloidogenic derivatives (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-02-07
    Description: The approximately 120-kilodalton amyloid beta protein precursor (beta APP) is processed into a complex set of 8- to 12-kilodalton carboxyl-terminal derivatives that includes potentially amyloidogenic forms with the approximately 4-kilodalton amyloid beta protein (beta AP) at or near their amino terminus. In order to determine if these derivatives are processed in a secretory pathway or by the endosomal-lysosomal system, (i) deletion mutants that produce the normal set of carboxyl-terminal derivatives and shortened secreted derivatives were analyzed and (ii) the effect of inhibitors of endosomal-lysosomal processing was examined. In the secretory pathway, cleavage of the beta APP occurs at a single site within the beta AP to generate one secreted derivative and one nonamyloidogenic carboxyl-terminal fragment, whereas, in the endosomal-lysosomal system, a complex set of carboxyl-terminal derivatives is produced that includes the potentially amyloidogenic forms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Golde, T E -- Estus, S -- Younkin, L H -- Selkoe, D J -- Younkin, S G -- New York, N.Y. -- Science. 1992 Feb 7;255(5045):728-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuropathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1738847" target="_blank"〉PubMed〈/a〉
    Keywords: Ammonium Chloride/pharmacology ; Amyloid/*biosynthesis ; Amyloid beta-Protein Precursor/genetics/*metabolism ; Base Sequence ; Cell Line ; Endopeptidases/metabolism ; Humans ; Leupeptins/pharmacology ; Lysosomes/metabolism ; Molecular Sequence Data ; Mutagenesis ; Peptide Fragments/*metabolism/secretion ; Transfection
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  • 100
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    Alternative forms of Max as enhancers or suppressors of Myc-ras cotransformation (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-04-17
    Description: Max is a basic-helix-loop-helix-leucine zipper protein capable of forming sequence-specific DNA binding complexes with Myc proteins. An alternatively spliced messenger RNA has been identified that encodes a form of Max truncated at the COOH-terminus. This delta Max protein retained the ability to bind to the CACGTG motif in a complex with c-Myc but lacks the nuclear localization signal and the putative regulatory domain of Max. When tested in a myc-ras cotransformation assay in rat embryo fibroblasts, Max suppressed, whereas delta Max enhanced, transformation. Thus, the max gene may encode both a negative and a positive regulator of c-Myc function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Makela, T P -- Koskinen, P J -- Vastrik, I -- Alitalo, K -- New York, N.Y. -- Science. 1992 Apr 17;256(5055):373-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Virology, University of Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1566084" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Basic-Leucine Zipper Transcription Factors ; Binding Sites ; Cell Nucleus/metabolism ; Cell Transformation, Neoplastic/*drug effects/genetics ; DNA/chemistry/metabolism ; DNA-Binding Proteins/genetics/metabolism/*pharmacology ; Fibroblasts ; *Genes, myc ; *Genes, ras ; Humans ; Immunosorbent Techniques ; Molecular Sequence Data ; Polymerase Chain Reaction ; Proto-Oncogene Proteins c-myc/genetics/metabolism ; RNA Splicing ; RNA, Messenger/genetics ; Rats ; Structure-Activity Relationship ; *Transcription Factors ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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