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  • Cell Line  (381)
  • American Association for the Advancement of Science (AAAS)  (381)
  • Springer Science + Business Media
  • American Chemical Society (ACS)
  • 1990-1994  (381)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (381)
  • Springer Science + Business Media
  • American Chemical Society (ACS)
Years
Year
  • 1
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    CD26 antigen and HIV fusion? (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patience, C -- McKnight, A -- Clapham, P R -- Boyd, M T -- Weiss, R A -- Schulz, T F -- G117/547/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 1994 May 20;264(5162):1159-60; author reply 1162-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7909960" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/*physiology ; Antigens, Differentiation, T-Lymphocyte/*physiology ; Base Sequence ; Cats ; Cell Line ; Dipeptidyl Peptidase 4 ; HIV-1/*physiology ; Humans ; Mink ; Molecular Sequence Data
    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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    Microtubule severing by elongation factor 1 alpha (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-14
    Description: An activity that severs stable microtubules is thought to be involved in microtubule reorganization during the cell cycle. Here, a 48-kilodalton microtubule-severing protein was purified from Xenopus eggs and identified as translational elongation factor 1 alpha (EF-1 alpha). Bacterially expressed human EF-1 alpha also displayed microtubule-severing activity in vitro and, when microinjected into fibroblasts, induced rapid and transient fragmentation of cytoplasmic microtubule arrays. Thus, EF-1 alpha, an essential component of the eukaryotic translational apparatus, appears to have a second role as a regulator of cytoskeletal rearrangements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shiina, N -- Gotoh, Y -- Kubomura, N -- Iwamatsu, A -- Nishida, E -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):282-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Molecular Biology, Kyoto University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939665" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/pharmacology ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Guanosine Triphosphate/analogs & derivatives/metabolism ; Humans ; Microtubules/drug effects/*metabolism ; Molecular Sequence Data ; Molecular Weight ; Oocytes ; Peptide Elongation Factor 1 ; Peptide Elongation Factors/chemistry/isolation & purification/*physiology ; Rats ; Recombinant Proteins/pharmacology ; Ribonucleoproteins/chemistry/isolation & purification/*physiology ; Sepharose/analogs & derivatives/metabolism ; Xenopus laevis
    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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    DNA loop repair by human cell extracts (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-04
    Description: An activity in human cell extracts is described that repairs DNA with loops of five or more unpaired bases. Repair is strand-specific and is directed by a nick located 5' or 3' to the loop. This repair is observed in a colorectal cancer cell line that is devoid of a wild-type hMLH1 gene and is deficient in repair of mismatches. However, a cell line with deletions in both hMSH2 alleles is deficient in repair of both loops and mismatches. Defects in loop repair may be relevant to the repetitive-sequence instability observed in cancers and other hereditary diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Umar, A -- Boyer, J C -- Kunkel, T A -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):814-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973637" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Base Composition ; Base Sequence ; Carrier Proteins ; Cell Extracts ; Cell Line ; Colorectal Neoplasms/*genetics ; *DNA Repair ; DNA, Satellite/genetics/metabolism ; *DNA-Binding Proteins ; HeLa Cells ; Humans ; Molecular Sequence Data ; MutS Homolog 2 Protein ; Neoplasm Proteins/*genetics/physiology ; Nuclear Proteins ; Nucleic Acid Heteroduplexes/*metabolism ; Proto-Oncogene Proteins/*genetics/physiology ; Repetitive Sequences, Nucleic Acid ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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  • 4
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    Suppression of Ras-induced transformation of NIH 3T3 cells by activated G alpha s (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-04
    Description: Conversion of external signals into proliferative responses may be mediated by interactions between signaling pathways that control cell proliferation. Interactions between G alpha s, the alpha subunit of the heterotrimeric guanine nucleotide binding protein that stimulates adenylyl cyclase, and Ras, an important element in growth factor signaling, were studied. Expression of activated G alpha s in NIH 3T3 cells increased intracellular concentrations of adenosine 3',5'-monophosphate (cAMP) and inhibited H-Ras-stimulated DNA synthesis and mitogen-activated protein kinase activity. Activated G alpha s and 8-Br-cAMP suppressed H-Ras-induced transformation of NIH 3T3 cells. Apparently, G alpha s inhibits proliferative signals from Ras by stimulating cAMP production and activating protein kinase A.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, J -- Iyengar, R -- CA-44998/CA/NCI NIH HHS/ -- DK-38761/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 4;263(5151):1278-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Mount Sinai School of Medicine, City University of New York, NY 10029.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8122111" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Animals ; Cell Division ; Cell Line ; *Cell Transformation, Neoplastic ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Enzyme Activation ; GTP-Binding Proteins/genetics/*physiology ; *Genes, ras ; Mice ; Mitogen-Activated Protein Kinase 1 ; Mutagenesis, Site-Directed ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Protein-Tyrosine Kinases/antagonists & inhibitors/metabolism ; Signal Transduction ; Transfection
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  • 5
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    Functional participation of the IL-2 receptor gamma chain in IL-7 receptor complexes (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-11
    Description: The gamma chain of the interleukin-2 (IL-2) receptor is shared with the functional IL-4 receptor and is causatively related to X-linked severe combined immunodeficiency (XSCID), which is ascribed to a profound T cell defect. Studies with monoclonal antibodies specific for the IL-2 receptor gamma chain showed that the gamma chain participates in the functional high-affinity receptor complexes for IL-7 that are involved in the differentiation of T and B cells. Participation of the gamma subunit in more than one receptor may enable the elucidation of the mechanisms of XSCID development and lymphocyte differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, M -- Takeshita, T -- Higuchi, M -- Nakamura, M -- Sudo, T -- Nishikawa, S -- Sugamura, K -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1453-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Tohoku University School of Medicine, Sendai, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128231" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; B-Lymphocytes/*immunology ; Cell Line ; Cells, Cultured ; Female ; Genetic Linkage ; Interleukin-7/*metabolism/pharmacology ; Mice ; Mice, Inbred C57BL ; Receptors, Interleukin/*metabolism ; Receptors, Interleukin-2/genetics/immunology/*metabolism ; Receptors, Interleukin-7 ; Severe Combined Immunodeficiency/genetics/immunology ; T-Lymphocytes/*immunology ; X Chromosome
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  • 6
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    Potentiated transmission and prevention of further LTP by increased CaMKII activity in postsynaptic hippocampal slice neurons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-16
    Description: Calcium-calmodulin-dependent protein kinase II (CaMKII) is a necessary component of the cellular machinery underlying learning and memory. Here, a constitutively active form of this enzyme, CaMKII(1-290), was introduced into neurons of hippocampal slices with a recombinant vaccinia virus to test the hypothesis that increased postsynaptic activity of this enzyme is sufficient to produce long-term synaptic potentiation (LTP), a prominent cellular model of learning and memory. Postsynaptic expression of CaMKII(1-290) increased CaMKII activity, enhanced synaptic transmission, and prevented more potentiation by an LTP-inducing protocol. These results, together with previous studies, suggest that postsynaptic CaMKII activity is necessary and sufficient to generate LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pettit, D L -- Perlman, S -- Malinow, R -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1881-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Program, University of Iowa, Iowa City 52242.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7997883" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Line ; Genetic Vectors ; Hippocampus/cytology/enzymology/*physiology ; In Vitro Techniques ; Long-Term Potentiation/drug effects/*physiology ; Membrane Potentials ; Patch-Clamp Techniques ; Pyramidal Cells/enzymology/*physiology ; Rats ; Recombinant Proteins/metabolism ; Synaptic Transmission/drug effects/*physiology ; Transfection ; Vaccinia virus/genetics/physiology
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  • 7
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    Inhibition of NF-kappa B by sodium salicylate and aspirin (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-12
    Description: The transcription factor nuclear factor-kappa B (NF-kappa B) is critical for the inducible expression of multiple cellular and viral genes involved in inflammation and infection including interleukin-1 (IL-1), IL-6, and adhesion molecules. The anti-inflammatory drugs sodium salicylate and aspirin inhibited the activation of NF-kappa B, which further explains the mechanism of action of these drugs. This inhibition prevented the degradation of the NF-kappa B inhibitor, I kappa B, and therefore NF-kappa B was retained in the cytosol. Sodium salicylate and aspirin also inhibited NF-kappa B-dependent transcription from the Ig kappa enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kopp, E -- Ghosh, S -- R01 AI 33443-01A1/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 12;265(5174):956-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06536.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8052854" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspirin/*pharmacology ; Cell Line ; Enhancer Elements, Genetic ; Gene Expression/drug effects ; Genes, Reporter ; HIV Long Terminal Repeat ; HIV-1/genetics ; Humans ; Immunoglobulin kappa-Chains/genetics ; Lipopolysaccharides/pharmacology ; Mice ; NF-kappa B/*antagonists & inhibitors/metabolism ; Phosphorylation ; Promoter Regions, Genetic ; Protein Biosynthesis/drug effects ; Proto-Oncogene Proteins/metabolism ; Sodium Salicylate/*pharmacology ; T-Lymphocytes/metabolism ; Transcription Factor RelB ; *Transcription Factors ; Transfection ; Tumor Cells, Cultured
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  • 8
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    Receptor and ligand domains for invasion of erythrocytes by Plasmodium falciparum (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-24
    Description: A 175-kilodalton erythrocyte binding protein, EBA-175, of the parasite Plasmodium falciparum mediates the invasion of erythrocytes. The erythrocyte receptor for EBA-175 is dependent on sialic acid. The domain of EBA-175 that binds erythrocytes was identified as region II with the use of truncated portions of EBA-175 expressed on COS cells. Region II, which contains a cysteine-rich motif, and native EBA-175 bind specifically to glycophorin A, but not to glycophorin B, on the erythrocyte membrane. Erythrocyte recognition of EBA-175 requires both sialic acid and the peptide backbone of glycophorin A. The identification of both the receptor and ligand domains may suggest rational designs for receptor blockade and vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sim, B K -- Chitnis, C E -- Wasniowska, K -- Hadley, T J -- Miller, L H -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1941-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Malaria Research, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009226" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, Protozoan ; Base Sequence ; Binding Sites ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Erythrocytes/metabolism/*parasitology ; Glycopeptides/chemistry/metabolism ; Glycophorin/chemistry/*metabolism ; Molecular Sequence Data ; Plasmodium falciparum/*metabolism ; Protozoan Proteins/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Sialic Acids/*metabolism
    Print ISSN: 0036-8075
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  • 9
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    Protection from Fas-mediated apoptosis by a soluble form of the Fas molecule (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-25
    Description: Fas is an apoptosis-signaling receptor molecule on the surface of a number of cell types. Molecular cloning and nucleotide sequence analysis revealed a human Fas messenger RNA variant capable of encoding a soluble Fas molecule lacking the transmembrane domain because of the deletion of an exon encoding this region. The expression of soluble Fas was confirmed by flow cytometry and immunocytochemical analysis. Supernatants from cells transfected with the variant messenger RNA blocked apoptosis induced by the antibody to Fas. Levels of soluble Fas were elevated in patients with systemic lupus erythematosus, and mice injected with soluble Fas displayed autoimmune features.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, J -- Zhou, T -- Liu, C -- Shapiro, J P -- Brauer, M J -- Kiefer, M C -- Barr, P J -- Mountz, J D -- P01 AR03555/AR/NIAMS NIH HHS/ -- P50 AI23694/AI/NIAID NIH HHS/ -- P60 AR20614/AR/NIAMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1759-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Alabama at Birmingham.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7510905" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies/immunology ; Antigens, CD95 ; Antigens, Surface/chemistry/genetics/immunology/*physiology ; *Apoptosis ; Arthritis, Rheumatoid/blood ; Base Sequence ; Cell Line ; Cell Membrane/chemistry ; Humans ; Lupus Erythematosus, Systemic/blood ; Mice ; Molecular Sequence Data ; RNA, Messenger/genetics ; Solubility ; T-Lymphocyte Subsets/immunology ; Transfection
    Print ISSN: 0036-8075
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  • 10
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    Mediation of c-Myc-induced apoptosis by p53 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-30
    Description: The cellular proto-oncogene c-myc is involved in cell proliferation and transformation but is also implicated in the induction of programmed cell death (apoptosis). The same characteristics have been described for the tumor suppressor gene p53, the most commonly mutated gene in human cancer. In quiescent mouse fibroblasts expressing wild-type p53 protein, activation of c-Myc was found to induce apoptosis and cell cycle reentry, preceded by stabilization of p53. In contrast, in quiescent p53-null fibroblasts, activation of c-Myc induced cell cycle reentry but not apoptosis. These results suggest that p53 mediates apoptosis as a safeguard mechanism to prevent cell proliferation induced by oncogene activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hermeking, H -- Eick, D -- New York, N.Y. -- Science. 1994 Sep 30;265(5181):2091-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Klinische Molekularbiologie und Tumorgenetik Forschungszentrum fur Umwelt und Gesundheit, GSF, Munchen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091232" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; *Apoptosis ; Cell Line ; Estradiol/pharmacology ; G1 Phase ; Gene Expression Regulation ; Genes, myc ; Genes, p53 ; Mice ; Proto-Oncogene Proteins c-myc/*metabolism ; Tamoxifen/analogs & derivatives/pharmacology ; Transfection ; Tumor Suppressor Protein p53/*metabolism
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  • 11
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    Promoter-selective transcriptional defect in cell cycle mutant ts13 rescued by hTAFII250 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: The TAFII250 subunit of the human transcription factor IID (TFIID) rescues the temperature-sensitive hamster cell line ts13 and overcomes a G1 arrest. Investigation of the transcriptional properties of ts13 nuclear extracts in vitro showed that activation by the site-specific regulators Sp1 and Gal4VP16 is temperature sensitive in ts13 extracts, whereas basal transcription remains unaffected. This transcriptional defect can be rescued by purified human TFIID or by expression of wild-type TAFII250 in ts13 cells. Expression from the cyclin A but not c-fos promoter is temperature sensitive in these mutant cells. Thus, the mutation in TAFII250 appears to have gene-specific effects that may lead to the ts13 cell cycle phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, E H -- Tjian, R -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):811-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303298" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cyclins/genetics ; DNA-Binding Proteins/*genetics/physiology ; Fungal Proteins/physiology ; *G1 Phase ; Genes, fos ; Genetic Complementation Test ; Genetic Vectors ; Histone Acetyltransferases ; Humans ; Mutation ; Nuclear Proteins/*genetics/physiology ; *Promoter Regions, Genetic ; Sp1 Transcription Factor/physiology ; *TATA-Binding Protein Associated Factors ; Temperature ; Trans-Activators/physiology ; Transcription Factor TFIID ; Transcription Factors/pharmacology ; *Transcription, Genetic ; Transfection
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  • 12
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    Transgenic X. laevis embryos from eggs transplanted with nuclei of transfected cultured cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-28
    Description: Transgenic Xenopus laevis embryos were produced by transplantation of transfected cultured cell nuclei into unfertilized eggs. A Xenopus cell line, X-C, was stably transfected with plasmids containing a hygromycin-resistance gene and genes for either beta-galactosidase with a heat shock promoter or chloramphenicol acetyltransferase (CAT) with a muscle-specific actin promoter. Nuclei transplanted from these cells into unfertilized eggs directed development of embryos containing stably integrated copies of the plasmids in each cell. Transgenic embryos showed somite-specific expression of CAT and uniform expression of beta-galactosidase. Transgenic embryos produced by nuclear transplantation should be useful for testing the function of cloned genes in amphibian development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kroll, K L -- Gerhart, J C -- GM07232/GM/NIGMS NIH HHS/ -- GM19363/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Oct 28;266(5185):650-3.〈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/7939720" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Cell Line ; Cell Nucleus/genetics/physiology ; Chloramphenicol O-Acetyltransferase/genetics ; *Cinnamates ; Drug Resistance ; Embryo, Nonmammalian/*physiology ; *Gene Expression ; Genes, Reporter ; Hygromycin B/analogs & derivatives/pharmacology ; *Nuclear Transfer Techniques ; Ovum/physiology ; Plasmids ; Promoter Regions, Genetic ; *Transfection ; Xenopus laevis ; beta-Galactosidase/genetics
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  • 13
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    Identification of the ron gene product as the receptor for the human macrophage stimulating protein (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-07
    Description: Macrophage-stimulating protein (MSP) is a member of the hepatocyte growth factor-scatter factor (HGF-SF) family. Labeled MSP bound to Madin-Darby canine kidney (MDCK) cells transfected with complementary DNA encoding Ron, a cell membrane protein tyrosine kinase. Cross-linking of 125I-labeled MSP to transfected cells (MDCK-RE7 cells) and immunoprecipitation by antibodies to Ron revealed a 220-kilodalton complex, a size consistent with that of MSP (80 kilodaltons) cross-linked to the beta chain of Ron (150 kilodaltons). The binding of 125I-labeled MSP to MDCK-RE7 cells was inhibited by unlabeled MSP, but not by HGF-SF. MSP caused phosphorylation of the beta chain of Ron and induced migration of MDCK-RE7 cells. These results establish the ron gene product as a specific cell-surface receptor for MSP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, M H -- Ronsin, C -- Gesnel, M C -- Coupey, L -- Skeel, A -- Leonard, E J -- Breathnach, R -- New York, N.Y. -- Science. 1994 Oct 7;266(5182):117-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunopathology Section, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939629" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Binding, Competitive ; Cell Line ; Cell Movement/drug effects ; Cross-Linking Reagents ; Dogs ; Growth Substances/*metabolism/pharmacology ; Hepatocyte Growth Factor/metabolism ; Humans ; Phosphorylation ; Plasminogen/metabolism ; *Proto-Oncogene Proteins ; Receptor Protein-Tyrosine Kinases/genetics/*metabolism ; Receptors, Cell Surface/genetics/*metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Binding of 14-3-3 proteins to the protein kinase Raf and effects on its activation (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-16
    Description: To identify proteins that may participate in the activation of the protein kinase Raf, proteins that interact with Raf were selected in a two-hybrid screen. Two members of the 14-3-3 protein family were isolated that interacted with both the amino terminal regulatory regions of Raf and the kinase domain of Raf, but did not compete with the guanine nucleotide-binding protein Ras for binding to Raf. 14-3-3 proteins associated with Raf in mammalian cells and accompanied Raf to the membrane in the presence of activated Ras. In yeast cells expressing Raf and MEK, mammalian 14-3-3 beta or 14-3-3 zeta activated Raf to a similar extent as did expression of Ras. Therefore, 14-3-3 proteins may participate in or be required for the regulation of Raf function. These findings suggest a role for 14-3-3 proteins in Raf-mediated signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freed, E -- Symons, M -- Macdonald, S G -- McCormick, F -- Ruggieri, R -- New York, N.Y. -- Science. 1994 Sep 16;265(5179):1713-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Onyx Pharmaceuticals, Richmond, CA 94806-5206.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8085158" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Amino Acid Sequence ; Animals ; Cell Line ; Cell Membrane/enzymology ; Cytosol/enzymology ; Enzyme Activation ; GTP-Binding Proteins/metabolism ; HeLa Cells ; Humans ; MAP Kinase Kinase 1 ; *Mitogen-Activated Protein Kinase Kinases ; Molecular Sequence Data ; Nerve Tissue Proteins/*metabolism ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Protein-Tyrosine Kinases/genetics/metabolism ; Proto-Oncogene Proteins/chemistry/*metabolism ; Proto-Oncogene Proteins c-raf ; Recombinant Proteins/metabolism ; Saccharomyces cerevisiae/genetics/growth & development ; Signal Transduction ; *Tyrosine 3-Monooxygenase ; Zinc Fingers
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  • 15
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    Association of the protein kinases c-Bcr and Bcr-Abl with proteins of the 14-3-3 family (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-07
    Description: In this study, a protein that interacts with sequences encoded by the first exon of the protein kinase Bcr was cloned. The Bcr-associated protein 1 (Bap-1) is a member of the 14-3-3 family of proteins. Bap-1 interacts with full-length c-Bcr and with the chimeric Bcr-Abl tyrosine kinase of Philadelphia chromosome (Ph1)-positive human leukemias. Bap-1 is a substrate for the Bcr serine-threonine kinase and is also phosphorylated on tyrosine by Bcr-Abl but not by c-Abl. Bap-1 may function in the regulation of c-Bcr and may contribute to the transforming activity of Bcr-Abl in vivo. 14-3-3 proteins are essential for cell proliferation and have a role in determining the timing of mitosis in yeast. Through direct binding to sequences present in Bcr and in other proteins implicated in signaling, the mammalian 14-3-3 proteins may link specific signaling protein components to mitogenic and cell-cycle control pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reuther, G W -- Fu, H -- Cripe, L D -- Collier, R J -- Pendergast, A M -- CA61033/CA/NCI NIH HHS/ -- DK01965/DK/NIDDK NIH HHS/ -- GM07184/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Oct 7;266(5182):129-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939633" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Animals ; Cell Division ; Cell Line ; Cell Transformation, Neoplastic ; Fusion Proteins, bcr-abl/*metabolism ; Humans ; Mice ; Phosphorylation ; Poly(ADP-ribose) Polymerases/metabolism ; Protein-Tyrosine Kinases/*metabolism ; Proteins/isolation & purification/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-bcr ; Rats ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; *Tyrosine 3-Monooxygenase
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  • 16
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    Targeting of G alpha i2 to the Golgi by alternative spliced carboxyl-terminal region (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-07
    Description: Heterotrimeric guanosine triphosphate (GTP)-binding proteins (G proteins) may participate in membrane traffic events. A complementary DNA (cDNA) was isolated from a mouse pituitary cDNA library that corresponded to an alternatively spliced form of the gene encoding the G protein alpha subunit G alpha i2. The cDNA was identical to that encoding G alpha i2 except that the region encoding for the carboxyl-terminal 24 amino acids was replaced by a longer region encoding 35 amino acids that have no sequence similarity with G alpha i2 or other members of the G protein family. This alternative spliced product and the corresponding protein (sGi2) were present in several tissues. Specific antibodies revealed that sGi2 was localized in the Golgi apparatus, suggesting a role in membrane transport. Thus, alternative splicing may generate from a single gene two G protein alpha subunits with differential cellular localization and function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montmayeur, J P -- Borrelli, E -- New York, N.Y. -- Science. 1994 Jan 7;263(5143):95-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes, CNRS, INSERM U184, Faculte de Medecine, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8272874" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cell Membrane/metabolism ; Coatomer Protein ; DNA, Complementary/genetics ; GTP-Binding Protein alpha Subunit, Gi2 ; *GTP-Binding Protein alpha Subunits, Gi-Go ; GTP-Binding Proteins/analysis/chemistry/genetics/*metabolism ; Golgi Apparatus/chemistry/*metabolism ; Mice ; Microtubule-Associated Proteins/analysis ; Molecular Sequence Data ; Oncogene Proteins/analysis/chemistry/genetics/*metabolism ; *Proto-Oncogene Proteins
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  • 17
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    Regulation of MHC class I transport by the molecular chaperone, calnexin (p88, IP90) (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-21
    Description: Assembled class I histocompatibility molecules, consisting of heavy chain, beta 2-microglobulin, and peptide ligand, are transported rapidly to the cell surface. In contrast, the intracellular transport of free heavy chains or peptide-deficient heavy chain-beta 2-microglobulin heterodimers is impaired. A 90-kilodalton membrane-bound chaperone of the endoplasmic reticulum (ER), termed calnexin, associates quantitatively with newly synthesized class I heavy chains, but the functions of calnexin in this interaction are unknown. Class I subunits were expressed alone or in combination with calnexin in Drosophila melanogaster cells. Calnexin retarded the intracellular transport of both peptide-deficient heavy chain-beta 2-microglobulin heterodimers and free heavy chains. Calnexin also impeded the rapid intracellular degradation of free heavy chains. The ability of calnexin to protect and retain class I assembly intermediates is likely to contribute to the efficient intracellular formation of class I-peptide complexes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jackson, M R -- Cohen-Doyle, M F -- Peterson, P A -- Williams, D B -- New York, N.Y. -- Science. 1994 Jan 21;263(5145):384-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8278813" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Transport ; Calcium-Binding Proteins/*metabolism ; Calnexin ; Cell Line ; Drosophila melanogaster ; Endoplasmic Reticulum/*metabolism ; Golgi Apparatus/metabolism ; Histocompatibility Antigens Class I/*metabolism ; Membrane Proteins/*metabolism ; Molecular Sequence Data ; Temperature ; Transfection ; beta 2-Microglobulin/*metabolism
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  • 18
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    Sequential interactions of the TCR with two distinct cytoplasmic tyrosine kinases (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-25
    Description: The T cell antigen receptor (TCR) initiates signals by interacting with cytoplasmic protein tyrosine kinases (PTKs) through a 17-residue sequence motif [called the antigen recognition activation motif (ARAM)] that is contained in the TCR zeta and CD3 chains. TCR stimulation induces the tyrosine phosphorylation of several cellular substrates, including the ARAMs. Lck kinase activity is required for phosphorylation of two conserved tyrosine residues in an ARAM. This phosphorylation leads to the recruitment of a second cytoplasmic PTK, ZAP-70, through both of the ZAP-70 Src homology 2 domains and its phosphorylation. Thus, TCR signal transduction is initiated by the sequential interaction of two PTKs with TCR ARAMs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iwashima, M -- Irving, B A -- van Oers, N S -- Chan, A C -- Weiss, A -- AR-20684/AR/NIAMS NIH HHS/ -- GM39553/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1136-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7509083" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD8/metabolism ; Cell Line ; Cytoplasm/enzymology ; Haplorhini ; Humans ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Membrane Proteins/*metabolism ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Phosphotyrosine ; Protein-Tyrosine Kinases/*metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Signal Transduction ; Tumor Cells, Cultured ; Tyrosine/analogs & derivatives/metabolism ; ZAP-70 Protein-Tyrosine Kinase
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  • 19
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    Autoantibodies to glutamate receptor GluR3 in Rasmussen's encephalitis (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-07-29
    Description: Rasmussen's encephalitis is a progressive childhood disease of unknown cause characterized by severe epilepsy, hemiplegia, dementia, and inflammation of the brain. During efforts to raise antibodies to recombinant glutamate receptors (GluRs), behaviors typical of seizures and histopathologic features mimicking Rasmussen's encephalitis were found in two rabbits immunized with GluR3 protein. A correlation was found between the presence of Rasmussen's encephalitis and serum antibodies to GluR3 detected by protein immunoblot analysis and by immunoreactivity to transfected cells expressing GluR3. Repeated plasma exchanges in one seriously ill child transiently reduced serum titers of GluR3 antibodies, decreased seizure frequency, and improved neurologic function. Thus, GluR3 is an autoantigen in Rasmussen's encephalitis, and an autoimmune process may underlie this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rogers, S W -- Andrews, P I -- Gahring, L C -- Whisenand, T -- Cauley, K -- Crain, B -- Hughes, T E -- Heinemann, S F -- McNamara, J O -- NS17771/NS/NINDS NIH HHS/ -- NS28709/NS/NINDS NIH HHS/ -- NS30990R29/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jul 29;265(5172):648-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salt Lake City Geriatric Research Education and Clinical Center, Veterans Affairs Medical Center, UT.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036512" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Specificity ; Autoantibodies/blood/*immunology ; Brain/pathology ; Cell Line ; Child ; Disease Models, Animal ; Encephalitis/complications/*immunology/pathology/therapy ; Female ; Humans ; Male ; Plasma Exchange ; Rabbits ; Receptors, Glutamate/*immunology ; Recombinant Fusion Proteins/immunology ; Seizures/etiology/immunology
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  • 20
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    Transcriptional activation modulated by homopolymeric glutamine and proline stretches (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-02-11
    Description: Many transcription factors contain proline- or glutamine-rich activation domains. Here it is shown that simple homopolymeric stretches of these amino acids can activate transcription when fused to the DNA binding domain of GAL4 factor. In vitro, activity increased with polymer length, whereas in cell transfection assays maximal activity was achieved by 10 to 30 glutamines or about 10 prolines. Similar results were obtained when glutamine stretches were placed within a [GAL4]-VP16 chimeric protein. Because these stretches are encoded by rapidly evolving triplet repeats (microsatellites), they may be the main cause for modulation of transcription factor activity and thus result in subtle or overt genomic effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerber, H P -- Seipel, K -- Georgiev, O -- Hofferer, M -- Hug, M -- Rusconi, S -- Schaffner, W -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):808-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Molekularbiologie II der Universitat Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303297" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Glutamine/*chemistry/pharmacology ; HeLa Cells ; Humans ; Molecular Sequence Data ; Peptides/*chemistry/pharmacology ; Recombinant Fusion Proteins/pharmacology ; Repetitive Sequences, Nucleic Acid ; Transcription Factors/*chemistry/pharmacology ; *Transcriptional Activation ; Transfection
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  • 21
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    Nitric oxide activation of poly(ADP-ribose) synthetase in neurotoxicity (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-02-04
    Description: Poly(adenosine 5'-diphosphoribose) synthetase (PARS) is a nuclear enzyme which, when activated by DNA strand breaks, adds up to 100 adenosine 5'-diphosphoribose (ADP-ribose) units to nuclear proteins such as histones and PARS itself. This activation can lead to cell death through depletion of beta-nicotinamide adenine dinucleotide (the source of ADP-ribose) and adenosine triphosphate. Nitric oxide (NO) stimulated ADP-ribosylation of PARS in rat brain. Benzamide and other derivatives, which inhibit PARS, blocked N-methyl-D-aspartate- and NO-mediated neurotoxicity with relative potencies paralleling their ability to inhibit PARS. Thus, NO appeared to elicit neurotoxicity by activating PARS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Dawson, V L -- Dawson, T M -- Snyder, S H -- DA-00074/DA/NIDA NIH HHS/ -- DA-00266/DA/NIDA NIH HHS/ -- DA-271-90-7408/DA/NIDA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):687-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, 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/8080500" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzamides/pharmacology ; Brain/cytology/drug effects/enzymology ; Cell Death/drug effects ; Cell Line ; Cells, Cultured ; Cerebral Cortex/cytology/drug effects/enzymology ; DNA Damage ; Enzyme Activation ; Humans ; N-Methylaspartate/*toxicity ; Neurons/cytology/*drug effects/enzymology ; Nitric Oxide/*toxicity ; Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases/*metabolism ; Rats ; Rats, Sprague-Dawley
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  • 22
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    Interaction of IL-2R beta and gamma c chains with Jak1 and Jak3: implications for XSCID and XCID (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-11-11
    Description: Interleukin-2 (IL-2) signaling requires the dimerization of the IL-2 receptor beta.(IL-2R beta) and common gamma (gamma c) chains. Mutations of gamma c can result in X-linked severe combined immunodeficiency (XSCID). IL-2, IL-4, IL-7 (whose receptors are known to contain gamma c), and IL-9 (whose receptor is shown here to contain gamma c) induced the tyrosine phosphorylation and activation of the Janus family tyrosine kinases Jak1 and Jak3. Jak1 and Jak3 associated with IL-2R beta and gamma c, respectively; IL-2 induced Jak3-IL-2R beta and increased Jak3-gamma c associations. Truncations of gamma c, and a gamma c, point mutation causing moderate X-linked combined immunodeficiency (XCID), decreased gamma c-Jak3 association. Thus, gamma c mutations in at least some XSCID and XCID patients prevent normal Jak3 activation, suggesting that mutations of Jak3 may result in an XSCID-like phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Russell, S M -- Johnston, J A -- Noguchi, M -- Kawamura, M -- Bacon, C M -- Friedmann, M -- Berg, M -- McVicar, D W -- Witthuhn, B A -- Silvennoinen, O -- P30 CA21765/CA/NCI NIH HHS/ -- R01 DK42932/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1042-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973658" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Enzyme Activation ; Humans ; Interleukin-2/pharmacology ; Janus Kinase 1 ; Janus Kinase 3 ; Mutation ; Phosphorylation ; Point Mutation ; Protein-Tyrosine Kinases/genetics/*metabolism ; Receptors, Interleukin-2/genetics/*metabolism ; Severe Combined Immunodeficiency/genetics/*immunology/metabolism ; Transfection ; Tyrosine/metabolism
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  • 23
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    A truncated erythropoietin receptor and cell death: a reanalysis (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-04-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakamura, Y -- Nakauchi, H -- New York, N.Y. -- Science. 1994 Apr 22;264(5158):588-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8160019" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Base Sequence ; Cell Division ; Cell Line ; Erythropoietin/pharmacology ; Hematopoietic Stem Cells/cytology/*metabolism ; Humans ; Molecular Sequence Data ; Receptors, Erythropoietin/chemistry/genetics/*physiology ; Signal Transduction ; Transfection
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  • 24
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    Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-03
    Description: Through the study of transcriptional activation in response to interferon alpha (IFN-alpha) and interferon gamma (IFN-gamma), a previously unrecognized direct signal transduction pathway to the nucleus has been uncovered: IFN-receptor interaction at the cell surface leads to the activation of kinases of the Jak family that then phosphorylate substrate proteins called STATs (signal transducers and activators of transcription). The phosphorylated STAT proteins move to the nucleus, bind specific DNA elements, and direct transcription. Recognition of the molecules involved in the IFN-alpha and IFN-gamma pathway has led to discoveries that a number of STAT family members exist and that other polypeptide ligands also use the Jak-STAT molecules in signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Darnell, J E Jr -- Kerr, I M -- Stark, G R -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1415-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Cell Biology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8197455" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA-Binding Proteins/*metabolism ; Genes ; Genetic Complementation Test ; Humans ; Interferon-Stimulated Gene Factor 3 ; Interferon-Stimulated Gene Factor 3, gamma Subunit ; Interferon-alpha/*pharmacology ; Interferon-gamma/*pharmacology ; Molecular Sequence Data ; Mutation ; Protein-Tyrosine Kinases/metabolism ; Regulatory Sequences, Nucleic Acid ; *Signal Transduction ; Transcription Factors/*metabolism ; *Transcriptional Activation
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  • 25
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    Modulation of epithelial cell growth by intraepithelial gamma delta T cells (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-11-18
    Description: The role played in immune surveillance by gamma delta T cells residing in various epithelia has not been clear. It is shown here that activated gamma delta T cells obtained from skin and intestine express the epithelial cell mitogen keratinocyte growth factor (KGF). In contrast, intraepithelial alpha beta T cells, as well as all lymphoid alpha beta and gamma delta T cell populations tested, did not produce KGF or promote the growth of cultured epithelial cells. These results suggest that intraepithelial gamma delta T cells function in surveillance and in repair of damaged epithelial tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boismenu, R -- Havran, W L -- AI32751/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1253-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973709" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Division ; Cell Line ; Cells, Cultured ; Cloning, Molecular ; Dendritic Cells/*physiology ; Epithelial Cells ; Fibroblast Growth Factor 10 ; Fibroblast Growth Factor 7 ; *Fibroblast Growth Factors ; Growth Substances/*biosynthesis/genetics ; Keratinocytes/*cytology ; Lymphocyte Activation ; Mice ; Molecular Sequence Data ; *Receptors, Antigen, T-Cell, gamma-delta ; T-Lymphocyte Subsets/immunology/metabolism/*physiology
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  • 26
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    Prevention of T cell anergy by signaling through the gamma c chain of the IL-2 receptor (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: When stimulated through their antigen receptor without requisite costimulation, T cells enter a state of antigen-specific unresponsiveness termed anergy. In this study, signaling through the common gamma chain of the interleukin-2 (IL-2), IL-4, and IL-7 receptors in the presence of antigen was found to be sufficient to prevent the induction of anergy. After culture with IL-2, IL-4, or IL-7, Jak3 kinase was tyrosine-phosphorylated, which correlated with the prevention of anergy. Therefore, a signal through the common gamma chain may regulate the decision of T cells to either clonally expand or enter a state of anergy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boussiotis, V A -- Barber, D L -- Nakarai, T -- Freeman, G J -- Gribben, J G -- Bernstein, G M -- D'Andrea, A D -- Ritz, J -- Nadler, L M -- AI 35225/AI/NIAID NIH HHS/ -- CA 40216/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1039-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematologic Malignancies, Dana-Farber Cancer Institute, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973657" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Clonal Anergy/*immunology ; Clone Cells ; HLA-DR7 Antigen/immunology ; Humans ; Interleukins/immunology ; Janus Kinase 3 ; Lymphocyte Activation ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Receptors, Antigen, T-Cell/metabolism ; Receptors, Interleukin-2/immunology/*metabolism ; *Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; Tumor Necrosis Factor-alpha/immunology
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    Gem: an induced, immediate early protein belonging to the Ras family (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-08
    Description: A gene encoding a 35-kilodalton guanosine triphosphate (GTP)-binding protein, Gem, was cloned from mitogen-induced human peripheral blood T cells. Gem and Rad, the product of a gene overexpressed in skeletal muscle in individuals with Type II diabetes, constitute a new family of Ras-related GTP-binding proteins. The distinct structural features of this family include the G3 GTP-binding motif, extensive amino- and carboxyl-terminal extensions beyond the Ras-related domain, and a motif that determines membrane association. Gem was transiently expressed in human peripheral blood T cells in response to mitogenic stimulation; the protein was phosphorylated on tyrosine residues and localized to the cytosolic face of the plasma membrane. Deregulated Gem expression prevented proliferation of normal and transformed 3T3 cells. These results suggest that Gem is a regulatory protein, possibly participating in receptor-mediated signal transduction at the plasma membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maguire, J -- Santoro, T -- Jensen, P -- Siebenlist, U -- Yewdell, J -- Kelly, K -- New York, N.Y. -- Science. 1994 Jul 8;265(5169):241-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Pathology, 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/7912851" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; CD4-Positive T-Lymphocytes/metabolism ; Cell Death ; Cell Division ; Cell Line ; Cell Line, Transformed ; Cell Membrane/metabolism ; GTP-Binding Proteins/chemistry/genetics/*metabolism ; Genes, ras ; Guanosine Triphosphate/metabolism ; Humans ; Immediate-Early Proteins/chemistry/genetics/*metabolism ; Mice ; Molecular Sequence Data ; *Monomeric GTP-Binding Proteins ; Mutation ; RNA, Messenger/genetics/metabolism ; Transfection ; *ras Proteins
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  • 28
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    Reconstitution of an operational MHC class II compartment in nonantigen-presenting cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-02
    Description: Professional antigen-presenting cells (APCs) have a distinct compartment in which class II molecules are proposed to acquire antigenic peptides. Genetic evidence suggests that human leukocyte antigen (HLA)-DM, an unusual class II molecule, participates in this process. Peptide acquisition was reconstituted in nonprofessional APCs by transfection of class II, invariant chain (li), and H-2M, the murine equivalent of DM. The H-2M heterodimer appeared in an endosomal compartment, not at the cell surface, and the localization was independent of li. The data presented show that H-2M, class II, and li are the minimally required components for efficient formation of stable class II-peptide complexes, and thus for a functional class II compartment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karlsson, L -- Peleraux, A -- Lindstedt, R -- Liljedahl, M -- Peterson, P A -- AI-26610/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1569-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉R. W. Johnson Pharmaceutical Research Institute, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985028" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Antigen Presentation ; Antigen-Presenting Cells/immunology ; *Antigens, Differentiation, B-Lymphocyte ; B-Lymphocytes/immunology ; Cell Line ; Cell Membrane/immunology ; Endosomes/*immunology ; Fluorescent Antibody Technique ; H-2 Antigens/analysis/genetics/*metabolism ; HLA-DR3 Antigen/*metabolism ; HeLa Cells ; Histocompatibility Antigens Class II/*metabolism ; Humans ; Mice ; Mice, Inbred Strains ; Molecular Sequence Data ; Transfection
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  • 29
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    Prevention of lipopolysaccharide-induced lethal toxicity by tyrosine kinase inhibitors (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-27
    Description: Septic shock results from excessive stimulation of the host immune system, especially macrophages, by lipopolysaccharide (LPS), or endotoxin, which resides on the outer membrane of bacteria. Protein tyrosine kinase inhibitors of the tyrphostin AG 126 family protect mice against LPS-induced lethal toxicity. The protection correlates with the ability of these agents to block LPS-induced production of tumor necrosis factor alpha (TNF-alpha) and nitric oxide in macrophages as well as LPS-induced production of TNF-alpha in vivo. Furthermore, this inhibitory effect correlated with the potency of AG 126 to block LPS-induced tyrosine phosphorylation of a p42MAPK protein substrate in the murine macrophage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Novogrodsky, A -- Vanichkin, A -- Patya, M -- Gazit, A -- Osherov, N -- Levitzki, A -- New York, N.Y. -- Science. 1994 May 27;264(5163):1319-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Felsenstein Medical Research Center, Petach Tikva, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8191285" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzylidene Compounds/*pharmacology ; Biological Assay ; Cell Line ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Enzyme-Linked Immunosorbent Assay ; Female ; Lipopolysaccharides/*toxicity ; Macrophage Activation ; Macrophages, Peritoneal/*drug effects/metabolism ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinase 1 ; Nitric Oxide/*biosynthesis ; Nitriles/*pharmacology ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Tumor Necrosis Factor-alpha/analysis/*biosynthesis/toxicity ; *Tyrphostins
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  • 30
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    Activation of the myogenic lineage by MEF2A, a factor that induces and cooperates with MyoD (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-18
    Description: Muscle enhancer factor-2A (MEF2A), a member of the MADS family, induced myogenic development when ectopically expressed in clones of nonmuscle cells of human clones, a function previously limited to the muscle basic helix-loop-helix (bHLH) proteins. During myogenesis, MEF2A and bHLH proteins cooperatively activate skeletal muscle genes and physically interact through the MADS domain of MEF2A and the three myogenic amino acids of the muscle bHLH proteins. Thus, skeletal myogenesis is mediated by two distinct families of mutually inducible and interactive muscle transcription factors, either of which can initiate the developmental cascade.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaushal, S -- Schneider, J W -- Nadal-Ginard, B -- Mahdavi, V -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1236-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Children's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973707" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Cell Differentiation ; Cell Line ; DNA/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; *Gene Expression Regulation ; Genes, Reporter ; Haplorhini ; Helix-Loop-Helix Motifs ; Humans ; MADS Domain Proteins ; MEF2 Transcription Factors ; Mice ; Molecular Sequence Data ; Muscle, Skeletal/*cytology/metabolism ; MyoD Protein/biosynthesis/*metabolism ; Myogenic Regulatory Factors ; Myogenin/biosynthesis/genetics/metabolism ; Transcription Factors/genetics/*metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 31
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    CD26 antigen and HIV fusion? (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Broder, C C -- Nussbaum, O -- Gutheil, W G -- Bachovchin, W W -- Berger, E A -- New York, N.Y. -- Science. 1994 May 20;264(5162):1156-9; author reply 1162-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7909959" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/*physiology ; Antigens, Differentiation, T-Lymphocyte/*physiology ; Base Sequence ; *Cell Fusion ; Cell Line ; Dipeptidyl Peptidase 4 ; Gene Products, env/*physiology ; Giant Cells/physiology ; HIV-1/*physiology ; Humans ; Hybrid Cells ; Molecular Sequence Data
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 32
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    Characterization of type I receptors for transforming growth factor-beta and activin (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-01
    Description: Transforming growth factor-beta (TGF-beta) and activin exert their effects by binding to heteromeric complexes of type I and type II receptors. The type II receptors for TGF-beta and activin are transmembrane serine-threonine kinases; a series of related receptors, denoted activin receptor-like kinase (ALK) 1 to 5, have recently been identified, and ALK-6 is described here. ALK-5 has been shown to be a functional TGF-beta type I receptor. A systematic analysis revealed that most ALKs formed heteromeric complexes with the type II receptors for TGF-beta and activin after overexpression in COS cells; however, among the six ALKs, only ALK-5 was a functional TGF-beta type I receptor for activation of plasminogen activator inhibitor-1, and only ALK-2 and ALK-4 bound activin with high affinity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉ten Dijke, P -- Yamashita, H -- Ichijo, H -- Franzen, P -- Laiho, M -- Miyazono, K -- Heldin, C H -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):101-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research, Uppsala, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8140412" target="_blank"〉PubMed〈/a〉
    Keywords: Activin Receptors ; Activins ; Amino Acid Sequence ; Animals ; Bone Morphogenetic Protein Receptors, Type I ; Cell Line ; Inhibins/*metabolism ; Ligands ; Mice ; Molecular Sequence Data ; Protein-Serine-Threonine Kinases/chemistry/*metabolism ; Receptors, Growth Factor/chemistry/*metabolism ; Receptors, Transforming Growth Factor beta/chemistry/*metabolism ; Transforming Growth Factor beta/*metabolism
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  • 33
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    Human severe combined immunodeficiency due to a defect in ZAP-70, a T cell tyrosine kinase (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: A homozygous mutation in the kinase domain of ZAP-70, a T cell receptor-associated protein tyrosine kinase, produced a distinctive form of human severe combined immunodeficiency. Manifestations of this disorder included profound immunodeficiency, absence of peripheral CD8+ T cells, and abundant peripheral CD4+ T cells that were refractory to T cell receptor-mediated activation. These findings demonstrate that ZAP-70 is essential for human T cell function and suggest that CD4+ and CD8+ T cells depend on different intracellular signaling pathways to support their development or survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elder, M E -- Lin, D -- Clever, J -- Chan, A C -- Hope, T J -- Weiss, A -- Parslow, T G -- AI29313/AI/NIAID NIH HHS/ -- GM43574/GM/NIGMS NIH HHS/ -- RR01271/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1596-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of California, San Francisco 94143-0110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202712" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cloning, Molecular ; Female ; Frameshift Mutation ; Gene Deletion ; Homozygote ; Humans ; Infant ; Male ; Molecular Sequence Data ; Polymerase Chain Reaction ; Protein-Tyrosine Kinases/*genetics/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Severe Combined Immunodeficiency/*genetics/immunology ; Signal Transduction ; T-Lymphocyte Subsets/*immunology ; Transfection ; Tumor Cells, Cultured ; ZAP-70 Protein-Tyrosine Kinase
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  • 34
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    A MAP kinase targeted by endotoxin and hyperosmolarity in mammalian cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-05
    Description: Mammalian cells respond to endotoxic lipopolysaccharide (LPS) by activation of protein kinase cascades that lead to new gene expression. A protein kinase, p38, that was tyrosine phosphorylated in response to LPS, was cloned. The p38 enzyme and the product of the Saccharomyces cerevisiae HOG1 gene, which are both members of the mitogen-activated protein (MAP) kinase family, have sequences at and adjacent to critical phosphorylation sites that distinguish these proteins from most other MAP kinase family members. Both HOG1 and p38 are tyrosine phosphorylated after extracellular changes in osmolarity. These findings link a signaling pathway in mammalian cells with a pathway in yeast that is responsive to physiological stress.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, J -- Lee, J D -- Bibbs, L -- Ulevitch, R J -- AI15136/AI/NIAID NIH HHS/ -- GM28485/GM/NIGMS NIH HHS/ -- GM37696/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 5;265(5173):808-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7914033" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*chemistry/genetics ; Cell Line ; Endotoxins/*pharmacology ; Genetic Complementation Test ; Lipopolysaccharides/pharmacology ; Macrophages, Peritoneal/enzymology ; Mice ; Mice, Inbred C3H ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Osmotic Pressure ; Paclitaxel/pharmacology ; Saccharomyces cerevisiae/genetics ; *Saccharomyces cerevisiae Proteins ; Sequence Homology, Amino Acid ; Water-Electrolyte Balance/*physiology ; p38 Mitogen-Activated Protein Kinases
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  • 35
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    Molecular basis of mammalian sexual determination: activation of Mullerian inhibiting substance gene expression by SRY (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-02
    Description: The pathway of male sexual development in mammals is initiated by SRY, a gene on the short arm of the Y chromosome. Its expression in the differentiating gonadal ridge directs testicular morphogenesis, characterized by elaboration of Mullerian inhibiting substance (MIS) and testosterone. SRY and MIS each belong to conserved gene families that function in the control of growth and differentiation. Structural and biochemical studies of the DNA binding domain of SRY (the HMG box) revealed a protein-DNA interaction consisting of partial side chain intercalation into a widened minor groove. Functional studies of SRY in a cell line from embryonic gonadal ridge demonstrated activation of a gene-regulatory pathway leading to expression of MIS. SRY molecules containing mutations associated with human sex reversal have altered structural interactions with DNA and failed to induce transcription of MIS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haqq, C M -- King, C Y -- Ukiyama, E -- Falsafi, S -- Haqq, T N -- Donahoe, P K -- Weiss, M A -- GM51558/GM/NIGMS NIH HHS/ -- HD30812/HD/NICHD NIH HHS/ -- P30HD28138/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1494-500.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pediatric Surgical Research Laboratory, Massachusetts General Hospital, Boston 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985018" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Anti-Mullerian Hormone ; Base Sequence ; Cell Line ; DNA/metabolism ; DNA-Binding Proteins/chemistry/*genetics/metabolism ; Female ; *Gene Expression Regulation, Developmental ; Genitalia, Male/*embryology ; *Glycoproteins ; Growth Inhibitors/biosynthesis/*genetics ; Humans ; Male ; Models, Biological ; Models, Molecular ; Molecular Sequence Data ; Mullerian Ducts ; *Nuclear Proteins ; Sex Differentiation/*genetics ; Sex-Determining Region Y Protein ; Testicular Hormones/biosynthesis/*genetics ; Transcription Factors/chemistry/*genetics/metabolism
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  • 36
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    Association of polyomavirus middle tumor antigen with 14-3-3 proteins (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-07-22
    Description: To carry out its transformation function, the middle tumor antigen (MT) of murine polyomavirus associates with a number of cellular proteins involved in regulation of cell proliferation, including pp60c-Src, phosphatidylinositol 3-kinase, protein phosphatase 2A, Src homologous and collagen protein and growth factor receptor-binding protein 2. Here, two additional MT-associated proteins were identified as members of the 14-3-3 family of proteins. Yeast homologs of 14-3-3 proteins have recently been shown to play a role in the timing of mitosis. Thus, regulation of 14-3-3 protein function by MT may contribute to the development of neoplasia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pallas, D C -- Fu, H -- Haehnel, L C -- Weller, W -- Collier, R J -- Roberts, T M -- CA30002/CA/NCI NIH HHS/ -- CA45285/CA/NCI NIH HHS/ -- CA50661/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jul 22;265(5171):535-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular and Molecular Biology, Dana-Farber Cancer Institute, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036498" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; 3T3 Cells ; Adenosine Diphosphate Ribose/metabolism ; Amino Acid Sequence ; Animals ; Antigens, Polyomavirus Transforming/immunology/*metabolism ; *Cell Division ; Cell Line ; *Cell Transformation, Neoplastic ; *Cell Transformation, Viral ; Humans ; Immune Sera ; Mice ; Molecular Sequence Data ; Nerve Tissue Proteins/chemistry/isolation & purification/*metabolism ; Poly(ADP-ribose) Polymerases/metabolism ; Precipitin Tests ; *Tyrosine 3-Monooxygenase
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  • 37
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    ZAP-70 deficiency in an autosomal recessive form of severe combined immunodeficiency (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: Protein tyrosine kinases (PTKs) play an integral role in T cell activation and differentiation. Defects in the Src-family PTKs in mice and in T cell lines have resulted in variable defects in thymic development and in T cell antigen receptor (TCR) signal transduction. Here, three siblings are described with an autosomal recessive form of severe combined immunodeficiency disease (SCID) in which ZAP-70, a non-Src PTK, is absent as a result of mutations in the ZAP-70 gene. This absence is associated with defects in TCR signal transduction, suggesting an important functional role for ZAP-70.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, A C -- Kadlecek, T A -- Elder, M E -- Filipovich, A H -- Kuo, W L -- Iwashima, M -- Parslow, T G -- Weiss, A -- AR-20684/AR/NIAMS NIH HHS/ -- GM39553/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1599-601.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, 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/8202713" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Calcium/metabolism ; Cell Line ; Child ; Female ; Gene Deletion ; *Genes, Recessive ; Humans ; Lymphocyte Activation ; Male ; Molecular Sequence Data ; Mutation ; Point Mutation ; Protein-Tyrosine Kinases/deficiency/*genetics/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Severe Combined Immunodeficiency/*genetics/immunology ; *Signal Transduction ; T-Lymphocyte Subsets/immunology ; ZAP-70 Protein-Tyrosine Kinase
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 38
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    Restoration of X-ray resistance and V(D)J recombination in mutant cells by Ku cDNA (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-14
    Description: Three genetic complementation groups of rodent cells are defective for both repair of x-ray-induced double-strand breaks and V(D)J recombination. Cells from one group lack a DNA end-binding activity that is biochemically and antigenically similar to the Ku autoantigen. Transfection of complementary DNA (cDNA) that encoded the 86-kilodalton subunit of Ku rescued these mutant cells for DNA end-binding activity, x-ray resistance, and V(D)J recombination activity. These results establish a role for Ku in DNA repair and recombination. Furthermore, as a component of a DNA-dependent protein kinase, Ku may initiate a signaling pathway induced by DNA damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smider, V -- Rathmell, W K -- Lieber, M R -- Chu, G -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):288-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Stanford University Medical Center, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, Nuclear ; Cell Line ; Cell Line, Transformed ; Cell Survival/*radiation effects ; Cricetinae ; DNA/*metabolism ; *DNA Helicases ; *DNA Repair ; DNA, Complementary ; DNA-Binding Proteins/genetics/*physiology ; Gene Rearrangement ; Genetic Complementation Test ; Humans ; Nuclear Proteins/genetics/*physiology ; Radiation Tolerance ; *Recombination, Genetic ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Interaction of the p53-regulated protein Gadd45 with proliferating cell nuclear antigen (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-25
    Description: GADD45 is a ubiquitously expressed mammalian gene that is induced by DNA damage and certain other stresses. Like another p53-regulated gene, p21WAF1/CIP1, whose product binds to cyclin-dependent kinases (Cdk's) and proliferating cell nuclear antigen (PCNA), GADD45 has been associated with growth suppression. Gadd45 was found to bind to PCNA, a normal component of Cdk complexes and a protein involved in DNA replication and repair. Gadd45 stimulated DNA excision repair in vitro and inhibited entry of cells into S phase. These results establish GADD45 as a link between the p53-dependent cell cycle checkpoint and DNA repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, M L -- Chen, I T -- Zhan, Q -- Bae, I -- Chen, C Y -- Gilmer, T M -- Kastan, M B -- O'Connor, P M -- Fornace, A J Jr -- ES05777/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1376-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973727" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division/drug effects ; Cell Line ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/metabolism ; DNA/biosynthesis ; DNA Damage ; *DNA Repair ; *Genes, p53 ; Humans ; Intracellular Signaling Peptides and Proteins ; Proliferating Cell Nuclear Antigen/*metabolism ; Proteins/*metabolism/pharmacology ; Recombinant Proteins/metabolism/pharmacology ; S Phase/*drug effects ; Transfection ; Tumor Cells, Cultured
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    Retention of unassembled components of integral membrane proteins by calnexin (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-21
    Description: Quality control mechanisms prevent the cell surface expression of incompletely assembled multisubunit receptors such as the T cell receptor (TCR). The molecular chaperone function of calnexin (IP90, p88), a 90-kilodalton protein that resides in the endoplasmic reticulum (ER), in the retention of representative chains of the TCR-CD3 complex in the ER was tested. Truncation mutants of calnexin, when transiently expressed in COS cells, were exported from the ER and either accumulated in the Golgi or progressed to the cell surface. CD3 epsilon chains cotransfected with the forms of calnexin that were not retained in the ER exited the ER and colocalized with calnexin. Since engineered calnexin determined the intracellular localization of the proteins associated with it, it is concluded that calnexin interacts with incompletely assembled TCR components and retains them in the ER.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rajagopalan, S -- Xu, Y -- Brenner, M B -- New York, N.Y. -- Science. 1994 Jan 21;263(5145):387-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Rheumatology and Immunology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8278814" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD3/*metabolism ; Base Sequence ; Calcium-Binding Proteins/analysis/chemistry/*metabolism ; Calnexin ; Cell Line ; Cell Membrane/metabolism ; Endoplasmic Reticulum/*metabolism ; Golgi Apparatus/metabolism ; Histocompatibility Antigens Class I/metabolism ; Lysosomes/metabolism ; Membrane Proteins/analysis/chemistry/*metabolism ; Molecular Sequence Data ; Nuclear Envelope/metabolism ; Receptor-CD3 Complex, Antigen, T-Cell/*metabolism ; Recombinant Proteins/metabolism ; Transfection
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    Old protein provides new clue to nerve regeneration puzzle (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1800-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7522343" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Cell Line ; Central Nervous System/*cytology ; Ganglia, Spinal/cytology ; Myelin Proteins/pharmacology/*physiology ; Myelin-Associated Glycoprotein ; Nerve Regeneration/*physiology ; Neurites/physiology ; Neurons/*physiology ; Neurons, Afferent/physiology ; Rats
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  • 42
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    An interleukin-4-induced transcription factor: IL-4 Stat (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-16
    Description: Interleukin-4 (IL-4) is an immunomodulatory cytokine secreted by activated T lymphocytes, basophils, and mast cells. It plays an important role in modulating the balance of T helper (Th) cell subsets, favoring expansion of the Th2 lineage relative to Th1. Imbalance of these T lymphocyte subsets has been implicated in immunological diseases including allergy, inflammation, and autoimmune disease. IL-4 may mediate its biological effects, at least in part, by activating a tyrosine-phosphorylated DNA binding protein. This protein has now been purified and its encoding gene cloned. Examination of the primary amino acid sequence of this protein indicates that it is a member of the signal transducers and activators of transcription (Stat) family of DNA binding proteins, hereby designated IL-4 Stat. Study of the inhibitory activities of phosphotyrosine-containing peptides derived from the intracellular domain of the IL-4 receptor provided evidence for direct coupling of receptor and transcription factor during the IL-4 Stat activation cycle. Such observations indicate that IL-4 Stat has the same functional domain for both receptor coupling and dimerization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hou, J -- Schindler, U -- Henzel, W J -- Ho, T C -- Brasseur, M -- McKnight, S L -- New York, N.Y. -- Science. 1994 Sep 16;265(5179):1701-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tularik, Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8085155" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Cloning, Molecular ; Cross-Linking Reagents ; DNA/metabolism ; DNA-Binding Proteins/chemistry/genetics/isolation & purification/*metabolism ; Humans ; Interleukin-4/*pharmacology ; Interleukin-4 Receptor alpha Subunit ; Models, Biological ; Molecular Sequence Data ; Monocytes/metabolism ; Phosphopeptides/metabolism/pharmacology ; Phosphorylation ; Polymers ; Receptors, Cell Surface ; Receptors, Interleukin-4 ; Receptors, Mitogen/*metabolism ; STAT6 Transcription Factor ; Trans-Activators/chemistry/genetics/isolation & purification/*metabolism ; Transcription Factors/chemistry/genetics/*metabolism
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  • 43
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    Autoproteolysis in hedgehog protein biogenesis (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-12-02
    Description: Extracellular signaling proteins encoded by the hedgehog (hh) multigene family are responsible for the patterning of a variety of embryonic structures in vertebrates and invertebrates. The Drosophila hh gene has now been shown to generate two predominant protein species that are derived by an internal autoproteolytic cleavage of a larger precursor. Mutations that reduced the efficiency of autoproteolysis in vitro diminished precursor cleavage in vivo and also impaired the signaling and patterning activities of the HH protein. The two HH protein species exhibited distinctive biochemical properties and tissue distribution, and these differences suggest a mechanism that could account for the long- and short-range signaling activities of HH in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, J J -- Ekker, S C -- von Kessler, D P -- Porter, J A -- Sun, B I -- Beachy, P A -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1528-37.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Biology and Genetics, Johns Hopkins School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985023" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Drosophila/embryology/genetics/*metabolism ; *Drosophila Proteins ; Embryo, Nonmammalian/*metabolism ; Embryonic Induction ; Gene Expression Regulation, Developmental ; Genes, Insect ; Hedgehog Proteins ; Models, Biological ; Molecular Sequence Data ; Mutation ; Protein Precursors/chemistry/genetics/metabolism ; *Protein Processing, Post-Translational ; Proteins/chemistry/genetics/*metabolism ; Serine Endopeptidases/chemistry ; *Signal Transduction
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  • 44
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    Coatomer interaction with di-lysine endoplasmic reticulum retention motifs (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-18
    Description: Although signals for retention in the endoplasmic reticulum (ER) have been identified in the cytoplasmic domain of various ER-resident type I transmembrane proteins, the mechanisms responsible for ER retention are still unknown. Yeast and mammalian ER retention motifs interacted specifically in cell lysates with the coatomer, a polypeptide complex implicated in membrane traffic. Mutations that affect the ER retention capacity of the motifs also abolished binding of the coatomer. These results suggest a role for the coatomer in the retrieval of transmembrane proteins to the ER in both yeast and mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cosson, P -- Letourneur, F -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1629-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128252" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Transport ; Cell Line ; Coatomer Protein ; Endoplasmic Reticulum/*metabolism ; Fungal Proteins/chemistry/*metabolism ; Golgi Apparatus/metabolism ; *Hexosyltransferases ; Lysine/chemistry/*metabolism ; Membrane Proteins/*metabolism ; Molecular Sequence Data ; Mutation ; Recombinant Fusion Proteins/chemistry/metabolism ; Transferases/chemistry/*metabolism
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  • 45
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    Calcium-calmodulin modulation of the olfactory cyclic nucleotide-gated cation channel (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-11-25
    Description: Although several ion channels have been reported to be directly modulated by calcium-calmodulin, they have not been conclusively shown to bind calmodulin, nor are the modulatory mechanisms understood. Study of the olfactory cyclic nucleotide-activated cation channel, which is modulated by calcium-calmodulin, indicates that calcium-calmodulin directly binds to a specific domain on the amino terminus of the channel. This binding reduces the effective affinity of the channel for cyclic nucleotides, apparently by acting on channel gating, which is tightly coupled to ligand binding. The data reveal a control mechanism that resembles those underlying the regulation of enzymes by calmodulin. The results also point to the amino-terminal part of the olfactory channel as an element for gating, which may have general significance in the operation of ion channels with similar overall structures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, M -- Chen, T Y -- Ahamed, B -- Li, J -- Yau, K W -- EY 06837/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1348-54.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Baltimore, MD.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7526466" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Calcium/*metabolism ; Calmodulin/*metabolism ; Cell Line ; Cyclic AMP/*metabolism ; Cyclic GMP/*metabolism ; Humans ; *Ion Channel Gating ; Ion Channels/chemistry/*metabolism ; Molecular Sequence Data ; Olfactory Receptor Neurons/metabolism ; Peptides/metabolism ; Protein Structure, Secondary ; Rats ; Recombinant Fusion Proteins/metabolism
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  • 46
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    Stat3: a STAT family member activated by tyrosine phosphorylation in response to epidermal growth factor and interleukin-6 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-01
    Description: The STAT family of proteins carries out a dual function: signal transduction and activation of transcription. A new family member, Stat3, becomes activated through phosphorylation on tyrosine as a DNA binding protein in response to epidermal growth factor (EGF) and interleukin-6 (IL-6) but not interferon gamma (IFN-gamma). It is likely that this phosphoprotein forms homodimers as well as heterodimers with the first described member of the STAT family, Stat91 (renamed Stat1 alpha), which is activated by the IFNs and EGF. Differential activation of different STAT proteins in response to different ligands should help to explain specificity in nuclear signaling from the cell surface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhong, Z -- Wen, Z -- Darnell, J E Jr -- AI32489/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):95-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Cell Biology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8140422" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA/metabolism ; DNA-Binding Proteins/chemistry/genetics/isolation & purification/*metabolism ; Epidermal Growth Factor/*pharmacology ; Humans ; Interferon-gamma ; Interleukin-6/*pharmacology ; Mice ; Molecular Sequence Data ; Phosphorylation ; Regulatory Sequences, Nucleic Acid ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; Sequence Alignment ; Trans-Activators/metabolism ; Transfection ; Tumor Cells, Cultured ; Tyrosine/metabolism
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    Interaction of MHC class I molecules with the transporter associated with antigen processing (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-27
    Description: The transporter associated with antigen processing (TAP) delivers cytosolic peptides into the endoplasmic reticulum (ER) where they bind to nascent class 1 histocompatibility molecules. Class 1-peptide complexes are then displayed at the cell surface for recognition by cytotoxic T lymphocytes. Immunoprecipitation of either TAP or class 1 molecules revealed an association between the transporter and diverse class 1 products. TAP bound preferentially to heterodimers of the class 1 heavy chain and beta 2-microglobulin, and the complex subsequently dissociated in parallel with transport of class 1 molecules from the ER to the Golgi apparatus. The TAP-class 1 complexes could also be dissociated in vitro by the addition of class 1-binding peptides. The association of class 1 molecules with TAP likely promotes efficient capture of peptides before their exposure to the lumen of the ER.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suh, W K -- Cohen-Doyle, M F -- Fruh, K -- Wang, K -- Peterson, P A -- Williams, D B -- New York, N.Y. -- Science. 1994 May 27;264(5163):1322-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8191286" target="_blank"〉PubMed〈/a〉
    Keywords: *ATP-Binding Cassette Transporters ; Amino Acid Sequence ; Animals ; *Antigen Presentation ; Biological Transport ; Carrier Proteins/immunology/*metabolism ; Cell Line ; Endoplasmic Reticulum/metabolism ; Golgi Apparatus/metabolism ; H-2 Antigens/*metabolism ; Immune Sera ; Mice ; Molecular Sequence Data ; Precipitin Tests ; Protein Binding ; beta 2-Microglobulin/metabolism
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    Analysis and expression of a cloned pre-T cell receptor gene (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-18
    Description: The T cell antigen receptor (TCR) beta chain regulates early T cell development in the absence of the TCR alpha chain. The developmentally controlled gene described here encodes the pre-TCR alpha (pT alpha) chain, which covalently associates with TCR beta and with the CD3 proteins forms a pre-TCR complex that transduces signals in immature thymocytes. Unlike the lambda 5 pre-B cell receptor protein, the pT alpha chain is a type I transmembrane protein whose cytoplasmic tail contains two potential phosphorylation sites and a Src homology 3 (SH3)-domain binding sequence. Pre-TCR alpha transfection experiments indicated that surface expression of the pre-TCR is controlled by additional developmentally regulated proteins. Identification of the pT alpha gene represents an essential step in the structure-function analysis of the pre-TCR complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saint-Ruf, C -- Ungewiss, K -- Groettrup, M -- Bruno, L -- Fehling, H J -- von Boehmer, H -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1208-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite INSERM 373, Institut Necker, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973703" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD3/metabolism ; Base Sequence ; Cell Line ; *Cloning, Molecular ; DNA, Complementary/genetics ; *Gene Expression Regulation, Developmental ; Gene Rearrangement ; Membrane Glycoproteins/chemistry/*genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Open Reading Frames ; Phosphorylation ; Polymerase Chain Reaction ; Rabbits ; Receptors, Antigen, T-Cell, alpha-beta/chemistry/*genetics/metabolism ; Signal Transduction ; T-Lymphocytes/*immunology ; Transfection
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  • 49
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    Requirement for CD8 beta chain in positive selection of CD8-lineage T cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-25
    Description: CD8 is either an alpha alpha homodimer or an alpha beta heterodimer, although most peripheral CD8-lineage T cells express only the CD8 alpha beta heterodimer. The physiological function of CD8 beta was elucidated with mice that were chimeric for the homozygous disruption of the CD8 beta gene. The CD8 beta-1- T cells developed normally to CD4+CD8+ stage, but did not efficiently differentiate further, which resulted in few peripheral CD8+ T cells. The number of peripheral CD8+ T cells was restored by transfer of an exogenous CD8 beta gene into CD8 beta-deficient T cells. Thus, CD8 beta is necessary for the maturation of CD8+ T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakayama, K -- Negishi, I -- Kuida, K -- Louie, M C -- Kanagawa, O -- Nakauchi, H -- Loh, D Y -- AI 34580/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1131-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, 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/8108731" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/genetics ; Antigens, CD8/chemistry/genetics/*physiology ; CD4-CD8 Ratio ; Cell Differentiation ; Cell Line ; Chimera ; Histocompatibility Antigens Class I/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutation ; Phenotype ; Receptors, Antigen, T-Cell/metabolism ; T-Lymphocyte Subsets/cytology/*immunology/metabolism ; Transfection
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  • 50
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    Accumulation of HLA-DM, a regulator of antigen presentation, in MHC class II compartments (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-02
    Description: The HLA-DM genes encode an unconventional HLA (human leukocyte antigen) class II molecule that is required for appropriate binding of peptide to classical HLA class II products. In the absence of DM, other class II molecules are unstable upon electrophoresis in sodium dodecyl sulfate and are largely associated with a nested set of peptides derived from the invariant chain called CLIP, for class II-associated invariant chain peptides. DMA and DMB associated and accumulated in multilaminar, intracellular compartments with classical class II molecules, but were found infrequently, if at all, at the cell surface. Thus, DM may facilitate peptide binding to class II molecules within these intracellular compartments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanderson, F -- Kleijmeer, M J -- Kelly, A -- Verwoerd, D -- Tulp, A -- Neefjes, J J -- Geuze, H J -- Trowsdale, J -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1566-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Immunogenetics Laboratory, Imperial Cancer Research Fund, Holborn, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985027" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Cell Compartmentation ; Cell Line ; Cell Membrane/immunology ; Endoplasmic Reticulum/immunology ; Genes, MHC Class II ; HLA-D Antigens/analysis/genetics/*metabolism ; Histocompatibility Antigens Class I/analysis ; Histocompatibility Antigens Class II/analysis/*metabolism ; Humans ; L Cells (Cell Line) ; Mice ; Microscopy, Immunoelectron ; Subcellular Fractions/immunology ; Tumor Cells, Cultured
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    Ligands for EPH-related receptor tyrosine kinases that require membrane attachment or clustering for activity (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-04
    Description: The EPH-related transmembrane tyrosine kinases constitute the largest known family of receptor-like tyrosine kinases, with many members displaying specific patterns of expression in the developing and adult nervous system. A family of cell surface-bound ligands exhibiting distinct, but overlapping, specificities for these EPH-related kinases was identified. These ligands were unable to act as conventional soluble factors. However, they did function when presented in membrane-bound form, suggesting that they require direct cell-to-cell contact to activate their receptors. Membrane attachment may serve to facilitate ligand dimerization or aggregation, because antibody-mediated clustering activated previously inactive soluble forms of these ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, S -- Gale, N W -- Aldrich, T H -- Maisonpierre, P C -- Lhotak, V -- Pawson, T -- Goldfarb, M -- Yancopoulos, G D -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):816-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, Tarrytown, NY 10591.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973638" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cell Membrane/*metabolism ; *DNA-Binding Proteins ; Ephrin-A1 ; Ephrin-B1 ; Humans ; Ligands ; Membrane Proteins/chemistry/*metabolism ; Molecular Sequence Data ; Neurons/metabolism ; Phosphorylation ; Proteins/chemistry/*metabolism ; *Proto-Oncogene Proteins ; Receptor Protein-Tyrosine Kinases/*metabolism ; *Receptor, EphA5 ; Recombinant Fusion Proteins/metabolism ; Retroviridae Proteins, Oncogenic/*metabolism ; Solubility ; *Transcription Factors ; Transfection ; Tumor Cells, Cultured ; ets-Domain Protein Elk-1
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    Transformation of mammalian cells by constitutively active MAP kinase kinase (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-12
    Description: Mitogen-activated protein (MAP) kinase kinase (MAPKK) activates MAP kinase in a signal transduction pathway that mediates cellular responses to growth and differentiation factors. Oncogenes such as ras, src, raf, and mos have been proposed to transform cells by prolonging the activated state of MAPKK and of components downstream in the signaling pathway. To test this hypothesis, constitutively active MAPKK mutants were designed that had basal activities up to 400 times greater than that of the unphosphorylated wild-type kinase. Expression of these mutants in mammalian cells activated AP-1-regulated transcription. The cells formed transformed foci, grew efficiently in soft agar, and were highly tumorigenic in nude mice. These findings indicate that constitutive activation of MAPKK is sufficient to promote cell transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mansour, S J -- Matten, W T -- Hermann, A S -- Candia, J M -- Rong, S -- Fukasawa, K -- Vande Woude, G F -- Ahn, N G -- GM48521/GM/NIGMS NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 12;265(5174):966-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of Colorado, Boulder 80309.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8052857" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Cell Division ; Cell Line ; *Cell Transformation, Neoplastic ; Enzyme Activation ; Genes, mos ; Mice ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase Kinases ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Protein Kinases/genetics/*metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins c-jun/metabolism ; Signal Transduction ; Transfection
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    An alternative to SH2 domains for binding tyrosine-phosphorylated proteins (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-16
    Description: Src homology 2 (SH2) domains bind specifically to tyrosine-phosphorylated proteins that participate in signaling by growth factors and oncogenes. A protein domain was identified that bound specifically to the tyrosine-phosphorylated form of its target protein but differs from known SH2 sequences. Phosphotyrosine-binding (PTB) domains were found in two proteins: SHC, a protein implicated in signaling through Ras; and SCK, encoded by a previously uncharacterized gene. The PTB domain of SHC specifically bound to a tyrosine-phosphorylated 145-kilodalton protein. PTB domains are an alternative to SH2 domains for specifically recruiting tyrosine-phosphorylated proteins into signaling complexes and are likely to take part in signaling by many growth factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kavanaugh, W M -- Williams, L T -- K11 HL02714/HL/NHLBI NIH HHS/ -- R01 HL32898/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1862-5.〈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/7527937" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; *Adaptor Proteins, Signal Transducing ; *Adaptor Proteins, Vesicular Transport ; Amino Acid Sequence ; Animals ; Cell Line ; Humans ; Mice ; Molecular Sequence Data ; Phosphoproteins/*metabolism ; Phosphorylation ; Phosphotyrosine ; Platelet-Derived Growth Factor/pharmacology ; Protein Binding ; Protein-Tyrosine Kinases/chemistry/metabolism ; Proteins/chemistry/*metabolism ; Shc Signaling Adaptor Proteins ; *Signal Transduction ; Tyrosine/*analogs & derivatives/metabolism
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  • 54
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    Lymphotactin: a cytokine that represents a new class of chemokine (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-25
    Description: In this study, the cytokine-producing profile of progenitor T cells (pro-T cells) was determined. During screening of a complementary DNA library generated from activated mouse pro-T cells, a cytokine designated lymphotactin was discovered. Lymphotactin is similar to members of both the Cys-Cys and Cys-X-Cys chemokine families but lacks two of the four cysteine residues that are characteristic of the chemokines. Lymphotactin is also expressed in activated CD8+ T cells and CD4-CD8- T cell receptor alpha beta + thymocytes. It has chemotactic activity for lymphocytes but not for monocytes or neutrophils. The gene encoding lymphotactin maps to chromosome one. Taken together, these observations suggest that lymphotactin represents a novel addition to the chemokine superfamily.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelner, G S -- Kennedy, J -- Bacon, K B -- Kleyensteuber, S -- Largaespada, D A -- Jenkins, N A -- Copeland, N G -- Bazan, J F -- Moore, K W -- Schall, T J -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1395-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, DNAX Research Institute of Cellular and Molecular Biology, Palo Alto, CA 94304.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973732" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Calcium/metabolism ; Cell Line ; Chemokine CCL4 ; *Chemokines, C ; *Chemotaxis, Leukocyte ; Cytokines/pharmacology ; Hematopoietic Stem Cells/*immunology ; Humans ; Lymphokines/chemistry/genetics/isolation & purification/pharmacology/*physiology ; Macrophage Inflammatory Proteins ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Monokines/pharmacology ; Recombinant Proteins ; Sequence Alignment ; Sialoglycoproteins/chemistry/genetics/isolation & ; purification/pharmacology/*physiology ; Signal Transduction ; T-Lymphocyte Subsets/*immunology
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  • 55
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    A biochemical function for ras--at last (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hall, A -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1413-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory for Molecular Cell Biology, University College London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8197454" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Line ; Cell Membrane/*enzymology ; GTP-Binding Proteins/*physiology ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Models, Biological ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-raf ; Signal Transduction
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  • 56
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    Differential adhesion of cells to enantiomorphous crystal surfaces (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-03-11
    Description: Interactions during cell adhesion to external surfaces may reach the level of discrimination of molecular chirality. Cultured epithelial cells interact differently with the [011] faces of the (R,R) and (S,S) calcium tartrate tetrahydrate crystals. In a modified version of the classical Pasteur experiment, the enantiomorphous crystals were sorted out from a 1:1 mixture by the selective adhesion of cells to the (R,R) crystals. This stereospecificity results from molecular recognition between chiral components on the cell surface and the structured crystal surface. Crystals may allow experimental differentiation between distinct stages in cell substrate contacts, providing mechanistic information not readily attainable on conventional heterogeneous surfaces.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanein, D -- Geiger, B -- Addadi, L -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1413-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Structural Biology, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128221" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Adhesion ; Cell Line ; Computer Graphics ; Crystallization ; Humans ; Oligopeptides/pharmacology ; Stereoisomerism ; Surface Properties ; *Tartrates ; Tumor Cells, Cultured ; Xenopus laevis
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  • 57
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    FGF-2: apical ectodermal ridge growth signal for chick limb development (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-01
    Description: The apical ectodermal ridge permits growth and elongation of amniote limb buds; removal causes rapid changes in mesodermal gene expression, patterned cell death, and truncation of the limb. Ectopic fibroblast growth factor (FGF)-2 supplied to the chick apical bud mesoderm after ridge removal will sustain normal gene expression and cell viability, and allow relatively normal limb development. A bioassay for FGFs demonstrated that FGF-2 was the only detectable FGF in chick limb bud extracts. By distribution and bioactivity, FGF-2 is the prime candidate for the chick limb bud apical ridge growth signal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fallon, J F -- Lopez, A -- Ros, M A -- Savage, M P -- Olwin, B B -- Simandl, B K -- 5T32GM07507/GM/NIGMS NIH HHS/ -- HD20743/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):104-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Anatomy Department, University of Wisconsin, Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7908145" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Assay ; Cell Death ; Cell Differentiation ; Cell Line ; Cell Survival ; Chick Embryo ; DNA-Binding Proteins/genetics ; Ectoderm/chemistry/*physiology ; Extremities/*embryology ; Fibroblast Growth Factors/analysis/metabolism/pharmacology/*physiology ; Gene Expression ; Genes, Homeobox ; *Homeodomain Proteins ; Humans ; MSX1 Transcription Factor ; Mesoderm/*cytology/metabolism ; Muscles/cytology ; Recombinant Proteins/metabolism/pharmacology ; *Transcription Factors
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    Association of insulin receptor substrate-1 with integrins (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-02
    Description: Insulin stimulation was found to promote association of the alpha v beta 3 integrin (a vitronectin receptor) with insulin receptor substrate-1 (IRS-1), an intracellular protein that mediates insulin signaling by binding other signaling molecules, including growth factor receptor-bound protein 2 (Grb2) and phosphatidylinositol-3' kinase. Insulin-treated cells expressing the alpha v beta 3 integrin showed 2.5 times more DNA synthesis when plated on vitronectin than on other substrates, whereas cells expressing another vitronectin receptor, alpha v beta 5, did not show this difference. The association between integrin and IRS-1 may be a mechanism for the synergistic action of growth factor and extracellular matrix receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vuori, K -- Ruoslahti, E -- CA 28896/CA/NCI NIH HHS/ -- CA 30199/CA/NCI NIH HHS/ -- CA 42507/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1576-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Center, La Jolla Cancer Research Foundation, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7527156" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Collagen ; DNA/biosynthesis ; Glycoproteins ; Humans ; Insulin/pharmacology ; Insulin Receptor Substrate Proteins ; Integrins/*metabolism ; Molecular Sequence Data ; Phosphoproteins/*metabolism ; Phosphorylation ; Rats ; Receptor, Insulin ; Receptors, Cytoadhesin/*metabolism ; Receptors, Vitronectin ; Transfection ; Tumor Cells, Cultured ; Vitronectin
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  • 59
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    Beta 2-microglobulin-independent MHC class Ib molecule expressed by human intestinal epithelium (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-07-08
    Description: A major histocompatibility complex class Ib protein, CD1d, is expressed by human intestinal epithelial cells (IECs) and is a ligand for CD8+ T cells. CD1d was found to be expressed on the surface of human IECs as a 37-kilodalton protein that was beta 2-microglobulin (beta 2M) independent with no N-linked carbohydrate. Transfection into a beta 2M- cell line confirmed that CD1d could be expressed at the cell surface in the absence of beta 2M. These data indicate that IECs use a specialized pathway for CD1d synthesis and that a beta 2M-independent class Ib protein may be the normal ligand for some intestinal T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balk, S P -- Burke, S -- Polischuk, J E -- Frantz, M E -- Yang, L -- Porcelli, S -- Colgan, S P -- Blumberg, R S -- R01 AI33911/AI/NIAID NIH HHS/ -- R01 DK44319/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1994 Jul 8;265(5169):259-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hematology-Oncology Division, Beth Israel Hospital, Harvard Medical School, Boston, MA 02215.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7517575" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD/analysis/*biosynthesis/chemistry ; Antigens, CD1 ; Antigens, CD8 ; Cell Line ; Cell Membrane/immunology ; Electrophoresis, Polyacrylamide Gel ; Epithelial Cells ; Epithelium/immunology ; Glycosylation ; Humans ; Immunoblotting ; Intestinal Mucosa/cytology/*immunology ; Molecular Weight ; Precipitin Tests ; T-Lymphocyte Subsets/immunology ; Transfection ; beta 2-Microglobulin/*physiology
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    Rational design of potent, bioavailable, nonpeptide cyclic ureas as HIV protease inhibitors (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-21
    Description: Mechanistic information and structure-based design methods have been used to design a series of nonpeptide cyclic ureas that are potent inhibitors of human immunodeficiency virus (HIV) protease and HIV replication. A fundamental feature of these inhibitors is the cyclic urea carbonyl oxygen that mimics the hydrogen-bonding features of a key structural water molecule. The success of the design in both displacing and mimicking the structural water molecule was confirmed by x-ray crystallographic studies. Highly selective, preorganized inhibitors with relatively low molecular weight and high oral bioavailability were synthesized.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lam, P Y -- Jadhav, P K -- Eyermann, C J -- Hodge, C N -- Ru, Y -- Bacheler, L T -- Meek, J L -- Otto, M J -- Rayner, M M -- Wong, Y N -- New York, N.Y. -- Science. 1994 Jan 21;263(5145):380-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Virology Research, DuPont Merck Pharmaceutical Company, Wilmington, DE 19880.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8278812" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Animals ; Azepines/*chemistry/metabolism/pharmacokinetics/pharmacology ; Binding Sites ; Biological Availability ; Cell Line ; Crystallography, X-Ray ; Dogs ; *Drug Design ; Drug Evaluation, Preclinical ; HIV Protease/chemistry/metabolism ; HIV Protease Inhibitors/*chemistry/metabolism/pharmacokinetics/pharmacology ; HIV-1/drug effects/physiology ; Hydrogen Bonding ; Models, Molecular ; Molecular Conformation ; Molecular Weight ; Rats ; Recombinant Proteins/chemistry/metabolism ; Urea ; Virus Replication/drug effects
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    Dependence of enhancer-mediated transcription of the immunoglobulin mu gene on nuclear matrix attachment regions (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-26
    Description: Transcription of the immunoglobulin mu heavy chain locus is regulated by an intronic enhancer that is flanked on both sides by nuclear matrix attachment regions (MARs). These MARs have now been shown to be essential for transcription of a rearranged mu gene in transgenic B lymphocytes, but they were not required in stably transfected tissue culture cells. Normal rates of transcriptional initiation at a variable region promoter and the formation of an extended deoxyribonuclease I (DNase I)--sensitive chromatin domain were dependent on MARs, although DNase I hypersensitivity at the enhancer was detected in the absence of MARs. Thus, transcriptional activation of the mu gene during normal lymphoid development requires a synergistic collaboration between the enhancer and flanking MARs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Forrester, W C -- van Genderen, C -- Jenuwein, T -- Grosschedl, R -- New York, N.Y. -- Science. 1994 Aug 26;265(5176):1221-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California at San Francisco (UCSF) 94143-0414.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066460" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Base Sequence ; Cell Line ; *Enhancer Elements, Genetic ; Gene Rearrangement ; *Genes, Immunoglobulin ; Immunoglobulin mu-Chains/*genetics ; Introns ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Nuclear Matrix/*metabolism ; *Regulatory Sequences, Nucleic Acid ; *Transcription, Genetic ; Transcriptional Activation ; Transfection
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  • 62
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    Association and activation of Jak-Tyk kinases by CNTF-LIF-OSM-IL-6 beta receptor components (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-07
    Description: A recently defined family of cytokines, consisting of ciliary neurotrophic factor (CNTF), leukemia inhibitory factor (LIF), oncostatin M (OSM), and interleukin-6 (IL-6), utilize the Jak-Tyk family of cytoplasmic tyrosine kinases. The beta receptor components for this cytokine family, gp130 and LIF receptor beta, constitutively associate with Jak-Tyk kinases. Activation of these kinases occurs as a result of ligand-induced dimerization of the receptor beta components. Unlike other cytokine receptors studied to date, the receptors for the CNTF cytokine family utilize all known members of the Jak-Tyk family, but induce distinct patterns of Jak-Tyk phosphorylation in different cell lines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stahl, N -- Boulton, T G -- Farruggella, T -- Ip, N Y -- Davis, S -- Witthuhn, B A -- Quelle, F W -- Silvennoinen, O -- Barbieri, G -- Pellegrini, S -- P30 CA21765/CA/NCI NIH HHS/ -- R01 DK42932/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1994 Jan 7;263(5143):92-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, Inc., Tarrytown, NY 10591.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8272873" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, CD ; Cell Line ; Ciliary Neurotrophic Factor ; Cytokine Receptor gp130 ; Cytokines/metabolism/*pharmacology ; Enzyme Activation ; *Growth Inhibitors ; *Interleukin-6 ; Janus Kinase 1 ; Janus Kinase 2 ; Leukemia Inhibitory Factor ; *Lymphokines ; Membrane Glycoproteins/*metabolism ; Nerve Tissue Proteins/metabolism/pharmacology ; Oncostatin M ; Peptides/metabolism/pharmacology ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Proteins/metabolism ; *Proto-Oncogene Proteins ; Receptor, Ciliary Neurotrophic Factor ; Receptors, Cytokine/*metabolism ; Receptors, Growth Factor/metabolism ; Receptors, Interleukin/metabolism ; Receptors, Interleukin-6 ; Receptors, OSM-LIF ; Receptors, Oncostatin M ; Tyrosine/metabolism
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    Regulation of MHC class II expression by interferon-gamma mediated by the transactivator gene CIITA (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-01
    Description: Major histocompatibility complex (MHC) class II genes are expressed constitutively in only a few cell types, but they can be induced in the majority of them, in particular by interferon-gamma (IFN-gamma). The MHC class II transactivator gene CIITA is defective in a form of primary MHC class II deficiency. Here it is shown that CIITA expression is controlled and induced by IFN-gamma. A functional CIITA gene is necessary for class II induction, and transfection of CIITA is sufficient to activate expression of MHC class II genes in class II-negative cells in the absence of IFN-gamma. CIITA is therefore a general regulator of both inducible and constitutive MHC class II expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steimle, V -- Siegrist, C A -- Mottet, A -- Lisowska-Grospierre, B -- Mach, B -- New York, N.Y. -- Science. 1994 Jul 1;265(5168):106-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Microbiology, University of Geneva Medical School, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8016643" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chromosome Mapping ; Chromosomes, Human, Pair 16 ; Fibroblasts ; *Gene Expression Regulation ; *Genes, MHC Class II ; Histocompatibility Antigens Class II/biosynthesis/*genetics ; Humans ; Interferon-gamma/*pharmacology ; Models, Genetic ; *Nuclear Proteins ; RNA, Messenger/genetics/metabolism ; Trans-Activators/biosynthesis/*genetics ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Functional activation of Jak1 and Jak3 by selective association with IL-2 receptor subunits (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: The interleukin-2 receptor (IL-2R) consists of three subunits: the IL-2R alpha, IL-2R beta, and IL-2R gamma chains, the last of which is also used in the receptors for IL-4, IL-7, and IL-9. Stimulation with IL-2 induces the tyrosine phosphorylation and activation of the Janus kinases Jak1 and Jak3. Jak1 and Jak3 were found to be selectively associated with the "serine-rich" region of IL-2R beta and the carboxyl-terminal region of IL-2R gamma, respectively. Both regions were necessary for IL-2 signaling. Furthermore, Jak3-negative fibroblasts expressing reconstituted IL-2R became responsive to IL-2 after the additional expression of Jak3 complementary DNA. Thus, activation of Jak1 and Jak3 may be a key event in IL-2 signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyazaki, T -- Kawahara, A -- Fujii, H -- Nakagawa, Y -- Minami, Y -- Liu, Z J -- Oishi, I -- Silvennoinen, O -- Witthuhn, B A -- Ihle, J N -- P30 CA21765/CA/NCI NIH HHS/ -- R01 DK42932/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1045-7.〈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/7973659" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Enzyme Activation ; Humans ; Interleukin-2/*pharmacology ; Janus Kinase 1 ; Janus Kinase 3 ; Protein-Tyrosine Kinases/*metabolism ; Receptors, Interleukin-2/chemistry/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Tyrosine/metabolism
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    Interaction of the protein kinase Raf-1 with 14-3-3 proteins (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-07
    Description: Members of a family of highly conserved proteins, termed 14-3-3 proteins, were found by several experimental approaches to associate with Raf-1, a central component of a key signal transduction pathway. Optimal complex formation required the amino-terminal regulatory domain of Raf-1. The association of 14-3-3 proteins and Raf-1 was not substantially affected by the activation state of Raf.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fu, H -- Xia, K -- Pallas, D C -- Cui, C -- Conroy, K -- Narsimhan, R P -- Mamon, H -- Collier, R J -- Roberts, T M -- AI22021/AI/NIAID NIH HHS/ -- CA57327/CA/NCI NIH HHS/ -- HD24926/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1994 Oct 7;266(5182):126-9.〈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/7939632" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; 3T3 Cells ; Animals ; Binding Sites ; Cell Line ; Enzyme Activation ; Humans ; Mice ; Nerve Tissue Proteins/metabolism ; Phosphorylation ; Poly(ADP-ribose) Polymerases/metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Proteins/chemistry/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-raf ; *Signal Transduction ; Spodoptera ; *Tyrosine 3-Monooxygenase ; Zinc Fingers
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    Activation of Raf as a result of recruitment to the plasma membrane (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-03
    Description: The small guanine nucleotide binding protein Ras participates in a growth promoting signal transduction pathway. The mechanism by which interaction of Ras with the protein kinase Raf leads to activation of Raf was studied. Raf was targeted to the plasma membrane by addition of the COOH-terminal localization signals of K-ras. This modified form of Raf (RafCAAX) was activated to the same extent as Raf coexpressed with oncogenic mutant Ras. Plasma membrane localization rather than farnesylation or the presence of the additional COOH-terminal sequence accounted for the activation of RafCAAX. The activation of RafCAAX was completely independent of Ras; it was neither potentiated by oncogenic mutant Ras nor abrogated by dominant negative Ras. Raf, once recruited to the plasma membrane, was not anchored there by Ras; most activated Raf in cells was associated with plasma membrane cytoskeletal elements, not the lipid bilayer. Thus, Ras functions in the activation of Raf by recruiting Raf to the plasma membrane where a separate, Ras-independent, activation of Raf occurs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokoe, D -- Macdonald, S G -- Cadwallader, K -- Symons, M -- Hancock, J F -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1463-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ONXY Pharmaceuticals, Richmond, CA 94806.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7811320" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cell Membrane/*enzymology ; Cytosol/enzymology ; Enzyme Activation ; GTP-Binding Proteins/*metabolism ; MAP Kinase Kinase 1 ; Mitogen-Activated Protein Kinase 1 ; *Mitogen-Activated Protein Kinase Kinases ; Models, Biological ; Molecular Sequence Data ; Protein-Serine-Threonine Kinases/chemistry/*metabolism ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins/chemistry/*metabolism ; Proto-Oncogene Proteins c-raf ; Recombinant Fusion Proteins/metabolism
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    A transforming growth factor beta type I receptor that signals to activate gene expression (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-07
    Description: Transforming growth factor beta (TGF-beta) is a multifunctional factor that regulates many aspects of cellular functions. TGF-beta signals through a heteromeric complex of the type I and type II TGF-beta receptors. However, the molecular mechanism of signal transduction by this receptor complex remains unresolved. The type II receptor belongs to a transmembrane receptor serine-threonine kinase family. A new member of this receptor family (R4) was identified and shown to be a functional TGF-beta type I receptor on the basis of its ability to restore a TGF-beta-induced gene response in mutant cell lines lacking endogenous type I receptor. Both ligand binding and signaling of the R4 protein were dependent on the presence of a functional type II receptor. The type I receptor has an intrinsic serine-threonine kinase activity, which was essential for signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bassing, C H -- Yingling, J M -- Howe, D J -- Wang, T -- He, W W -- Gustafson, M L -- Shah, P -- Donahoe, P K -- Wang, X F -- DK45746/DK/NIDDK NIH HHS/ -- NICHD T32HD07396/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1994 Jan 7;263(5143):87-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8272871" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Gene Expression Regulation ; Genes, Reporter ; Mutagenesis, Site-Directed ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Transforming Growth Factor beta/*metabolism ; *Signal Transduction ; Transfection ; Transforming Growth Factor beta/*metabolism/pharmacology
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    Integration and germ-line transmission of a pseudotyped retroviral vector in zebrafish (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-29
    Description: The zebrafish is rapidly becoming a popular model system for the study of vertebrate development because it is ideal for both embryological studies and genetic analysis. To determine if a retroviral vector pseudotyped with the envelope glycoprotein of the vesicular stomatitis virus could infect zebrafish embryos, and in particular, the cells destined to become the germ line, a pseudotyped virus was injected into blastula-stage zebrafish embryos. Fifty-one embryos were allowed to develop and eight transmitted proviral DNA to their progeny. Founders were mosaic, but as expected, transgenic F1's transmitted proviral DNA in a Mendelian fashion to the F2 progeny. Transgenic F1 fish inherited a single integrated provirus, and a single founder could transmit more than one viral integration to its progeny. These results demonstrate that this pantropic pseudotyped vector, originally developed for human gene therapy, will make the use of retroviral vectors in zebrafish possible.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, S -- Gaiano, N -- Culp, P -- Burns, J C -- Friedmann, T -- Yee, J K -- Hopkins, N -- CA14051/CA/NCI NIH HHS/ -- HD-20034/HD/NICHD NIH HHS/ -- HL-01855/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jul 29;265(5172):666-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036514" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Base Sequence ; Cell Line ; DNA, Viral/analysis ; Genetic Vectors/*genetics ; Molecular Sequence Data ; Moloney murine leukemia virus/*genetics ; Proviruses/*genetics ; Vesicular stomatitis Indiana virus/*genetics ; Virus Integration/*genetics ; Zebrafish/embryology/*genetics
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    Inhibition of Ras-induced DNA synthesis by expression of the phosphatase MKP-1 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-14
    Description: Mitogen-activated protein kinases (MAP kinases) are common components of signaling pathways induced by diverse growth stimuli. Although the guanidine nucleotide-binding Ras proteins are known to be upstream activators of MAP kinases, the extent to which MAP kinases directly contribute to the mitogenic effect of Ras is as yet undefined. In this study, inhibition of MAP kinases by the MAP kinase phosphatase MKP-1 blocked the induction of DNA synthesis in quiescent rat embryonic fibroblast REF-52 cells by an activated mutant of Ras, V12Ras. These results suggest an essential role for activation of MAP kinases in the transition from the quiescent to the DNA replication phase of the eukaryotic cell cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, H -- Tonks, N K -- Bar-Sagi, D -- CA53840/CA/NCI NIH HHS/ -- CA55360/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):285-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, NY 11724-2208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939666" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors ; *Cell Cycle Proteins ; Cell Line ; DNA/*biosynthesis ; Dual Specificity Phosphatase 1 ; Enzyme Activation ; G0 Phase ; HeLa Cells ; Humans ; Immediate-Early Proteins/*metabolism/pharmacology ; JNK Mitogen-Activated Protein Kinases ; Mitogen-Activated Protein Kinase 1 ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Mutation ; *Phosphoprotein Phosphatases ; Protein Phosphatase 1 ; Protein Tyrosine Phosphatases/*metabolism/pharmacology ; Protein-Serine-Threonine Kinases/*antagonists & inhibitors/metabolism ; Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Rats ; S Phase ; Signal Transduction ; Transfection ; ras Proteins/genetics/*metabolism
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    Gh: a GTP-binding protein with transglutaminase activity and receptor signaling function (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: The alpha 1-adrenergic receptors activate a phospholipase C enzyme by coupling to members of the large molecular size (approximately 74 to 80 kilodaltons) G alpha h family of guanosine triphosphate (GTP)-binding proteins. Rat liver G alpha h is now shown to be a tissue transglutaminase type II (TGase II). The transglutaminase activity of rat liver TGase II expressed in COS-1 cells was inhibited by the nonhydrolyzable GTP analog guanosine 5'-O-(3-thiotriphosphate) or by alpha 1-adrenergic receptor activation. Rat liver TGase II also mediated alpha 1-adrenergic receptor stimulation of phospholipase C activity. Thus, G alpha h represents a new class of GTP-binding proteins that participate in receptor signaling and may be a component of a complex regulatory network in which receptor-stimulated GTP binding switches the function of G alpha h from transglutamination to receptor signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakaoka, H -- Perez, D M -- Baek, K J -- Das, T -- Husain, A -- Misono, K -- Im, M J -- Graham, R M -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1593-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiovascular Biology, Cleveland Clinic Foundation, OH 44195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7911253" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Epinephrine/pharmacology ; GTP-Binding Proteins/chemistry/genetics/*metabolism ; Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology ; Guinea Pigs ; Inositol Phosphates/metabolism ; Liver/enzymology ; Molecular Sequence Data ; Prazosin/pharmacology ; Rats ; Receptors, Adrenergic, alpha/genetics/*metabolism ; *Signal Transduction ; Transfection ; Transglutaminases/chemistry/genetics/*metabolism ; Type C Phospholipases/metabolism
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    Anergic T cells as suppressor cells in vitro (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-06-10
    Description: T cell-mediated suppression is an established phenomenon, but its underlying mechanisms are obscure. An in vitro system was used to test the possibility that anergic T cells can act as specific suppressor cells. Anergic human T cells caused inhibition of antigen-specific and allospecific T cell proliferation. In order for the inhibition to occur, the anergic T cells had to be specific for the same antigen-presenting cells (APCs) as the T cells that were suppressed. The mechanism of this suppression appears to be competition for the APC surface and for locally produced interleukin-2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lombardi, G -- Sidhu, S -- Batchelor, R -- Lechler, R -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1587-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Royal Postgraduate Medical School, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202711" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen-Presenting Cells/immunology ; Cell Line ; Cells, Cultured ; *Clonal Anergy ; Humans ; Interleukin-10/immunology ; Interleukin-2/immunology/secretion ; Interleukin-4/immunology ; Lymphocyte Activation ; Recombinant Proteins/immunology ; T-Lymphocytes, Helper-Inducer/*immunology ; T-Lymphocytes, Regulatory/*immunology ; Transforming Growth Factor beta/immunology
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    Generation of lymphohematopoietic cells from embryonic stem cells in culture (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-08-19
    Description: An efficient system was developed that induced the differentiation of embryonic stem (ES) cells into blood cells of erythroid, myeloid, and B cell lineages by coculture with the stromal cell line OP9. This cell line does not express functional macrophage colony-stimulating factor (M-CSF). The presence of M-CSF had inhibitory effects on the differentiation of ES cells to blood cells other than macrophages. Embryoid body formation or addition of exogenous growth factors was not required, and differentiation was highly reproducible even after the selection of ES cells with the antibiotic G418. Combined with the ability to genetically manipulate ES cells, this system will facilitate the study of molecular mechanisms involved in development and differentiation of hematopoietic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakano, T -- Kodama, H -- Honjo, T -- New York, N.Y. -- Science. 1994 Aug 19;265(5175):1098-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Faculty of Medicine, Kyoto University Yoshida, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066449" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/cytology ; Base Sequence ; Cell Differentiation ; Cell Line ; Cells, Cultured ; Culture Media ; Erythrocytes/cytology ; Erythropoiesis ; Gene Rearrangement ; *Hematopoiesis ; Hematopoietic Stem Cells/*cytology ; Lymphocytes/*cytology ; Macrophage Colony-Stimulating Factor/pharmacology ; Macrophages/cytology ; Mesoderm/cytology ; Mice ; Molecular Sequence Data ; Recombinant Proteins/pharmacology ; Stromal Cells/cytology
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    Ability of HIV to promote a TH1 to TH0 shift and to replicate preferentially in TH2 and TH0 cells (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-07-08
    Description: Both interferon gamma (IFN-gamma) produced by T helper 1 (TH1) lymphocytes and interleukin-4 (IL-4) produced by TH2 lymphocytes were reduced in either bulk circulating mononuclear cells or mitogen-induced CD4+ T cell clones from the peripheral blood of individuals infected with human immunodeficiency virus (HIV). There was a preferential reduction in clones producing IL-4 and IL-5 in the advanced phases of infection. However, enhanced proportions of CD4+ T cell clones producing both TH1-type and TH2-type cytokines (TH0 clones) were generated from either skin-infiltrating T cells that had been activated in vivo or peripheral blood T cells stimulated by antigen in vitro when cells were isolated from HIV-infected individuals. All TH2 and most TH0 clones supported viral replication, although viral replication was not detected in any of the TH1 clones infected in vitro with HIV. These results suggest that HIV (i) does not induce a definite TH1 to TH2 switch, but can favor a shift to the TH0 phenotype in response to recall antigens, and (ii) preferentially replicates in CD4+ T cells producing TH2-type cytokines (TH2 and TH0).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maggi, E -- Mazzetti, M -- Ravina, A -- Annunziato, F -- de Carli, M -- Piccinni, M P -- Manetti, R -- Carbonari, M -- Pesce, A M -- del Prete, G -- New York, N.Y. -- Science. 1994 Jul 8;265(5169):244-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Clinical Immunology and Allergy, University of Florence, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023142" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; Cell Line ; Cells, Cultured ; HIV/*physiology ; HIV Infections/*immunology/microbiology ; HIV Seropositivity/immunology ; Humans ; Immunologic Memory ; Interferon-gamma/*biosynthesis ; Interleukin-4/biosynthesis ; Interleukin-5/biosynthesis ; Interleukins/*biosynthesis ; Lymphocyte Activation ; Phenotype ; T-Lymphocytes, Helper-Inducer/*immunology/microbiology ; Virus Replication
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    Reversal of terminal differentiation mediated by p107 in Rb-/- muscle cells (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-06-03
    Description: The terminal differentiation of mammalian muscle cells requires the tumor suppressor retinoblastoma protein (Rb). Unlike their wild-type counterparts, multinucleated myotubes from mouse cells deficient in Rb (Rb-/-) were induced by serum to re-enter the cell cycle. Development of the myogenic phenotype in Rb-/- cells correlated with increased expression of p107, which interacted with myogenic transcription factors. Serum-induced cell cycle reentry, on the other hand, correlated with decreased p107 expression. Thus, although p107 could substitute for Rb as a cofactor for differentiation, it could not maintain the terminally differentiated state in Rb-/- myotubes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schneider, J W -- Gu, W -- Zhu, L -- Mahdavi, V -- Nadal-Ginard, B -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1467-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Children's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8197461" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood ; Cell Cycle ; Cell Differentiation ; Cell Line ; Culture Media ; Gene Expression ; Helix-Loop-Helix Motifs ; Humans ; Mice ; Muscles/*cytology/metabolism ; Myogenin/metabolism ; *Nuclear Proteins ; Proteins/genetics/*physiology ; Recombinant Fusion Proteins/metabolism ; Retinoblastoma Protein/genetics/*physiology ; Retinoblastoma-Like Protein p107 ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured
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    Differential complementation of Bcr-Abl point mutants with c-Myc (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-04-15
    Description: A complementation strategy was developed to define the signaling pathways activated by the Bcr-Abl tyrosine kinase. Transformation inactive point mutants of Bcr-Abl were tested for complementation with c-Myc. Single point mutations in the Src-homology 2 (SH2) domain, the major tyrosine autophosphorylation site of the kinase domain, and the Grb-2 binding site in the Bcr region impaired the transformation of fibroblasts by Bcr-Abl. Hyperexpression of c-Myc efficiently restored transformation activity only to the Bcr-Abl SH2 mutant. These data support a model in which Bcr-Abl activates at least two independent pathways for transformation. This strategy may be useful for discerning signaling pathways activated by other oncogenes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Afar, D E -- Goga, A -- McLaughlin, J -- Witte, O N -- Sawyers, C L -- CA 01551/CA/NCI NIH HHS/ -- CA 53867/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Apr 15;264(5157):424-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, University of California-Los Angeles 90024-1489.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8153630" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; Cell Line ; *Cell Transformation, Neoplastic ; Fusion Proteins, bcr-abl/*genetics/physiology ; GRB2 Adaptor Protein ; Gene Expression ; *Genes, abl ; *Genes, myc ; Genetic Complementation Test ; Molecular Sequence Data ; Phosphorylation ; Point Mutation ; Proteins/metabolism ; Proto-Oncogene Proteins c-myc/genetics/physiology ; Rats ; Retroviridae/physiology ; Signal Transduction ; Transfection ; Tyrosine/metabolism
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    Tissue-specific targeting of retroviral vectors through ligand-receptor interactions (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-25
    Description: The development of retroviral vectors that target specific cell types could have important implications for the design of gene therapy strategies. A chimeric protein containing the polypeptide hormone erythropoietin and part of the env protein of ecotropic Moloney murine leukemia virus was engineered into the virus. This murine virus became several times more infectious for murine cells bearing the erythropoietin receptor, and it also became infectious for human cells bearing the erythropoietin receptor. This type of tissue-specific targeting by means of ligand-receptor interactions may have broad applications to a variety of gene delivery systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kasahara, N -- Dozy, A M -- Kan, Y W -- AM16666/AM/NIADDK NIH HHS/ -- HL 20985/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1373-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Laboratory Medicine, University of California, San Francisco 94143-0724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973726" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Base Sequence ; Cell Line ; Erythrocytes/chemistry/*virology ; Erythropoietin/genetics/metabolism ; Genetic Therapy/methods ; Genetic Vectors/*genetics/physiology ; HeLa Cells ; Humans ; Ligands ; Mice ; Molecular Sequence Data ; Moloney murine leukemia virus/*genetics/physiology ; Receptors, Erythropoietin/*metabolism ; Receptors, Virus/metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection ; Tumor Cells, Cultured ; Viral Envelope Proteins/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Subsets of HLA-DR1 molecules defined by SEB and TSST-1 binding (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-16
    Description: Superantigens bind to major histocompatibility complex class II molecules on antigen-presenting cells and stimulate T cells. Staphylococcus aureus enterotoxin B (SEB) and toxic shock syndrome toxin-1 (TSST-1) bind to the same region of human lymphocyte antigen (HLA)-DR1 but do not compete with each other, which indicates that they bind to different subsets of DR1 molecules. Here, a mutation in the peptide-binding groove disrupted the SEB and TSST-1 binding sites, which suggests that peptides can influence the interaction with bacterial toxins. In support of this, the expression of the DR1 molecule in various cell types differentially affected the binding of these toxins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thibodeau, J -- Cloutier, I -- Lavoie, P M -- Labrecque, N -- Mourad, W -- Jardetzky, T -- Sekaly, R P -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1874-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire d'Immunologie, Institut de Recherches Cliniques de Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7997881" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; *Bacterial Toxins ; Binding Sites ; Binding, Competitive ; Cell Line ; Enterotoxins/chemistry/*metabolism ; HLA-DR1 Antigen/chemistry/genetics/*metabolism ; HeLa Cells ; Humans ; Hybridomas ; Mice ; Mutation ; Protein Structure, Secondary ; *Staphylococcus aureus ; Superantigens/chemistry/*metabolism ; T-Lymphocytes/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 78
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    Protein-protein interactions contributing to the specificity of intracellular vesicular trafficking (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-25
    Description: Intracellular vesicles destined to fuse with the plasma membrane and secrete their contents must have a mechanism for specifically interacting with the appropriate target membrane. Such a mechanism is now suggested by the demonstration of specific interaction between vesicular proteins and plasma membrane proteins. The vesicle-associated membrane proteins (VAMPs) 1 and 2 specifically bind the acceptor membrane proteins syntaxin 1A and 4 but not syntaxin 2 or 3. The binding site is within amino acids 194 to 267 of syntaxin 1A, and the approximate equilibrium dissociation constants is 4.7 x 10(-6) molar. These data suggest a physical basis for the specificity of intracellular vesicular transport.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Calakos, N -- Bennett, M K -- Peterson, K E -- Scheller, R H -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1146-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Stanford University Medical Center, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8108733" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, Surface/*metabolism ; Binding Sites ; Cell Line ; Cell Membrane/metabolism ; Cytoplasm/metabolism ; Haplorhini ; Kinetics ; Membrane Proteins/*metabolism ; Molecular Sequence Data ; Nerve Tissue Proteins/*metabolism ; R-SNARE Proteins ; Recombinant Fusion Proteins/metabolism ; Synaptic Vesicles/*metabolism ; Syntaxin 1
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  • 79
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    CD26 antigen and HIV fusion? (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Camerini, D -- Planelles, V -- Chen, I S -- New York, N.Y. -- Science. 1994 May 20;264(5162):1160-1; author reply 1162-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7909961" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/*physiology ; Antigens, Differentiation, T-Lymphocyte/*physiology ; Base Sequence ; *Cell Fusion ; Cell Line ; Dipeptidyl Peptidase 4 ; Gene Products, env/physiology ; Giant Cells/physiology ; HIV-1/*physiology ; Humans ; Molecular Sequence Data
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 80
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    Estrogen receptor-associated proteins: possible mediators of hormone-induced transcription (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-03
    Description: The estrogen receptor is a transcription factor which, when bound to estradiol, binds DNA and regulates expression of estrogen-responsive genes. A 160-kilodalton estrogen receptor-associated protein, ERAP160, was identified that exhibits estradiol-dependent binding to the receptor. Mutational analysis of the receptor shows that its ability to activate transcription parallels its ability to bind ERAP160. Antiestrogens are unable to promote ERAP160 binding and can block the estrogen-dependent interaction of the receptor and ERAP160 in a dose-dependent manner. This evidence suggests that ERAP160 may mediate estradiol-dependent transcriptional activation by the estrogen receptor. Furthermore, the ability of antiestrogens to block estrogen receptor-ERAP160 complex formation could account for their therapeutic effects in breast cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Halachmi, S -- Marden, E -- Martin, G -- MacKay, H -- Abbondanza, C -- Brown, M -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1455-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Biological and Biomedical Sciences, Harvard Medical School, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8197458" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Carrier Proteins/*metabolism ; Cell Line ; Diethylstilbestrol/pharmacology ; Estradiol/*metabolism ; Estrogen Antagonists/*pharmacology ; Humans ; Molecular Sequence Data ; Point Mutation ; Receptors, Estrogen/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Tamoxifen/pharmacology ; *Transcriptional Activation ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 81
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    Soluble beta-amyloid induction of Alzheimer's phenotype for human fibroblast K+ channels (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-08
    Description: Although beta-amyloid is the main constituent of neurite plaques and may play a role in the pathophysiology of Alzheimer's disease, mechanisms by which soluble beta-amyloid might produce early symptoms such as memory loss before diffuse plaque deposition have not been implicated. Treatment of fibroblasts with beta-amyloid (10 nM) induced the same potassium channel dysfunction previously shown to occur specifically in fibroblasts from patients with Alzheimer's disease--namely, the absence of a 113-picosiemen potassium channel. A tetraethylammonium-induced increase of intracellular concentrations of calcium, [Ca2+]i, a response that depends on functional 113-picosiemen potassium channels, was also eliminated or markedly reduced by 10 nM beta-amyloid. Increased [Ca2+]i induced by high concentrations of extracellular potassium and 166-picosiemen potassium channels were unaffected by 10 nM beta-amyloid. In Alzheimer's disease, then, beta-amyloid might alter potassium channels and thus impair neuronal function to produce symptoms such as memory loss by a means other than plaque formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Etcheberrigaray, R -- Ito, E -- Kim, C S -- Alkon, D L -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):276-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Adaptive Systems, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146663" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*metabolism ; Amyloid beta-Peptides/*pharmacology ; Bombesin/pharmacology ; Calcium/metabolism ; Cell Line ; Cells, Cultured ; Dimethyl Sulfoxide/pharmacology ; Female ; Fibroblasts/*drug effects/metabolism ; Humans ; Male ; Phenotype ; Potassium Channel Blockers ; Potassium Channels/*drug effects/metabolism ; Potassium Chloride/pharmacology ; Solubility ; Tetraethylammonium ; Tetraethylammonium Compounds/pharmacology
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  • 82
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    Specific association of human telomerase activity with immortal cells and cancer (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-23
    Description: Synthesis of DNA at chromosome ends by telomerase may be necessary for indefinite proliferation of human cells. A highly sensitive assay for measuring telomerase activity was developed. In cultured cells representing 18 different human tissues, 98 of 100 immortal and none of 22 mortal populations were positive for telomerase. Similarly, 90 of 101 biopsies representing 12 human tumor types and none of 50 normal somatic tissues were positive. Normal ovaries and testes were positive, but benign tumors such as fibroids were negative. Thus, telomerase appears to be stringently repressed in normal human somatic tissues but reactivated in cancer, where immortal cells are likely required to maintain tumor growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, N W -- Piatyszek, M A -- Prowse, K R -- Harley, C B -- West, M D -- Ho, P L -- Coviello, G M -- Wright, W E -- Weinrich, S L -- Shay, J W -- AG07992/AG/NIA NIH HHS/ -- CA50195/CA/NCI NIH HHS/ -- CA65178/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 23;266(5193):2011-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Geron Corporation, Menlo Park, CA 94025.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7605428" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Division ; Cell Line ; Cell Line, Transformed/enzymology ; DNA Nucleotidylexotransferase/*metabolism ; Enzyme Activation ; Enzyme Repression ; Female ; Humans ; Male ; Molecular Sequence Data ; Neoplasms/*enzymology ; Ovary/enzymology ; Polymerase Chain Reaction ; Testis/enzymology ; Tumor Cells, Cultured
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  • 83
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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
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  • 84
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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
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  • 85
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    Inhibition by cAMP of Ras-dependent activation of Raf (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-12
    Description: Activation of the Raf and extracellular signal-regulated kinases (ERKs) (or mitogen-activated protein kinases) are key events in mitogenic signalling, but little is known about interactions with other signaling pathways. Agents that raise levels of intracellular cyclic adenosine 3',5'-monophosphate (cAMP) blocked DNA synthesis and signal transduction in Rat1 cells exposed to epidermal growth factor (EGF) or lysophosphatidic acid. In the case of EGF, receptor tyrosine kinase activity and association with the signaling molecules Grb2 and Shc were unaffected by cAMP. Likewise, EGF-dependent accumulation of the guanosine 5'-triphosphate-bound form of Ras was unaffected. In contrast, activation of Raf-1 and ERK kinases was inhibited. Thus, cAMP appears to inhibit signal transmission from Ras by preventing Ras-dependent activation of Raf-1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook, S J -- McCormick, F -- UO1 CA51992-03/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Nov 12;262(5136):1069-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Onyx Pharmaceuticals, Richmond, CA 94806.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7694367" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-3-isobutylxanthine/pharmacology ; Animals ; Bucladesine/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Line ; Cholera Toxin/pharmacology ; Cyclic AMP/*pharmacology ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Enzyme Activation ; Epidermal Growth Factor/pharmacology ; Interphase ; Lysophospholipids/pharmacology ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-raf ; Proto-Oncogene Proteins p21(ras)/*metabolism ; Rats ; Receptor, Epidermal Growth Factor/metabolism ; *Signal Transduction
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  • 86
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    Disappearance of the lymphoid system in Bcl-2 homozygous mutant chimeric mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-17
    Description: The bcl-2 proto-oncogene can prevent the death of many cell types. Mice were generated that were chimeric for the homozygous inactivation of bcl-2. Lymphocytes without Bcl-2 differentiated into phenotypically mature cells. However, in vitro, the mature T cells that lacked Bcl-2 had shorter life-spans and increased sensitivity to glucocorticoids and gamma-irradiation. In contrast, stimulation of CD3 inhibited the death of these cells. T and B cells with no Bcl-2 disappeared from the bone marrow, thymus, and periphery by 4 weeks of age. Thus, Bcl-2 was dispensable for lymphocyte maturation, but was required for a stable immune system after birth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakayama, K -- Negishi, I -- Kuida, K -- Shinkai, Y -- Louie, M C -- Fields, L E -- Lucas, P J -- Stewart, V -- Alt, F W -- AI 15322/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 17;261(5128):1584-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, 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/8372353" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3/immunology ; Apoptosis ; B-Lymphocytes/cytology/*immunology ; Base Sequence ; Bone Marrow/immunology ; Bone Marrow Cells ; Cell Line ; Chimera ; Homozygote ; Humans ; Lymphoid Tissue/cytology/immunology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Proto-Oncogene Proteins/genetics/*physiology ; Proto-Oncogene Proteins c-bcl-2 ; Proto-Oncogenes ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/cytology/*immunology
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  • 87
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    Shutdown of class switch recombination by deletion of a switch region control element (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-12
    Description: Upon activation, B lymphocytes can change the class of the antibody they express by immunoglobulin class switch recombination. Cytokines can direct this recombination to distinct classes by the specific activation of repetitive recombinogenic DNA sequences, the switch regions. Recombination to a particular switch region (s gamma 1) was abolished in mice that were altered to lack sequences that are 5' to the s gamma 1 region. This result directly implicates the functional importance of 5' switch region flanking sequences in the control of class switch recombination. Mutant mice exhibit a selective agammaglobulinemia and may be useful in the assessment of the biological importance of immunoglobulin G1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jung, S -- Rajewsky, K -- Radbruch, A -- New York, N.Y. -- Science. 1993 Feb 12;259(5097):984-7.〈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/8438159" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Base Sequence ; Cell Line ; Chimera ; Drug Resistance/genetics ; Embryo, Mammalian ; *Gene Deletion ; Immunoglobulin G/genetics ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin Switch Region/*genetics ; Interleukin-4/pharmacology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutagenesis ; Neomycin ; *Recombination, Genetic ; Stem Cells
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  • 88
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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
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  • 89
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    Cloning of B7-2: a CTLA-4 counter-receptor that costimulates human T cell proliferation (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-05
    Description: Although presentation of antigen to the T cell receptor is necessary for the initiation of an immune response, additional molecules expressed on antigen-presenting cells deliver essential costimulatory signals. T cell activation, in the absence of costimulation, results in T cell anergy. The B7-1 protein is a costimulator molecule that regulates interleukin-2 (IL-2) secretion by signaling through the pathway that uses CD28 and CTLA-4 (hereafter referred to as the CD28 pathway). We have cloned a counter-receptor of CD28 and CTLA-4, termed B7-2. Although only 26 percent identical to B7-1, B7-2 also costimulates IL-2 production and T cell proliferation. Unlike B7-1, B7-2 messenger RNA is constitutively expressed in unstimulated B cells. It is likely that B7-2 provides a critical early costimulatory signal determining if the T cell will contribute to an immune response or become anergic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freeman, G J -- Gribben, J G -- Boussiotis, V A -- Ng, J W -- Restivo, V A Jr -- Lombard, L A -- Gray, G S -- Nadler, L M -- CA 40216/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Nov 5;262(5135):909-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematologic Malignancies, Dana-Farber Cancer Institute.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7694363" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Amino Acid Sequence ; Animals ; *Antigens, CD ; Antigens, CD28/metabolism ; Antigens, CD80/chemistry/genetics/*immunology/metabolism ; Antigens, CD86 ; Antigens, Differentiation/*metabolism ; B-Lymphocytes/*immunology/metabolism ; CTLA-4 Antigen ; Cell Line ; *Cloning, Molecular ; DNA, Complementary/genetics ; Humans ; *Immunoconjugates ; *Lymphocyte Activation ; *Membrane Glycoproteins ; Molecular Sequence Data ; Sequence Alignment ; Signal Transduction ; T-Lymphocytes/*immunology
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  • 90
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    The role of TH1 and TH2 cells in a rodent malaria infection (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-25
    Description: CD4+ T cells play a major role in protective immunity against the blood stage of malaria, but the mechanism of protection is unclear. By adoptive transfer of cloned T cell lines, direct evidence is provided that both TH1 and TH2 subsets of CD4+ T cells can protect mice against Plasmodium chabaudi chabaudi infection. TH1 cells protect by a nitric oxide-dependent mechanism, whereas TH2 cells protect by the enhancement and accelerated production of specific immunoglobulin G1 antibody.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taylor-Robinson, A W -- Phillips, R S -- Severn, A -- Moncada, S -- Liew, F Y -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1931-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Laboratories for Experimental Parasitology, University of Glasgow, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8100366" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Protozoan/biosynthesis ; Arginine/analogs & derivatives/pharmacology ; CD4-Positive T-Lymphocytes/*immunology ; Cell Line ; Female ; Immunoglobulin G/*biosynthesis ; Lymphocyte Depletion ; Malaria/*immunology ; Mice ; Mice, Inbred Strains ; Nitrates/blood ; Nitric Oxide/*metabolism ; Plasmodium chabaudi/*immunology ; T-Lymphocyte Subsets/*immunology ; omega-N-Methylarginine
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  • 91
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    Blood-brain barrier penetration and in vivo activity of an NGF conjugate (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-15
    Description: Nerve growth factor (NGF) is essential for the survival of both peripheral ganglion cells and central cholinergic neurons of the basal forebrain. The accelerated loss of central cholinergic neurons during Alzheimer's disease may be a determinant of dementia in these patients and may therefore suggest a therapeutic role for NGF. However, NGF does not significantly penetrate the blood-brain barrier, which makes its clinical utility dependent on invasive neurosurgical procedures. When conjugated to an antibody to the transferrin receptor, however, NGF crossed the blood-brain barrier after peripheral injection. This conjugated NGF increased the survival of both cholinergic and noncholinergic neurons of the medial septal nucleus that had been transplanted into the anterior chamber of the rat eye. This approach may prove useful for the treatment of Alzheimer's disease and other neurological disorders that are amenable to treatment by proteins that do not readily cross the blood-brain barrier.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Friden, P M -- Walus, L R -- Watson, P -- Doctrow, S R -- Kozarich, J W -- Backman, C -- Bergman, H -- Hoffer, B -- Bloom, F -- Granholm, A C -- NS29601-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 15;259(5093):373-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Alkermes, Inc., Cambridge, MA 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8420006" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Chamber/metabolism ; Antibodies/*metabolism ; *Blood-Brain Barrier ; Brain/blood supply/metabolism ; Capillaries ; Cell Line ; Cross-Linking Reagents ; Dose-Response Relationship, Drug ; Drug Carriers ; Immunohistochemistry ; Nerve Growth Factors/administration & dosage/*pharmacokinetics/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Transferrin/*immunology
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  • 92
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    Generation of allospecific natural killer cells by stimulation across a polymorphism of HLA-C (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-21
    Description: The cytotoxicity of human natural killer (NK) cells is modulated by the major histocompatibility complex human leukocyte antigen (HLA)-C molecules on the surface of the target cell. Alloreactive NK cells specific for the NK-1 alloantigen could be reproducibly generated from individuals that were homozygous for HLA-C with asparagine at residue 77 and lysine at residue 80 [HLA-C(Asn77,Lys80)] by stimulation with target cells that were homozygous for HLA-C(Ser77,Asn80); the reciprocal stimulation yielded NK cells specific for the NK-2 alloantigen. However, neither homozygous target cell stimulated the generation of alloreactive NK cells from heterozygous individuals. Thus, these data reveal an unanticipated difference between human NK alloreactivity defined by this system and murine "hybrid resistance."〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Colonna, M -- Brooks, E G -- Falco, M -- Ferrara, G B -- Strominger, J L -- CA 47554/CA/NCI NIH HHS/ -- KO8 AI01064/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 May 21;260(5111):1121-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunogenetics, Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493555" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Base Sequence ; Cell Line ; *Cytotoxicity, Immunologic ; Genotype ; HLA-C Antigens/genetics/*immunology ; Heterozygote ; Homozygote ; Humans ; Isoantigens/*immunology ; Killer Cells, Natural/*immunology ; Mice ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Polymorphism, Genetic
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  • 93
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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
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  • 94
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    Association of the APC gene product with beta-catenin (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-10
    Description: Mutations in the human APC gene are linked to familial adenomatous polyposis and to the progression of sporadic colorectal and gastric tumors. To gain insight into APC function, APC-associated proteins were identified by immunoprecipitation experiments. Antibodies to APC precipitated a 95-kilodalton protein that was purified and identified by sequencing as beta-catenin, a protein that binds to the cell adhesion molecule E-cadherin. An antibody specific to beta-catenin also recognized the 95-kilodalton protein in the immunoprecipitates. These results suggest that APC is involved in cell adhesion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rubinfeld, B -- Souza, B -- Albert, I -- Muller, O -- Chamberlain, S H -- Masiarz, F R -- Munemitsu, S -- Polakis, P -- New York, N.Y. -- Science. 1993 Dec 10;262(5140):1731-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Onyx Pharmaceuticals, Richmond, CA 94806.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8259518" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Amino Acid Sequence ; Antibodies ; Cadherins/*metabolism ; Cell Adhesion ; Cell Line ; Colonic Neoplasms/genetics/*metabolism ; Cytoskeletal Proteins/chemistry/isolation & purification/*metabolism ; *Genes, APC ; Humans ; Molecular Sequence Data ; Neoplasm Proteins/genetics/immunology/*metabolism ; Precipitin Tests ; *Trans-Activators ; Tumor Cells, Cultured ; beta Catenin
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  • 95
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    Alterations of a zinc finger-encoding gene, BCL-6, in diffuse large-cell lymphoma (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-29
    Description: The molecular pathogenesis of diffuse large-cell lymphoma (DLCL), the most frequent and clinically relevant type of lymphoma, is unknown. A gene was cloned from chromosomal translocations affecting band 3q27, which are common in DLCL. This gene, BCL-6, codes for a 79-kilodalton protein that is homologous with zinc finger-transcription factors. In 33 percent (13 of 39) of DLCL samples, but not in other types of lymphoid malignancies, the BCL-6 gene is truncated within its 5' noncoding sequences, suggesting that its expression is deregulated. Thus, BCL-6 may be a proto-oncogene specifically involved in the pathogenesis of DLCL.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ye, B H -- Lista, F -- Lo Coco, F -- Knowles, D M -- Offit, K -- Chaganti, R S -- Dalla-Favera, R -- CA 44029/CA/NCI NIH HHS/ -- CA 48236/CA/NCI NIH HHS/ -- EY 06337/EY/NEI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Oct 29;262(5134):747-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, 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/8235596" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Line ; Chromosomes, Human, Pair 3 ; DNA, Complementary ; DNA-Binding Proteins/genetics ; Exons ; Gene Rearrangement ; Humans ; Introns ; Lymphoma, Large B-Cell, Diffuse/*genetics ; Molecular Sequence Data ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins c-bcl-6 ; Proto-Oncogenes/*genetics ; Sequence Homology, Amino Acid ; Transcription Factors/genetics ; Translocation, Genetic ; Zinc Fingers/*genetics
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  • 96
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    Inhibition of adenylyl cyclase by Gi alpha (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-09
    Description: Evidence suggests that both alpha and beta gamma subunits of heterotrimeric guanine nucleotide-binding regulatory proteins (G proteins) inhibit adenylyl cyclase. Although type I adenylyl cyclase is inhibited directly by exogenous beta gamma, inhibition of adenylyl cyclase by Gi alpha has not been convincingly demonstrated in vitro. Concentration-dependent inhibition of adenylyl cyclases by purified Gi alpha subunits is described. Activated Gi alpha but not G(o) alpha was effective, and myristoylation of Gi alpha was required. The characteristics of the inhibitory effect were dependent on the type of adenylyl cyclase and the nature of the activator of the enzyme. The concentrations of Gi alpha required to inhibit adenylyl cyclase were substantially higher than those normally thought to be relevant physiologically. However, analysis indicates that these concentrations may be relevant and reasonable.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taussig, R -- Iniguez-Lluhi, J A -- Gilman, A G -- GM34497/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 9;261(5118):218-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas 75235-9041.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8327893" target="_blank"〉PubMed〈/a〉
    Keywords: *Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/metabolism ; Animals ; Calmodulin/pharmacology ; Cell Line ; Colforsin/pharmacology ; Dose-Response Relationship, Drug ; Enzyme Activation ; GTP-Binding Proteins/*metabolism ; Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology ; Guanosine Triphosphate/metabolism ; Moths ; Myristic Acid ; Myristic Acids/metabolism ; Recombinant Proteins/pharmacology
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  • 97
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    MHC-restricted depletion of human myelin basic protein-reactive T cells by T cell vaccination (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: Activated autoreactive T cells are potentially pathogenic and regulated by clonotypic networks. Experimental autoimmune diseases can be treated by inoculation with autoreactive T cells (T cell vaccination). In the present study, patients with multiple sclerosis were inoculated with irradiated myelin basic protein (MBP)-reactive T cells. T cell responses to the inoculates were induced to deplete circulating MBP-reactive T cells in the recipients. Regulatory T cell lines isolated from the recipients inhibited T cells used for vaccination. The cytotoxicity of the CD8+ T cell lines was restricted by major histocompatibility antigens. Thus, clonotypic interactions regulating autoreactive T cells in humans can be induced by T cell vaccination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Medaer, R -- Stinissen, P -- Hafler, D -- Raus, J -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1451-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Multiple Sclerosis Research Unit, Dr. L. Willems Instituut, Diepenbeek, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7690157" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antigens, CD4/analysis ; Antigens, CD8/analysis ; Cell Line ; Epitopes/immunology ; Female ; Humans ; *Immunotherapy, Adoptive ; Lymphocyte Activation ; Male ; Middle Aged ; Multiple Sclerosis/immunology/*therapy ; Myelin Basic Protein/*immunology ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; T-Lymphocytes/*immunology ; Vaccination
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  • 98
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    GDNF: a glial cell line-derived neurotrophic factor for midbrain dopaminergic neurons (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-21
    Description: A potent neurotrophic factor that enhances survival of midbrain dopaminergic neurons was purified and cloned. Glial cell line-derived neurotrophic factor (GDNF) is a glycosylated, disulfide-bonded homodimer that is a distantly related member of the transforming growth factor-beta superfamily. In embryonic midbrain cultures, recombinant human GDNF promoted the survival and morphological differentiation of dopaminergic neurons and increased their high-affinity dopamine uptake. These effects were relatively specific; GDNF did not increase total neuron or astrocyte numbers nor did it increase transmitter uptake by gamma-aminobutyric-containing and serotonergic neurons. GDNF may have utility in the treatment of Parkinson's disease, which is marked by progressive degeneration of midbrain dopaminergic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, L F -- Doherty, D H -- Lile, J D -- Bektesh, S -- Collins, F -- New York, N.Y. -- Science. 1993 May 21;260(5111):1130-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Synergen, Inc., Boulder, CO 80301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Astrocytes/cytology/drug effects ; Base Sequence ; Cell Differentiation/drug effects ; Cell Line ; Cell Survival/drug effects ; Cells, Cultured ; Cloning, Molecular ; Dopamine/*biosynthesis ; Glial Cell Line-Derived Neurotrophic Factor ; Humans ; Mesencephalon/cytology/*drug effects/metabolism ; Molecular Sequence Data ; Molecular Weight ; *Nerve Growth Factors ; Nerve Tissue Proteins/chemistry/genetics/isolation & purification/*pharmacology ; Neuroglia/*metabolism ; Neurons/cytology/*drug effects/metabolism ; Parkinson Disease/drug therapy ; Rats
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  • 99
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    Genotypic and phenotypic characterization of HIV-1 patients with primary infection (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-27
    Description: Better characterization of human immunodeficiency virus-type 1 (HIV-1) in patients with primary infection has important implications for the development of an acquired immunodeficiency syndrome (AIDS) vaccine because vaccine strategies should target viral isolates with the properties of transmitted viruses. In five HIV-1 seroconverters, the viral phenotype was found to be uniformly macrophage-tropic and non-syncytium-inducing. Furthermore, the viruses were genotypically homogeneous within each patient, but a common signature sequence was not discernible among transmitted viruses. In the two cases where the sexual partners were also studied, the sequences of the transmitted viruses matched best with minor variants in the blood of the transmitters. There was also a stronger pressure to conserve sequences in gp120 than in gp41, nef, and p17, suggesting that a selective mechanism is involved in transmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, T -- Mo, H -- Wang, N -- Nam, D S -- Cao, Y -- Koup, R A -- Ho, D D -- AI24030/AI/NIAID NIH HHS/ -- AI25541/AI/NIAID NIH HHS/ -- AI27742/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Aug 27;261(5125):1179-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Aaron Diamond AIDS Research Center, New York University School of Medicine, NY 10016.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8356453" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Female ; Gene Products, gag/chemistry/genetics ; Genes, Viral ; Genotype ; Giant Cells/physiology ; HIV Antigens/chemistry/genetics ; HIV Envelope Protein gp120/chemistry/*genetics ; HIV Envelope Protein gp41/chemistry/genetics ; HIV Infections/*microbiology/transmission ; HIV Seropositivity/microbiology ; HIV-1/chemistry/*genetics/*physiology ; Humans ; Macrophages ; Male ; Molecular Sequence Data ; Phenotype ; Sequence Alignment ; Sexual Partners ; *Viral Proteins ; Virus Replication ; gag Gene Products, Human Immunodeficiency Virus
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  • 100
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    Molecular cloning of an apolipoprotein B messenger RNA editing protein (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-18
    Description: Mammalian apolipoprotein B (apo B) exists in two forms, each the product of a single gene. The shorter form, apo B48, arises by posttranscriptional RNA editing whereby cytidine deamination produces a UAA termination codon. A full-length complementary DNA clone encoding an apo B messenger RNA editing protein (REPR) was isolated from rat small intestine. The 229-residue protein contains consensus phosphorylation sites and leucine zipper domains. HepG2 cell extracts acquire editing activity when mixed with REPR from oocyte extracts. REPR is essential for apo B messenger RNA editing, and the isolation and characterization of REPR may lead to the identification of other eukaryotic RNA editing proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Teng, B -- Burant, C F -- Davidson, N O -- DK-42086/DK/NIDDK NIH HHS/ -- HL-38180/HL/NHLBI NIH HHS/ -- KO-4 HL-02166/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 18;260(5115):1816-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8511591" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apolipoproteins B/*genetics ; Base Sequence ; Cell Line ; *Cloning, Molecular ; Cytidine Deaminase/chemistry/*genetics ; Humans ; Intestine, Small/chemistry ; Leucine Zippers ; Molecular Sequence Data ; Molecular Weight ; Open Reading Frames ; Phosphorylation ; *RNA Editing ; Rats ; Tumor Cells, Cultured
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