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  • 1
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    The RNA component of human telomerase (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-09-01
    Description: Eukaryotic chromosomes are capped with repetitive telomere sequences that protect the ends from damage and rearrangements. Telomere repeats are synthesized by telomerase, a ribonucleic acid (RNA)-protein complex. Here, the cloning of the RNA component of human telomerase, termed hTR, is described. The template region of hTR encompasses 11 nucleotides (5'-CUAACCCUAAC) complementary to the human telomere sequence (TTAGGG)n. Germline tissues and tumor cell lines expressed more hTR than normal somatic cells and tissues, which have no detectable telomerase activity. Human cell lines that expressed hTR mutated in the template region generated the predicted mutant telomerase activity. HeLa cells transfected with an antisense hTR lost telomeric DNA and began to die after 23 to 26 doublings. Thus, human telomerase is a critical enzyme for the long-term proliferation of immortal tumor cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng, J -- Funk, W D -- Wang, S S -- Weinrich, S L -- Avilion, A A -- Chiu, C P -- Adams, R R -- Chang, E -- Allsopp, R C -- Yu, J -- AG09383/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1995 Sep 1;269(5228):1236-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Geron Corporation, Menlo Park, CA 94025, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7544491" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Death ; *Cell Division ; Cell Line ; Cloning, Molecular ; DNA Nucleotidylexotransferase/antagonists & ; inhibitors/chemistry/genetics/*metabolism ; HeLa Cells ; Humans ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacology ; Polymerase Chain Reaction ; RNA/chemistry/genetics/*metabolism ; Templates, Genetic ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Cloning and characterization of a G protein-activated human phosphoinositide-3 kinase (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-08-04
    Description: Phosphoinositide-3 kinase activity is implicated in diverse cellular responses triggered by mammalian cell surface receptors and in the regulation of protein sorting in yeast. Receptors with intrinsic and associated tyrosine kinase activity recruit heterodimeric phosphoinositide-3 kinases that consist of p110 catalytic subunits and p85 adaptor molecules containing Src homology 2 (SH2) domains. A phosphoinositide-3 kinase isotype, p110 gamma, was cloned and characterized. The p110 gamma enzyme was activated in vitro by both the alpha and beta gamma subunits of heterotrimeric guanosine triphosphate (GTP)-binding proteins (G proteins) and did not interact with p85. A potential pleckstrin homology domain is located near its amino terminus. The p110 gamma isotype may link signaling through G protein-coupled receptors to the generation of phosphoinositide second messengers phosphorylated in the D-3 position.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stoyanov, B -- Volinia, S -- Hanck, T -- Rubio, I -- Loubtchenkov, M -- Malek, D -- Stoyanova, S -- Vanhaesebroeck, B -- Dhand, R -- Nurnberg, B -- New York, N.Y. -- Science. 1995 Aug 4;269(5224):690-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Research Unit in Growth Factor Signal Transduction, Medical Faculty, University of Jena, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7624799" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Cloning, Molecular ; Enzyme Activation ; GTP-Binding Proteins/*physiology ; Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology ; Humans ; Hydrogen-Ion Concentration ; Molecular Sequence Data ; Phosphatidylinositol 3-Kinases ; Phosphatidylinositols/metabolism ; Phosphotransferases (Alcohol Group Acceptor)/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Substrate Specificity ; Tumor Cells, Cultured
    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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  • 3
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    Activation of RET as a dominant transforming gene by germline mutations of MEN2A and MEN2B (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-01-20
    Description: Multiple endocrine neoplasia types 2A and 2B (MEN2A and MEN2B) and familial medullary thyroid carcinoma are dominantly inherited cancer syndromes. All three syndromes are associated with mutations in RET, which encodes a receptor-like tyrosine kinase. The altered RET alleles were shown to be transforming genes in NIH 3T3 cells as a consequence of constitutive activation of the RET kinase. The MEN2A mutation resulted in RET dimerization at steady state, whereas the MEN2B mutation altered RET catalytic properties both quantitatively and qualitatively. Oncogenic conversion of RET in these neoplastic syndromes establishes germline transmission of dominant transforming genes in human cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santoro, M -- Carlomagno, F -- Romano, A -- Bottaro, D P -- Dathan, N A -- Grieco, M -- Fusco, A -- Vecchio, G -- Matoskova, B -- Kraus, M H -- New York, N.Y. -- Science. 1995 Jan 20;267(5196):381-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centro di Endocrinologia ed Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (CNR), Napoli, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7824936" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Alleles ; Animals ; Cell Transformation, Neoplastic/*genetics ; *Drosophila Proteins ; Genetic Vectors ; Humans ; Mice ; Multiple Endocrine Neoplasia Type 2a/*genetics ; Multiple Endocrine Neoplasia Type 2b/*genetics ; Mutation ; Phosphorylation ; Proto-Oncogene Proteins/chemistry/*genetics/metabolism ; Proto-Oncogene Proteins c-ret ; *Proto-Oncogenes ; Receptor Protein-Tyrosine Kinases/chemistry/*genetics/metabolism ; Substrate Specificity ; Transfection ; Tumor Cells, Cultured
    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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  • 4
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    Fibroblasts as efficient antigen-presenting cells in lymphoid organs (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-02
    Description: Only so-called "professional" antigen-presenting cells (APCs) of hematopoietic origin are believed capable of inducing T lymphocyte responses. However, fibroblasts transfected with viral proteins directly induced antiviral cytotoxic T lymphocyte responses in vivo, without involvement of host APCs. Fibroblasts induced T cells only in the milieu of lymphoid organs. Thus, antigen localization affects self-nonself discrimination and cell-based vaccine strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kundig, T M -- Bachmann, M F -- DiPaolo, C -- Simard, J J -- Battegay, M -- Lother, H -- Gessner, A -- Kuhlcke, K -- Ohashi, P S -- Hengartner, H -- New York, N.Y. -- Science. 1995 Jun 2;268(5215):1343-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Experimental Immunology, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7761853" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/*immunology ; Cytotoxicity, Immunologic ; Fibroblasts/*immunology ; Glycoproteins/immunology ; Histocompatibility Antigens Class I/immunology ; L Cells (Cell Line) ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic choriomeningitis virus/*immunology ; Lymphoid Tissue/*immunology ; Mice ; Mice, Inbred C57BL ; Neoplasms/immunology ; T-Lymphocytes, Cytotoxic/*immunology ; Transfection ; Tumor Cells, Cultured ; Viral Proteins/*immunology
    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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  • 5
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    Inactivation of the type II TGF-beta receptor in colon cancer cells with microsatellite instability (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-02
    Description: Transforming growth factor-beta (TGF-beta) is a potent inhibitor of epithelial cell growth. Human colon cancer cell lines with high rates of microsatellite instability were found to harbor mutations in the type II TGF-beta receptor (RII) gene. Eight such examples, due to three different mutations, were identified. The mutations were clustered within small repeated sequences in the RII gene, were accompanied by the absence of cell surface RII receptors, and were usually associated with small amounts of RII transcript. RII mutation, by inducing the escape of cells from TGF-beta-mediated growth control, links DNA repair defects with a specific pathway of tumor progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Markowitz, S -- Wang, J -- Myeroff, L -- Parsons, R -- Sun, L -- Lutterbaugh, J -- Fan, R S -- Zborowska, E -- Kinzler, K W -- Vogelstein, B -- CA38173/CA/NCI NIH HHS/ -- CA50457/CA/NCI NIH HHS/ -- CA63480/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 Jun 2;268(5215):1336-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University Hospitals of Cleveland, OH, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7761852" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Colonic Neoplasms/*genetics/metabolism/pathology ; Colorectal Neoplasms, Hereditary Nonpolyposis/*genetics/metabolism/pathology ; DNA Repair ; DNA, Neoplasm/genetics ; DNA, Satellite/*genetics ; Disease Progression ; Frameshift Mutation ; Humans ; Mice ; Molecular Sequence Data ; Neoplasm Transplantation ; Phenotype ; RNA, Messenger/genetics ; Receptors, Transforming Growth Factor beta/*genetics/metabolism ; Repetitive Sequences, Nucleic Acid ; Sequence Deletion ; Transforming Growth Factor beta/metabolism ; Tumor Cells, Cultured
    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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  • 6
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    Mutations of GTBP in genetically unstable cells (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-30
    Description: The molecular defects responsible for tumor cell hypermutability in humans have not yet been fully identified. Here the gene encoding a G/T mismatch-binding protein (GTBP) was localized to within 1 megabase of the related hMSH2 gene on chromosome 2 and was found to be inactivated in three hypermutable cell lines. Unlike cells defective in other mismatch repair genes, which display widespread alterations in mononucleotide, dinucleotide, and other simple repeated sequences, the GTBP-deficient cells showed alterations primarily in mononucleotide tracts. These results suggest that GTBP is important for maintaining the integrity of the human genome and document molecular defects accounting for variation in mutator phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papadopoulos, N -- Nicolaides, N C -- Liu, B -- Parsons, R -- Lengauer, C -- Palombo, F -- D'Arrigo, A -- Markowitz, S -- Willson, J K -- Kinzler, K W -- CA35494/CA/NCI NIH HHS/ -- CA47527/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 Jun 30;268(5219):1915-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins Oncology Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7604266" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Chromosome Mapping ; Chromosomes, Human, Pair 2 ; Codon ; Colorectal Neoplasms/*genetics ; Colorectal Neoplasms, Hereditary Nonpolyposis/genetics ; DNA Repair/*genetics ; DNA, Neoplasm/*genetics ; DNA, Satellite/genetics ; DNA-Binding Proteins/*genetics ; *Frameshift Mutation ; Genetic Markers ; Germ-Line Mutation ; Humans ; Molecular Sequence Data ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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