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  • Transfection  (5)
  • 2005-2009
  • 1995-1999  (5)
  • 1945-1949
  • 1940-1944
  • 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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    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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  • 3
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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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  • 4
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    Massive cell death of immature hematopoietic cells and neurons in Bcl-x-deficient mice (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-10
    Description: bcl-x is a member of the bcl-2 gene family, which may regulate programmed cell death. Mice were generated that lacked Bcl-x. The Bcl-x-deficient mice died around embryonic day 13. Extensive apoptotic cell death was evident in postmitotic immature neurons of the developing brain, spinal cord, and dorsal root ganglia. Hematopoietic cells in the liver were also apoptotic. Analyses of bcl-x double-knockout chimeric mice showed that the maturation of Bcl-x-deficient lymphocytes was diminished. The life-span of immature lymphocytes, but not mature lymphocytes, was shortened. Thus, Bcl-x functions to support the viability of immature cells during the development of the nervous and hematopoietic systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Motoyama, N -- Wang, F -- Roth, K A -- Sawa, H -- Nakayama, K -- Negishi, I -- Senju, S -- Zhang, Q -- Fujii, S -- New York, N.Y. -- Science. 1995 Mar 10;267(5203):1506-10.〈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/7878471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Bone Marrow Cells ; Brain/cytology/embryology ; Cell Differentiation ; Cell Survival ; Cells, Cultured ; Ganglia, Spinal/cytology/embryology ; Hematopoietic Stem Cells/*cytology ; Liver/cytology/embryology ; Lymphocytes/*cytology ; Mice ; Mice, Knockout ; Nerve Degeneration ; Neurons/*cytology ; Proto-Oncogene Proteins/deficiency/*physiology ; *Proto-Oncogene Proteins c-bcl-2 ; Spinal Cord/cytology/embryology ; Transfection ; bcl-X Protein
    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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  • 5
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    Inhibition of ICE family proteases by baculovirus antiapoptotic protein p35 (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-09-29
    Description: The baculovirus antiapoptotic protein p35 inhibited the proteolytic activity of human interleukin-1 beta converting enzyme (ICE) and three of its homologs in enzymatic assays. Coexpression of p35 prevented the autoproteolytic activation of ICE from its precursor form and blocked ICE-induced apoptosis. Inhibition of enzymatic activity correlated with the cleavage of p35 and the formation of a stable ICE-p35 complex. The ability of p35 to block apoptosis in different pathways and in distantly related organisms suggests a central and conserved role for ICE-like proteases in the induction of apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bump, N J -- Hackett, M -- Hugunin, M -- Seshagiri, S -- Brady, K -- Chen, P -- Ferenz, C -- Franklin, S -- Ghayur, T -- Li, P -- AI 38262/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1995 Sep 29;269(5232):1885-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BASF Bioresearch Corporation, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7569933" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Apoptosis ; Binding Sites ; Binding, Competitive ; Caspase 1 ; Cell Line ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/genetics/*metabolism/pharmacology ; Enzyme Activation/drug effects ; Humans ; Inhibitor of Apoptosis Proteins ; Molecular Sequence Data ; Recombinant Proteins/pharmacology ; Transfection ; Viral Proteins/genetics/*metabolism/pharmacology
    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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