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  • Tumor Cells, Cultured  (85)
  • American Association for the Advancement of Science (AAAS)  (85)
  • 1995-1999  (85)
  • 1999  (36)
  • 1997  (49)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (85)
Years
  • 1995-1999  (85)
Year
  • 1
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    CD3- and CD28-dependent induction of PDE7 required for T cell activation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-05
    Description: Costimulation of both the CD3 and CD28 receptors is essential for T cell activation. Induction of adenosine 3',5'-monophosphate (cAMP)-specific phosphodiesterase-7 (PDE7) was found to be a consequence of such costimulation. Increased PDE7 in T cells correlated with decreased cAMP, increased interleukin-2 expression, and increased proliferation. Selectively reducing PDE7 expression with a PDE7 antisense oligonucleotide inhibited T cell proliferation; inhibition was reversed by blocking the cAMP signaling pathways that operate through cAMP-dependent protein kinase (PKA). Thus, PDE7 induction and consequent suppression of PKA activity is required for T cell activation, and inhibition of PDE7 could be an approach to treating T cell-dependent disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, L -- Yee, C -- Beavo, J A -- DK21723/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 5;283(5403):848-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Molecular and Cellular Biology Program, Box 357280, University of Washington School of Medicine, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9933169" target="_blank"〉PubMed〈/a〉
    Keywords: 3',5'-Cyclic-AMP Phosphodiesterases/*biosynthesis/genetics/metabolism ; Antibodies ; Antigens, CD28/immunology/*physiology ; Antigens, CD3/immunology/*physiology ; CD4-Positive T-Lymphocytes/enzymology/immunology ; Cells, Cultured ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Cyclic Nucleotide Phosphodiesterases, Type 7 ; Enzyme Induction ; Humans ; Interleukin-2/biosynthesis ; Isoenzymes/*biosynthesis/genetics/metabolism ; *Lymphocyte Activation ; Oligonucleotides, Antisense/pharmacology ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; T-Lymphocytes/*enzymology/*immunology/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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  • 2
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    An activating immunoreceptor complex formed by NKG2D and DAP10 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Many immune receptors are composed of separate ligand-binding and signal-transducing subunits. In natural killer (NK) and T cells, DAP10 was identified as a cell surface adaptor protein in an activating receptor complex with NKG2D, a receptor for the stress-inducible and tumor-associated major histocompatibility complex molecule MICA. Within the DAP10 cytoplasmic domain, an Src homology 2 (SH2) domain-binding site was capable of recruiting the p85 subunit of the phosphatidylinositol 3-kinase (PI 3-kinase), providing for NKG2D-dependent signal transduction. Thus, NKG2D-DAP10 receptor complexes may activate NK and T cell responses against MICA-bearing tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, J -- Song, Y -- Bakker, A B -- Bauer, S -- Spies, T -- Lanier, L L -- Phillips, J H -- AI30581/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):730-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNAX Research Institute, 901 California Avenue, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426994" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Cell Line ; Cytotoxicity, Immunologic ; Humans ; Killer Cells, Natural/*immunology/metabolism ; Ligands ; *Lymphocyte Activation ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Molecular Sequence Data ; NK Cell Lectin-Like Receptor Subfamily K ; Neoplasms/immunology ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Receptors, Immunologic/chemistry/genetics/*metabolism ; Receptors, Natural Killer Cell ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; Tumor Cells, Cultured ; src Homology Domains
    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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    Antiangiogenic activity of the cleaved conformation of the serpin antithrombin (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: Antithrombin, a member of the serpin family, functions as an inhibitor of thrombin and other enzymes. Cleavage of the carboxyl-terminal loop of antithrombin induces a conformational change in the molecule. Here it is shown that the cleaved conformation of antithrombin has potent antiangiogenic and antitumor activity in mouse models. The latent form of intact antithrombin, which is similar in conformation to the cleaved molecule, also inhibited angiogenesis and tumor growth. These data provide further evidence that the clotting and fibrinolytic pathways are directly involved in the regulation of angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Reilly, M S -- Pirie-Shepherd, S -- Lane, W S -- Folkman, J -- P01-CA45548/CA/NCI NIH HHS/ -- R01-CA64481/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1926-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Children's Hospital, Departments of Surgery and Cellular Biology, Harvard Microchemistry Facility, 16 Divinity Avenue, Cambridge, MA 02138, USA. oreilly@hub.tch.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489375" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/chemistry/isolation & purification/metabolism/*pharmacology ; Antithrombins/chemistry/isolation & purification/metabolism/*pharmacology ; Carcinoma, Small Cell/blood supply/drug therapy ; Cell Line ; Culture Media, Conditioned ; Drug Screening Assays, Antitumor ; Humans ; Lung Neoplasms/blood supply/drug therapy ; Mice ; Mice, SCID ; Neoplasm Transplantation ; Neovascularization, Pathologic/*drug therapy ; Peptide Fragments/chemistry/metabolism/pharmacology ; Protein Conformation ; 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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    Efficient persistence of extrachromosomal KSHV DNA mediated by latency-associated nuclear antigen (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: Primary effusion lymphoma (PEL) cells harbor Kaposi's sarcoma-associated herpesvirus (KSHV) episomes and express a KSHV-encoded latency-associated nuclear antigen (LANA). In PEL cells, LANA and KSHV DNA colocalized in dots in interphase nuclei and along mitotic chromosomes. In the absence of KSHV DNA, LANA was diffusely distributed in the nucleus or on mitotic chromosomes. In lymphoblasts, LANA was necessary and sufficient for the persistence of episomes containing a specific KSHV DNA fragment. Furthermore, LANA colocalized with the artificial KSHV DNA episomes in nuclei and along mitotic chromosomes. These results support a model in which LANA tethers KSHV DNA to chromosomes during mitosis to enable the efficient segregation of KSHV episomes to progeny cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ballestas, M E -- Chatis, P A -- Kaye, K M -- CA67380-04/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):641-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213686" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Viral/analysis/genetics/metabolism ; Cell Nucleus/chemistry ; Chromosomes/chemistry/*metabolism ; Cosmids ; DNA, Viral/analysis/genetics/*metabolism ; Herpesvirus 8, Human/*genetics/physiology ; Humans ; Interphase ; Lymphocytes/chemistry ; Microscopy, Confocal ; *Mitosis ; Nuclear Proteins/analysis/genetics/*metabolism ; *Plasmids ; 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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  • 5
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    Pigment epithelium-derived factor: a potent inhibitor of angiogenesis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-10
    Description: In the absence of disease, the vasculature of the mammalian eye is quiescent, in part because of the action of angiogenic inhibitors that prevent vessels from invading the cornea and vitreous. Here, an inhibitor responsible for the avascularity of these ocular compartments is identified as pigment epithelium-derived factor (PEDF), a protein previously shown to have neurotrophic activity. The amount of inhibitory PEDF produced by retinal cells was positively correlated with oxygen concentrations, suggesting that its loss plays a permissive role in ischemia-driven retinal neovascularization. These results suggest that PEDF may be of therapeutic use, especially in retinopathies where pathological neovascularization compromises vision and leads to blindness.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawson, D W -- Volpert, O V -- Gillis, P -- Crawford, S E -- Xu, H -- Benedict, W -- Bouck, N P -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):245-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology-Immunology, Department of Pathology, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Medical School, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10398599" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antibodies/immunology ; Cattle ; Cells, Cultured ; Chemotaxis/drug effects ; Culture Media, Conditioned ; Endothelial Growth Factors/metabolism ; Endothelium, Vascular/cytology/drug effects/physiology ; Eye/blood supply ; *Eye Proteins ; Humans ; Lymphokines/metabolism ; Mice ; Neovascularization, Pathologic/*drug therapy/metabolism/pathology ; Neovascularization, Physiologic/*drug effects ; *Nerve Growth Factors ; Oxygen/physiology ; Proteins/genetics/immunology/*pharmacology/*physiology ; RNA, Messenger/genetics/metabolism ; Rats ; Retina/*metabolism/pathology ; Retinal Neovascularization/*drug therapy ; Retinal Vessels/growth & development ; Serpins/genetics/immunology/*pharmacology/*physiology ; Tumor Cells, Cultured ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Dynamic control of CaMKII translocation and localization in hippocampal neurons by NMDA receptor stimulation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-02
    Description: Calcium-calmodulin-dependent protein kinase II (CaMKII) is thought to increase synaptic strength by phosphorylating postsynaptic density (PSD) ion channels and signaling proteins. It is shown that N-methyl-D-aspartate (NMDA) receptor stimulation reversibly translocates green fluorescent protein-tagged CaMKII from an F-actin-bound to a PSD-bound state. The translocation time was controlled by the ratio of expressed beta-CaMKII to alpha-CaMKII isoforms. Although F-actin dissociation into the cytosol required autophosphorylation of or calcium-calmodulin binding to beta-CaMKII, PSD translocation required binding of calcium-calmodulin to either the alpha- or beta-CaMKII subunits. Autophosphorylation of CaMKII indirectly prolongs its PSD localization by increasing the calmodulin-binding affinity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, K -- Meyer, T -- GM-48113/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):162-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Department of Pharmacology and Cancer Biology, Box 3709, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10102820" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Calcium/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cells, Cultured ; Cytosol/metabolism ; Dendrites/*enzymology ; Electric Stimulation ; Glutamic Acid/pharmacology ; Green Fluorescent Proteins ; Hippocampus/cytology/*enzymology ; Isoenzymes/metabolism ; Luminescent Proteins ; Microscopy, Fluorescence ; Nerve Tissue Proteins/analysis ; Neurons/*enzymology ; Phosphorylation ; Rats ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Synapses/*enzymology ; 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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  • 7
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    BRCA1 inhibition of estrogen receptor signaling in transfected cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Mutations of the breast cancer susceptibility gene BRCA1 confer increased risk for breast, ovarian, and prostatic cancers, but it is not clear why the mutations are associated with these particular tumor types. In transient transfection assays, BRCA1 was found to inhibit signaling by the ligand-activated estrogen receptor (ER-alpha) through the estrogen-responsive enhancer element and to block the transcriptional activation function AF-2 of ER-alpha. These results raise the possibility that wild-type BRCA1 suppresses estrogen-dependent transcriptional pathways related to mammary epithelial cell proliferation and that loss of this ability contributes to tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fan, S -- Wang, J -- Yuan, R -- Ma, Y -- Meng, Q -- Erdos, M R -- Pestell, R G -- Yuan, F -- Auborn, K J -- Goldberg, I D -- Rosen, E M -- R01-CA75503/CA/NCI NIH HHS/ -- R01-ES09169/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1999 May 21;284(5418):1354-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, Long Island Jewish Medical Center, The Long Island Campus for the Albert Einstein College of Medicine, 270-05 76th Avenue, New Hyde Park, NY 11040, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334989" target="_blank"〉PubMed〈/a〉
    Keywords: BRCA1 Protein/*physiology ; Breast/cytology ; Breast Neoplasms/etiology ; Cell Division ; Enhancer Elements, Genetic ; Epithelial Cells/cytology ; Estradiol/metabolism ; Estrogen Receptor alpha ; Female ; Genes, BRCA1 ; Genes, Reporter ; Humans ; Ligands ; Male ; Receptors, Estrogen/*metabolism ; *Signal Transduction ; Transcription Factors/metabolism ; *Transcriptional Activation ; 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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  • 8
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    Potential target found for antimetastasis drugs (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finkel, E -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):33-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10428697" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/therapeutic use ; Clinical Trials as Topic ; Cloning, Molecular ; *Glucuronidase ; Glycoside Hydrolases/*antagonists & inhibitors/*genetics/isolation & ; purification/metabolism ; Humans ; Mice ; Neoplasm Metastasis/*prevention & control ; Rats ; 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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  • 9
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    Signaling from Rho to the actin cytoskeleton through protein kinases ROCK and LIM-kinase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-07
    Description: The actin cytoskeleton undergoes extensive remodeling during cell morphogenesis and motility. The small guanosine triphosphatase Rho regulates such remodeling, but the underlying mechanisms of this regulation remain unclear. Cofilin exhibits actin-depolymerizing activity that is inhibited as a result of its phosphorylation by LIM-kinase. Cofilin was phosphorylated in N1E-115 neuroblastoma cells during lysophosphatidic acid-induced, Rho-mediated neurite retraction. This phosphorylation was sensitive to Y-27632, a specific inhibitor of the Rho-associated kinase ROCK. ROCK, which is a downstream effector of Rho, did not phosphorylate cofilin directly but phosphorylated LIM-kinase, which in turn was activated to phosphorylate cofilin. Overexpression of LIM-kinase in HeLa cells induced the formation of actin stress fibers in a Y-27632-sensitive manner. These results indicate that phosphorylation of LIM-kinase by ROCK and consequently increased phosphorylation of cofilin by LIM-kinase contribute to Rho-induced reorganization of the actin cytoskeleton.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maekawa, M -- Ishizaki, T -- Boku, S -- Watanabe, N -- Fujita, A -- Iwamatsu, A -- Obinata, T -- Ohashi, K -- Mizuno, K -- Narumiya, S -- New York, N.Y. -- Science. 1999 Aug 6;285(5429):895-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Kyoto University Faculty of Medicine, Kyoto 606-8315, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10436159" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*metabolism ; Actin Depolymerizing Factors ; Actins/metabolism ; Amides/pharmacology ; Animals ; COS Cells ; DNA-Binding Proteins/metabolism ; Enzyme Activation ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; HeLa Cells ; Humans ; Intracellular Signaling Peptides and Proteins ; Lim Kinases ; Lysophospholipids/pharmacology ; Membrane Proteins/*metabolism ; Microfilament Proteins/metabolism ; Phosphorylation ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Pyridines/pharmacology ; *Signal Transduction ; Tumor Cells, Cultured ; rho-Associated Kinases ; rhoB GTP-Binding Protein
    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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  • 10
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    Association of BRCA1 with the hRad50-hMre11-p95 complex and the DNA damage response (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: BRCA1 encodes a tumor suppressor that is mutated in familial breast and ovarian cancers. Here, it is shown that BRCA1 interacts in vitro and in vivo with hRad50, which forms a complex with hMre11 and p95/nibrin. Upon irradiation, BRCA1 was detected in discrete foci in the nucleus, which colocalize with hRad50. Formation of irradiation-induced foci positive for BRCA1, hRad50, hMre11, or p95 was dramatically reduced in HCC/1937 breast cancer cells carrying a homozygous mutation in BRCA1 but was restored by transfection of wild-type BRCA1. Ectopic expression of wild-type, but not mutated, BRCA1 in these cells rendered them less sensitive to the DNA damage agent, methyl methanesulfonate. These data suggest that BRCA1 is important for the cellular responses to DNA damage that are mediated by the hRad50-hMre11-p95 complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhong, Q -- Chen, C F -- Li, S -- Chen, Y -- Wang, C C -- Xiao, J -- Chen, P L -- Sharp, Z D -- Lee, W H -- CA 30195/CA/NCI NIH HHS/ -- CA 58183/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):747-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Medicine, Institute of Biotechnology, University of Texas Health Science Center at San Antonio, 15355 Lambda Drive, San Antonio, TX 78245, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426999" target="_blank"〉PubMed〈/a〉
    Keywords: BRCA1 Protein/*metabolism ; Cell Cycle Proteins/*metabolism ; Cell Nucleus/*metabolism ; Cell Survival ; *DNA Damage ; *DNA Repair Enzymes ; DNA-Binding Proteins/*metabolism ; Gamma Rays ; Genes, BRCA1 ; Humans ; Methyl Methanesulfonate/pharmacology ; Mutagens/pharmacology ; Mutation ; *Nuclear Proteins ; Rad51 Recombinase ; Recombination, Genetic ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Identification of a nuclear receptor for bile acids (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Bile acids are essential for the solubilization and transport of dietary lipids and are the major products of cholesterol catabolism. Results presented here show that bile acids are physiological ligands for the farnesoid X receptor (FXR), an orphan nuclear receptor. When bound to bile acids, FXR repressed transcription of the gene encoding cholesterol 7alpha-hydroxylase, which is the rate-limiting enzyme in bile acid synthesis, and activated the gene encoding intestinal bile acid-binding protein, which is a candidate bile acid transporter. These results demonstrate a mechanism by which bile acids transcriptionally regulate their biosynthesis and enterohepatic transport.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Makishima, M -- Okamoto, A Y -- Repa, J J -- Tu, H -- Learned, R M -- Luk, A -- Hull, M V -- Lustig, K D -- Mangelsdorf, D J -- Shan, B -- New York, N.Y. -- Science. 1999 May 21;284(5418):1362-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pharmacology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9050, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334992" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/biosynthesis/*metabolism ; Biological Transport ; Carrier Proteins/*genetics/metabolism ; Cell Line ; Chenodeoxycholic Acid/*metabolism ; Cholesterol/metabolism ; Cholesterol 7-alpha-Hydroxylase/*genetics ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Gene Expression Regulation ; Histone Acetyltransferases ; Homeostasis ; Humans ; *Hydroxysteroid Dehydrogenases ; Ligands ; Liver/metabolism ; *Membrane Glycoproteins ; Mice ; Nuclear Receptor Coactivator 1 ; *Organic Anion Transporters, Sodium-Dependent ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; *Symporters ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection ; Tumor Cells, Cultured
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  • 12
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    A giant protease with potential to substitute for some functions of the proteasome (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-12
    Description: An alanyl-alanyl-phenylalanyl-7-amino-4-methylcoumarin-hydrolyzing protease particle copurifying with 26S proteasomes was isolated and identified as tripeptidyl peptidase II (TPPII), a cytosolic subtilisin-like peptidase of unknown function. The particle is larger than the 26S proteasome and has a rod-shaped, dynamic supramolecular structure. TPPII exhibits enhanced activity in proteasome inhibitor-adapted cells and degrades polypeptides by exo- as well as predominantly trypsin-like endoproteolytic cleavage. TPPII may thus participate in extralysosomal polypeptide degradation and may in part account for nonproteasomal epitope generation as postulated for certain major histocompatibility complex class I alleles. In addition, TPPII may be able to substitute for some metabolic functions of the proteasome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geier, E -- Pfeifer, G -- Wilm, M -- Lucchiari-Hartz, M -- Baumeister, W -- Eichmann, K -- Niedermann, G -- New York, N.Y. -- Science. 1999 Feb 12;283(5404):978-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck Institute of Immunobiology, Stubeweg 51, D-79108 Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9974389" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcysteine/analogs & derivatives/pharmacology ; Alleles ; Amino Acid Chloromethyl Ketones/pharmacology ; Aminopeptidases ; Animals ; Cell Survival ; Coumarins/metabolism ; Cysteine Endopeptidases/*metabolism ; Cytosol/enzymology ; Dipeptidyl-Peptidases and Tripeptidyl-Peptidases ; Epitopes/metabolism ; Genes, MHC Class I ; Hydrolysis ; Mice ; Molecular Weight ; Multienzyme Complexes/*metabolism ; Oligopeptides/metabolism ; Proteasome Endopeptidase Complex ; Serine Endopeptidases/chemistry/isolation & purification/*metabolism ; Serine Proteinase Inhibitors/pharmacology ; Substrate Specificity ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    UDP-GlcNAc 2-epimerase: a regulator of cell surface sialylation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Modification of cell surface molecules with sialic acid is crucial for their function in many biological processes, including cell adhesion and signal transduction. Uridine diphosphate-N-acetylglucosamine 2-epimerase (UDP-GlcNAc 2-epimerase) is an enzyme that catalyzes an early, rate-limiting step in the sialic acid biosynthetic pathway. UDP-GlcNAc 2-epimerase was found to be a major determinant of cell surface sialylation in human hematopoietic cell lines and a critical regulator of the function of specific cell surface adhesion molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keppler, O T -- Hinderlich, S -- Langner, J -- Schwartz-Albiez, R -- Reutter, W -- Pawlita, M -- New York, N.Y. -- Science. 1999 May 21;284(5418):1372-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Applied Tumor Virology Program, Tumor Immunology Program, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Antigens, CD14/biosynthesis ; Antigens, CD15/biosynthesis ; Antigens, Differentiation, B-Lymphocyte/metabolism ; Carbohydrate Epimerases/genetics/metabolism ; Cell Adhesion Molecules/metabolism ; Cell Membrane/*metabolism ; Culture Media ; *Escherichia coli Proteins ; Glycoconjugates/*metabolism ; HL-60 Cells ; Histocompatibility Antigens Class I/biosynthesis ; Humans ; Lectins/metabolism ; Oligosaccharides/biosynthesis ; Rats ; Sialic Acid Binding Ig-like Lectin 2 ; Sialic Acids/*biosynthesis ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    HIV vaccines. Magic of the occult? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montefiori, D -- Moore, J P -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):336-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for AIDS Research, Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA. monte005@mc.duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9925493" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/*immunology ; Animals ; COS Cells ; Cell Fusion ; Coculture Techniques ; Epitopes/immunology ; HIV Antibodies/biosynthesis/*immunology ; HIV Antigens/*immunology ; HIV Envelope Protein gp120/immunology ; HIV Envelope Protein gp41/immunology ; HIV-1/*immunology/physiology ; Mice ; Neutralization Tests ; 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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  • 15
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    Two distinct cytokines released from a human aminoacyl-tRNA synthetase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-02
    Description: Aminoacyl-tRNA synthetases catalyze aminoacylation of transfer RNAs (tRNAs). It is shown that human tyrosyl-tRNA synthetase can be split into two fragments with distinct cytokine activities. The endothelial monocyte-activating polypeptide II-like carboxy-terminal domain has potent leukocyte and monocyte chemotaxis activity and stimulates production of myeloperoxidase, tumor necrosis factor-alpha, and tissue factor. The catalytic amino-terminal domain binds to the interleukin-8 type A receptor and functions as an interleukin-8-like cytokine. Under apoptotic conditions in cell culture, the full-length enzyme is secreted, and the two cytokine activities can be generated by leukocyte elastase, an extracellular protease. Secretion of this tRNA synthetase may contribute to apoptosis both by arresting translation and producing needed cytokines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wakasugi, K -- Schimmel, P -- GM23562/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):147-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Skaggs Institute for Chemical Biology, The Scripps Research Institute, Beckman Center, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10102815" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antigens, CD/metabolism ; Apoptosis ; Binding, Competitive ; Catalytic Domain ; Chemotaxis, Leukocyte ; *Cytokines ; Humans ; Interleukin-8/*metabolism/pharmacology ; Leukocyte Elastase/metabolism ; Molecular Sequence Data ; Monocytes/physiology ; Neoplasm Proteins/*metabolism/pharmacology ; Neutrophils/metabolism/physiology ; RNA-Binding Proteins/*metabolism/pharmacology ; Receptors, Interleukin/metabolism ; Receptors, Interleukin-8A ; Recombinant Proteins/metabolism ; Signal Transduction ; Tumor Cells, Cultured ; Tyrosine-tRNA Ligase/chemistry/*metabolism/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    A chemical inhibitor of p53 that protects mice from the side effects of cancer therapy (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-11
    Description: Chemotherapy and radiation therapy for cancer often have severe side effects that limit their efficacy. Because these effects are in part determined by p53-mediated apoptosis, temporary suppression of p53 has been suggested as a therapeutic strategy to prevent damage of normal tissues during treatment of p53-deficient tumors. To test this possibility, a small molecule was isolated for its ability to reversibly block p53-dependent transcriptional activation and apoptosis. This compound, pifithrin-alpha, protected mice from the lethal genotoxic stress associated with anticancer treatment without promoting the formation of tumors. Thus, inhibitors of p53 may be useful drugs for reducing the side effects of cancer therapy and other types of stress associated with p53 induction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Komarov, P G -- Komarova, E A -- Kondratov, R V -- Christov-Tselkov, K -- Coon, J S -- Chernov, M V -- Gudkov, A V -- CA60730/CA/NCI NIH HHS/ -- CA75179/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Sep 10;285(5434):1733-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Illinois at Chicago, Chicago, IL 60607, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10481009" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*adverse effects/pharmacology ; Apoptosis/*drug effects ; Benzothiazoles ; Cell Division/drug effects ; Cell Line ; Cell Nucleus/drug effects/metabolism ; Cytoplasm/drug effects/metabolism ; DNA/biosynthesis ; DNA Damage ; G2 Phase/drug effects ; Gamma Rays/*adverse effects ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Nude ; Neoplasms/drug therapy/radiotherapy/*therapy ; Radiation Tolerance/*drug effects ; Thiazoles/*pharmacology ; Time Factors ; Toluene/*analogs & derivatives/pharmacology ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/*antagonists & inhibitors/physiology ; Ultraviolet Rays/adverse effects
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  • 17
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    In vivo protein transduction: delivery of a biologically active protein into the mouse (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-08
    Description: Delivery of therapeutic proteins into tissues and across the blood-brain barrier is severely limited by the size and biochemical properties of the proteins. Here it is shown that intraperitoneal injection of the 120-kilodalton beta-galactosidase protein, fused to the protein transduction domain from the human immunodeficiency virus TAT protein, results in delivery of the biologically active fusion protein to all tissues in mice, including the brain. These results open new possibilities for direct delivery of proteins into patients in the context of protein therapy, as well as for epigenetic experimentation with model organisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwarze, S R -- Ho, A -- Vocero-Akbani, A -- Dowdy, S F -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1569-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10477521" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood-Brain Barrier ; Brain/metabolism ; Cell Membrane/metabolism ; Drug Carriers ; *Drug Delivery Systems ; Fluorescein-5-isothiocyanate ; Gene Products, tat/administration & dosage/*metabolism ; Humans ; Injections, Intraperitoneal ; Jurkat Cells ; Lipid Bilayers ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Microscopy, Fluorescence ; Muscle, Skeletal/metabolism ; Recombinant Fusion Proteins/administration & dosage/*metabolism ; Spleen/metabolism ; Tissue Distribution ; Tumor Cells, Cultured ; beta-Galactosidase/administration & dosage/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Regulation of beta-catenin signaling by the B56 subunit of protein phosphatase 2A (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-26
    Description: Dysregulation of Wnt-beta-catenin signaling disrupts axis formation in vertebrate embryos and underlies multiple human malignancies. The adenomatous polyposis coli (APC) protein, axin, and glycogen synthase kinase 3beta form a Wnt-regulated signaling complex that mediates the phosphorylation-dependent degradation of beta-catenin. A protein phosphatase 2A (PP2A) regulatory subunit, B56, interacted with APC in the yeast two-hybrid system. Expression of B56 reduced the abundance of beta-catenin and inhibited transcription of beta-catenin target genes in mammalian cells and Xenopus embryo explants. The B56-dependent decrease in beta-catenin was blocked by oncogenic mutations in beta-catenin or APC, and by proteasome inhibitors. B56 may direct PP2A to dephosphorylate specific components of the APC-dependent signaling complex and thereby inhibit Wnt signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seeling, J M -- Miller, J R -- Gil, R -- Moon, R T -- White, R -- Virshup, D M -- 3P30CA42014/CA/NCI NIH HHS/ -- R01 CA71074/CA/NCI NIH HHS/ -- T32CA09602/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):2089-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84132, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10092233" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Line ; Cysteine Endopeptidases/metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Cytoskeletal Proteins/genetics/*metabolism ; Down-Regulation ; Genes, Reporter ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinases ; Humans ; Leupeptins/pharmacology ; Multienzyme Complexes/metabolism ; Mutation ; Phosphoprotein Phosphatases/chemistry/genetics/*metabolism ; Phosphorylation ; Proteasome Endopeptidase Complex ; Protein Phosphatase 2 ; Proto-Oncogene Proteins/*metabolism ; *Signal Transduction ; *Trans-Activators ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; Wnt Proteins ; Xenopus ; Xenopus Proteins ; *Zebrafish Proteins ; beta Catenin
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  • 19
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    Genetic mechanisms of age regulation of human blood coagulation factor IX (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Blood coagulation capacity increases with age in healthy individuals. Through extensive longitudinal analyses of human factor IX gene expression in transgenic mice, two essential age-regulatory elements, AE5' and AE3', have been identified. These elements are required and together are sufficient for normal age regulation of factor IX expression. AE5', a PEA-3 related element present in the 5' upstream region of the gene encoding factor IX, is responsible for age-stable expression of the gene. AE3', in the middle of the 3' untranslated region, is responsible for age-associated elevation in messenger RNA levels. In a concerted manner, AE5' and AE3' recapitulate natural patterns of the advancing age-associated increase in factor IX gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kurachi, S -- Deyashiki, Y -- Takeshita, J -- Kurachi, K -- AG13283/AG/NIA NIH HHS/ -- HL38644/HL/NHLBI NIH HHS/ -- HL53713/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):739-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, University of Michigan Medical School, Ann Arbor, MI 48109-0618, USA. kkurachi@umich.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426997" target="_blank"〉PubMed〈/a〉
    Keywords: *3' Untranslated Regions ; Aging/blood/*genetics ; Animals ; Consensus Sequence ; DNA Footprinting ; Dinucleotide Repeats ; Factor IX/*genetics/metabolism ; Female ; *Gene Expression Regulation ; Genetic Vectors ; Humans ; Male ; Mice ; Mice, Transgenic ; RNA, Messenger/genetics/metabolism ; *Regulatory Sequences, Nucleic Acid ; Transcription Factors/genetics/metabolism ; Transcription, Genetic ; Tumor Cells, Cultured
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  • 20
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    Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Apoptosis is implicated in the generation and resolution of inflammation in response to bacterial pathogens. All bacterial pathogens produce lipoproteins (BLPs), which trigger the innate immune response. BLPs were found to induce apoptosis in THP-1 monocytic cells through human Toll-like receptor-2 (hTLR2). BLPs also initiated apoptosis in an epithelial cell line transfected with hTLR2. In addition, BLPs stimulated nuclear factor-kappaB, a transcriptional activator of multiple host defense genes, and activated the respiratory burst through hTLR2. Thus, hTLR2 is a molecular link between microbial products, apoptosis, and host defense mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aliprantis, A O -- Yang, R B -- Mark, M R -- Suggett, S -- Devaux, B -- Radolf, J D -- Klimpel, G R -- Godowski, P -- Zychlinsky, A -- AI 37720-04/AI/NIAID NIH HHS/ -- AI-38894/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):736-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute and Department of Microbiology, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426996" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Antigens, CD14/analysis ; *Apoptosis ; Bacterial Proteins/metabolism/*pharmacology ; Cell Line/metabolism ; Cycloheximide/pharmacology ; Cytotoxicity, Immunologic ; *Drosophila Proteins ; Genes, Reporter ; Humans ; Lipopolysaccharides/immunology ; Lipoproteins/metabolism/*pharmacology ; Membrane Glycoproteins/immunology/*metabolism ; Monocytes/*cytology/immunology/metabolism ; NF-kappa B/metabolism ; Protein Synthesis Inhibitors/pharmacology ; Reactive Oxygen Species/metabolism ; Receptors, Cell Surface/immunology/*metabolism ; Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; Toll-Like Receptor 2 ; Toll-Like Receptors ; Transfection ; Tumor Cells, Cultured
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  • 21
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    Fusion-competent vaccines: broad neutralization of primary isolates of HIV (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-15
    Description: Current recombinant human immunodeficiency virus (HIV) gp120 protein vaccine candidates are unable to elicit antibodies capable of neutralizing infectivity of primary isolates from patients. Here, "fusion-competent" HIV vaccine immunogens were generated that capture the transient envelope-CD4-coreceptor structures that arise during HIV binding and fusion. In a transgenic mouse immunization model, these formaldehyde-fixed whole-cell vaccines elicited antibodies capable of neutralizing infectivity of 23 of 24 primary HIV isolates from diverse geographic locations and genetic clades A to E. Development of these fusion-dependent immunogens may lead to a broadly effective HIV vaccine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LaCasse, R A -- Follis, K E -- Trahey, M -- Scarborough, J D -- Littman, D R -- Nunberg, J H -- AI33856/AI/NIAID NIH HHS/ -- AI41165/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):357-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Montana Biotechnology Center and Division of Biological Sciences, University of Montana, Missoula, MT 59812, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9888845" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/*immunology ; Animals ; Antigens, CD4/metabolism ; Cell Fusion ; Coculture Techniques ; Epitopes/immunology ; Gene Products, env/chemistry/*immunology/metabolism ; Giant Cells ; HIV Antibodies/biosynthesis/*immunology ; HIV Antigens/chemistry/*immunology ; HIV Envelope Protein gp120/chemistry/immunology/metabolism ; HIV Envelope Protein gp41/chemistry/immunology/metabolism ; HIV Infections/virology ; HIV-1/*immunology/isolation & purification/physiology ; Humans ; Mice ; Mice, Transgenic ; Neutralization Tests ; Protein Conformation ; Receptors, CCR5/metabolism ; Tumor Cells, Cultured
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  • 22
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    A mammalian H+ channel generated through alternative splicing of the NADPH oxidase homolog NOH-1 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-30
    Description: Voltage-gated proton (H+) channels are found in many human and animal tissues and play an important role in cellular defense against acidic stress. However, a molecular identification of these unique ion conductances has so far not been achieved. A 191-amino acid protein is described that, upon heterologous expression, has properties indistinguishable from those of native H+ channels. This protein is generated through alternative splicing of messenger RNA derived from the gene NOH-1 (NADPH oxidase homolog 1, where NADPH is the reduced form of nicotinamide adenine dinucleotide phosphate).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Banfi, B -- Maturana, A -- Jaconi, S -- Arnaudeau, S -- Laforge, T -- Sinha, B -- Ligeti, E -- Demaurex, N -- Krause, K H -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):138-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biology of Aging Laboratory, Department of Geriatrics, Geneva University Hospitals, Geneva Medical School, CH-1211 Geneva 4, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10615049" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Amino Acid Sequence ; Cell Line ; Cytosol/metabolism ; Electric Conductivity ; Electron Transport ; Expressed Sequence Tags ; Humans ; Hydrogen/*metabolism ; Hydrogen-Ion Concentration ; Ion Channel Gating ; Ion Channels/chemistry/*genetics/metabolism ; Membrane Glycoproteins/chemistry/*genetics ; Molecular Sequence Data ; NADPH Oxidase/chemistry/*genetics ; Patch-Clamp Techniques ; Protons ; Transfection ; Tumor Cells, Cultured ; Zinc/pharmacology
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  • 23
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    An adhesin of the yeast pathogen Candida glabrata mediating adherence to human epithelial cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-27
    Description: Candida glabrata is an important fungal pathogen of humans that is responsible for about 15 percent of mucosal and systemic candidiasis. Candida glabrata adhered avidly to human epithelial cells in culture. By means of a genetic approach and a strategy allowing parallel screening of mutants, it was possible to clone a lectin from a Candida species. Deletion of this adhesin reduced adherence of C. glabrata to human epithelial cells by 95 percent. The adhesin, encoded by the EPA1 gene, is likely a glucan-cross-linked cell-wall protein and binds to host-cell carbohydrate, specifically recognizing asialo-lactosyl-containing carbohydrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cormack, B P -- Ghori, N -- Falkow, S -- New York, N.Y. -- Science. 1999 Jul 23;285(5427):578-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Stanford University School of Medicine, Fairchild D039, 299 Campus Drive, Stanford, CA 94305-5124, USA. bcormack@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10417386" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/metabolism ; Candida/*genetics/*pathogenicity/physiology ; Candidiasis, Vulvovaginal/microbiology ; Carbohydrates/pharmacology ; Cell Adhesion ; Cloning, Molecular ; Epithelial Cells/*microbiology ; Female ; *Fungal Proteins ; Genes, Fungal ; Humans ; Lectins/chemistry/*genetics/metabolism ; Ligands ; Mice ; Mice, Inbred DBA ; Molecular Sequence Data ; Mutagenesis, Insertional ; Mutation ; Plasmids ; Polymerase Chain Reaction ; Transformation, Genetic ; Tumor Cells, Cultured ; Virulence/genetics
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  • 24
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    Activation of NK cells and T cells by NKG2D, a receptor for stress-inducible MICA (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Stress-inducible MICA, a distant homolog of major histocompatibility complex (MHC) class I, functions as an antigen for gammadelta T cells and is frequently expressed in epithelial tumors. A receptor for MICA was detected on most gammadelta T cells, CD8+ alphabeta T cells, and natural killer (NK) cells and was identified as NKG2D. Effector cells from all these subsets could be stimulated by ligation of NKG2D. Engagement of NKG2D activated cytolytic responses of gammadelta T cells and NK cells against transfectants and epithelial tumor cells expressing MICA. These results define an activating immunoreceptor-MHC ligand interaction that may promote antitumor NK and T cell responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bauer, S -- Groh, V -- Wu, J -- Steinle, A -- Phillips, J H -- Lanier, L L -- Spies, T -- P01 CA18221/CA/NCI NIH HHS/ -- R01 AI30581/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):727-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center, Clinical Research Division, 1100 Fairview Avenue North, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426993" target="_blank"〉PubMed〈/a〉
    Keywords: Cytotoxicity, Immunologic ; Histocompatibility Antigens Class I/*immunology/metabolism ; Humans ; Jurkat Cells ; Killer Cells, Natural/*immunology ; Ligands ; *Lymphocyte Activation ; Lymphocyte Subsets/immunology ; Membrane Proteins/metabolism ; NK Cell Lectin-Like Receptor Subfamily K ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; Receptors, Immunologic/chemistry/genetics/*immunology/metabolism ; Receptors, Natural Killer Cell ; Signal Transduction ; T-Lymphocytes/*immunology ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Negative feedback regulation of TGF-beta signaling by the SnoN oncoprotein (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: Smad proteins mediate transforming growth factor-beta (TGF-beta) signaling to regulate cell growth and differentiation. The SnoN oncoprotein was found to interact with Smad2 and Smad4 and to repress their abilities to activate transcription through recruitment of the transcriptional corepressor N-CoR. Immediately after TGF-beta stimulation, SnoN is rapidly degraded by the nuclear accumulation of Smad3, allowing the activation of TGF-beta target genes. By 2 hours, TGF-beta induces a marked increase in SnoN expression, resulting in termination of Smad-mediated transactivation. Thus, SnoN maintains the repressed state of TGF-beta-responsive genes in the absence of ligand and participates in negative feedback regulation of TGF-beta signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stroschein, S L -- Wang, W -- Zhou, S -- Zhou, Q -- Luo, K -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):771-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Life Sciences Division, Lawrence Berkeley National Laboratory, and Department of Molecular and Cell Biology, University of California, Berkeley, 229 Stanley Hall, Mail Code 3206, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531062" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division ; Cell Line ; Cell Nucleus/metabolism ; DNA/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Feedback ; *Gene Expression Regulation ; Humans ; Intracellular Signaling Peptides and Proteins ; Nuclear Proteins/metabolism ; Nuclear Receptor Co-Repressor 1 ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/genetics/*metabolism ; Repressor Proteins/metabolism ; *Signal Transduction ; Smad2 Protein ; Smad3 Protein ; Smad4 Protein ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics/*metabolism ; Transcriptional Activation ; Transfection ; Transforming Growth Factor beta/*metabolism ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    New type of blood vessel found in tumors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1475.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10498529" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/therapeutic use ; Endothelium, Vascular/pathology ; Gene Expression Regulation, Neoplastic ; Humans ; Melanoma/*blood supply/drug therapy/genetics/pathology ; *Neovascularization, Pathologic/drug therapy ; Tumor Cells, Cultured ; Uveal Neoplasms/*blood supply/drug therapy/genetics/pathology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 27
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    Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: The generation of cell-mediated immunity against many infectious pathogens involves the production of interleukin-12 (IL-12), a key signal of the innate immune system. Yet, for many pathogens, the molecules that induce IL-12 production by macrophages and the mechanisms by which they do so remain undefined. Here it is shown that microbial lipoproteins are potent stimulators of IL-12 production by human macrophages, and that induction is mediated by Toll-like receptors (TLRs). Several lipoproteins stimulated TLR-dependent transcription of inducible nitric oxide synthase and the production of nitric oxide, a powerful microbicidal pathway. Activation of TLRs by microbial lipoproteins may initiate innate defense mechanisms against infectious pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brightbill, H D -- Libraty, D H -- Krutzik, S R -- Yang, R B -- Belisle, J T -- Bleharski, J R -- Maitland, M -- Norgard, M V -- Plevy, S E -- Smale, S T -- Brennan, P J -- Bloom, B R -- Godowski, P J -- Modlin, R L -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):732-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Howard Hughes Medical Institute, University of California Los Angeles School of Medicine, Los Anges, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/chemistry/*immunology/metabolism ; Cell Line ; *Drosophila Proteins ; Gene Expression Regulation ; Humans ; Interleukin-12/*biosynthesis/genetics ; Lipopolysaccharides/immunology ; Lipoproteins/chemistry/*immunology/metabolism ; Macrophages/*immunology/metabolism ; Membrane Glycoproteins/*metabolism ; Mice ; Monocytes/*immunology/metabolism ; Mycobacterium tuberculosis/*immunology ; NF-kappa B/biosynthesis ; Nitric Oxide Synthase/genetics ; Nitric Oxide Synthase Type II ; Promoter Regions, Genetic ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; Toll-Like Receptors ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 28
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    Phosphorylation and regulation of Raf by Akt (protein kinase B) (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-27
    Description: Activation of the protein kinase Raf can lead to opposing cellular responses such as proliferation, growth arrest, apoptosis, or differentiation. Akt (protein kinase B), a member of a different signaling pathway that also regulates these responses, interacted with Raf and phosphorylated this protein at a highly conserved serine residue in its regulatory domain in vivo. This phosphorylation of Raf by Akt inhibited activation of the Raf-MEK-ERK signaling pathway and shifted the cellular response in a human breast cancer cell line from cell cycle arrest to proliferation. These observations provide a molecular basis for cross talk between two signaling pathways at the level of Raf and Akt.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zimmermann, S -- Moelling, K -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1741-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Medical Virology, University of Zurich, Gloriastrasse 30/32, CH-8028 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576742" target="_blank"〉PubMed〈/a〉
    Keywords: *Cell Division ; Cell Line ; Chromones/pharmacology ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/metabolism ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Epidermal Growth Factor/pharmacology ; Flavonoids/pharmacology ; Humans ; *MAP Kinase Signaling System ; Morpholines/pharmacology ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors/metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-raf/antagonists & inhibitors/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Somatomedins/pharmacology ; Tetradecanoylphorbol Acetate/pharmacology ; Tumor Cells, Cultured ; ras Proteins/metabolism
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  • 29
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    Synergy between tumor suppressor APC and the beta-catenin-Tcf4 target Tcf1 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: Mutations in APC or beta-catenin inappropriately activate the transcription factor Tcf4, thereby transforming intestinal epithelial cells. Here it is shown that one of the target genes of Tcf4 in epithelial cells is Tcf1. The most abundant Tcf1 isoforms lack a beta-catenin interaction domain. Tcf1(-/-) mice develop adenomas in the gut and mammary glands. Introduction of a mutant APC allele into these mice substantially increases the number of these adenomas. Tcf1 may act as a feedback repressor of beta-catenin-Tcf4 target genes and thus may cooperate with APC to suppress malignant transformation of epithelial cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roose, J -- Huls, G -- van Beest, M -- Moerer, P -- van der Horn, K -- Goldschmeding, R -- Logtenberg, T -- Clevers, H -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1923-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Center for Biomedical Genetics, Department of Pathology, University Medical Center Utrecht, Post Office Box 85500, 3508 GA Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489374" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/genetics/metabolism/pathology ; Adenomatous Polyposis Coli Protein ; Animals ; Cytoskeletal Proteins/*metabolism ; DNA-Binding Proteins/*genetics/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Hepatocyte Nuclear Factor 1-alpha ; Humans ; Intestinal Neoplasms/genetics/metabolism/pathology ; Lymphoid Enhancer-Binding Factor 1 ; Male ; Mammary Neoplasms, Experimental/genetics/metabolism/pathology ; Mice ; Neoplasm Proteins/metabolism ; Promoter Regions, Genetic ; T Cell Transcription Factor 1 ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/*genetics/*metabolism ; Transfection ; Tumor Cells, Cultured ; beta Catenin
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  • 30
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    p53- and ATM-dependent apoptosis induced by telomeres lacking TRF2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-26
    Description: Although broken chromosomes can induce apoptosis, natural chromosome ends (telomeres) do not trigger this response. It is shown that this suppression of apoptosis involves the telomeric-repeat binding factor 2 (TRF2). Inhibition of TRF2 resulted in apoptosis in a subset of mammalian cell types. The response was mediated by p53 and the ATM (ataxia telangiectasia mutated) kinase, consistent with activation of a DNA damage checkpoint. Apoptosis was not due to rupture of dicentric chromosomes formed by end-to-end fusion, indicating that telomeres lacking TRF2 directly signal apoptosis, possibly because they resemble damaged DNA. Thus, in some cells, telomere shortening may signal cell death rather than senescence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karlseder, J -- Broccoli, D -- Dai, Y -- Hardy, S -- de Lange, T -- GM49046/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 26;283(5406):1321-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, The Rockefeller University, New York, NY 10021, USA. Cell Genesys, Foster City, CA 94405, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10037601" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics/physiology ; Animals ; *Apoptosis ; Ataxia Telangiectasia/pathology ; Ataxia Telangiectasia Mutated Proteins ; B-Lymphocytes/cytology ; Cell Cycle Proteins ; Cell Line ; Cells, Cultured ; Cloning, Molecular ; DNA Damage ; DNA-Binding Proteins/chemistry/genetics/*physiology ; Genetic Vectors ; Humans ; In Situ Nick-End Labeling ; Mice ; Mitosis ; Phosphorylation ; *Protein-Serine-Threonine Kinases ; Proteins/metabolism ; T-Lymphocytes/cytology ; Telomere/*physiology ; Telomeric Repeat Binding Protein 2 ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/*metabolism ; Tumor Suppressor Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The conditional mutator phenotype in human tumor cells: correction (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meuth, M -- Richards, B -- Schneider, B -- New York, N.Y. -- Science. 1999 Jan 29;283(5402):641.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9988656" target="_blank"〉PubMed〈/a〉
    Keywords: *Blood ; Cell Culture Techniques ; *Cell Division ; Culture Media ; Humans ; *Mutation ; Neoplasms/*genetics/pathology ; Phenotype ; Tumor Cells, Cultured
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  • 32
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    Mouse tumor model for neurofibromatosis type 1 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-11
    Description: Neurofibromatosis type 1 (NF1) is an autosomal dominant disorder characterized by increased incidence of benign and malignant tumors of neural crest origin. Mutations that activate the protooncogene ras, such as loss of Nf1, cooperate with inactivating mutations at the p53 tumor suppressor gene during malignant transformation. One hundred percent of mice harboring null Nf1 and p53 alleles in cis synergize to develop soft tissue sarcomas between 3 and 7 months of age. These sarcomas exhibit loss of heterozygosity at both gene loci and express phenotypic traits characteristic of neural crest derivatives and human NF1 malignancies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079436/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079436/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, K S -- Klesse, L J -- Velasco-Miguel, S -- Meyers, K -- Rushing, E J -- Parada, L F -- NS34296/NS/NINDS NIH HHS/ -- R01 NS034296/NS/NINDS NIH HHS/ -- R01 NS034296-04/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 10;286(5447):2176-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Developmental Biology and Department of Pathology, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd., Dallas, TX 75235-9133, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10591653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers, Tumor ; Cell Differentiation ; Cell Transformation, Neoplastic ; Crosses, Genetic ; *Disease Models, Animal ; Female ; *Genes, Neurofibromatosis 1 ; *Genes, p53 ; Heterozygote ; Humans ; Loss of Heterozygosity ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Neural Crest/metabolism/pathology ; Neurofibromatosis 1/*genetics/*pathology ; Sarcoma/genetics/*pathology ; Schwann Cells/metabolism/pathology ; Tumor Cells, Cultured
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    Looking for a few good mutants (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldman, W E -- New York, N.Y. -- Science. 1999 Jul 23;285(5427):539, 541.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University, St. Louis, MO 63110, USA. goldman@borcim.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10447486" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Candida/*genetics/*pathogenicity/physiology ; Cell Adhesion ; DNA Transposable Elements ; Epithelial Cells/*microbiology ; *Fungal Proteins ; Genes, Fungal ; Humans ; Lectins/*genetics/metabolism ; Mice ; *Mutagenesis, Insertional ; Mutation ; Polymerase Chain Reaction ; Tumor Cells, Cultured ; Virulence/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 34
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    Use of chemokine receptors by poxviruses (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-03
    Description: Chemokine receptors serve as portals of entry for certain intracellular pathogens, most notably human immunodeficiency virus (HIV). Myxoma virus is a member of the poxvirus family that induces a lethal systemic disease in rabbits, but no poxvirus receptor has ever been defined. Rodent fibroblasts (3T3) that cannot be infected with myxoma virus could be made fully permissive for myxoma virus infection by expression of any one of several human chemokine receptors, including CCR1, CCR5, and CXCR4. Conversely, infection of 3T3-CCR5 cells can be inhibited by RANTES, anti-CCR5 polyclonal antibody, or herbimycin A but not by monoclonal antibodies that block HIV-1 infection or by pertussis toxin. These findings suggest that poxviruses, like HIV, are able to use chemokine receptors to infect specific cell subtypes, notably migratory leukocytes, but that their mechanisms of receptor interactions are distinct.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lalani, A S -- Masters, J -- Zeng, W -- Barrett, J -- Pannu, R -- Everett, H -- Arendt, C W -- McFadden, G -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1968-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The John P. Robarts Research Institute and Department of Immunology, The University of Western Ontario, London, Ontario N6G 2V4, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583963" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Antibodies/immunology ; Benzoquinones ; Cell Line ; Cercopithecus aethiops ; Chemokine CCL5/pharmacology ; Gene Expression ; Humans ; Lactams, Macrocyclic ; Mice ; Myxoma virus/genetics/*metabolism ; Pertussis Toxin ; Quinones/pharmacology ; Receptors, CCR1 ; Receptors, CCR5/immunology/metabolism ; Receptors, CXCR4/metabolism ; Receptors, Chemokine/*metabolism ; Receptors, Virus/*metabolism ; Rifabutin/analogs & derivatives ; Signal Transduction ; Tumor Cells, Cultured ; Virulence Factors, Bordetella/pharmacology ; beta-Galactosidase/biosynthesis
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  • 35
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    Small molecule inhibitor of mitotic spindle bipolarity identified in a phenotype-based screen (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-05
    Description: Small molecules that perturb specific protein functions are valuable tools for dissecting complex processes in mammalian cells. A combination of two phenotype-based screens, one based on a specific posttranslational modification, the other visualizing microtubules and chromatin, was used to identify compounds that affect mitosis. One compound, here named monastrol, arrested mammalian cells in mitosis with monopolar spindles. In vitro, monastrol specifically inhibited the motility of the mitotic kinesin Eg5, a motor protein required for spindle bipolarity. All previously known small molecules that specifically affect the mitotic machinery target tubulin. Monastrol will therefore be a particularly useful tool for studying mitotic mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mayer, T U -- Kapoor, T M -- Haggarty, S J -- King, R W -- Schreiber, S L -- Mitchison, T J -- CA78048/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 29;286(5441):971-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, and Institute of Chemistry and Cell Biology, Harvard Medical School, Boston, MA 02115, USA. Thomas_Mayer@hms.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10542155" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/drug effects ; Animals ; Cattle ; Cell Line ; Cytoskeleton/drug effects ; Golgi Apparatus/drug effects ; Kinesin/*drug effects ; Microtubules/drug effects ; Mitosis/*drug effects ; Molecular Motor Proteins/drug effects ; Phenotype ; Phosphoproteins/metabolism ; Protein Processing, Post-Translational ; Pyrimidines/*pharmacology ; RNA-Binding Proteins/metabolism ; Spindle Apparatus/*drug effects ; Thiones/*pharmacology ; Tumor Cells, Cultured ; Xenopus ; *Xenopus Proteins
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    Identification of a conserved receptor-binding site on the fiber proteins of CAR-recognizing adenoviridae (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: The human adenovirus serotype 5 (Ad5) is used widely for applications in human gene therapy. Cellular attachment of Ad5 is mediated by binding of the carboxyl-terminal knob of its fiber coat protein to the Coxsackie adenovirus receptor (CAR) protein. However, Ad5 binding to CAR hampers the development of adenovirus vectors capable of specifically targeting (diseased) tissues or organs. Through sequence analysis and mutagenesis, a conserved receptor-binding region was identified on the side of three divergent CAR-binding knobs. The feasibility of simultaneous CAR ablation and redirection of an adenovirus to a new receptor is demonstrated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roelvink, P W -- Mi Lee, G -- Einfeld, D A -- Kovesdi, I -- Wickham, T J -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1568-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research and Development, GenVec Inc., 65 West Watkins Mill Road, Gaithersburg, MD 20879, USA. genecloner@genvec.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567265" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviruses, Human/*chemistry/metabolism ; Amino Acid Sequence ; Binding Sites ; Capsid/*chemistry/genetics/*metabolism ; *Capsid Proteins ; Cell Line ; Conserved Sequence ; Coxsackie and Adenovirus Receptor-Like Membrane Protein ; Genetic Vectors ; Humans ; Models, Molecular ; Mutagenesis, Site-Directed ; Point Mutation ; Protein Conformation ; Protein Structure, Secondary ; Receptors, Virus/*metabolism ; Sequence Deletion ; Transfection ; Tumor Cells, Cultured
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    Conditional mutator phenotypes in hMSH2-deficient tumor cell lines (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-05
    Description: Two human tumor cell lines that are deficient in the mismatch repair protein hMSH2 show little or no increase in mutation rate relative to that of a mismatch repair-proficient cell line when the cells are maintained in culture conditions allowing rapid growth. However, mutations accumulate at a high rate in these cells when they are maintained at high density. Thus the mutator phenotype of some mismatch repair-deficient cell lines is conditional and strongly depends on growth conditions. These observations have implications for tumor development because they suggest that mutations may accumulate in tumor cells when growth is limited.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Richards, B -- Zhang, H -- Phear, G -- Meuth, M -- R01-CA-62244/CA/NCI NIH HHS/ -- T32-CA-09602/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 5;277(5331):1523-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncological Sciences, Eccles Institute of Human Genetics, University of Utah, Salt Lake City, UT, 84112, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9278518" target="_blank"〉PubMed〈/a〉
    Keywords: *Cell Count ; *Cell Division ; *DNA Repair ; DNA Replication ; *DNA-Binding Proteins ; Drug Resistance, Neoplasm ; Female ; Frameshift Mutation ; Humans ; Hypoxanthine Phosphoribosyltransferase/genetics ; Microsatellite Repeats ; MutS Homolog 2 Protein ; *Mutation ; Neoplasms/*genetics/pathology ; Ouabain/pharmacology ; Ovarian Neoplasms/genetics/pathology ; Phenotype ; Proto-Oncogene Proteins/genetics/*physiology ; Tumor Cells, Cultured ; Uterine Neoplasms/genetics/pathology
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    Trafficking of matrix collagens through bone-resorbing osteoclasts (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-11
    Description: An intracellular pathway for proteins liberated from mineralized matrix during resorption was identified in osteoclasts. Analysis by confocal microscopy of sites of active bone resorption showed that released matrix proteins, including degraded type I collagen, were endocytosed along the ruffled border within the resorption compartment and transcytosed through the osteoclast to the basolateral membrane. Intracellular trafficking of degraded collagen, as typified by the resorbing osteoclast, may provide the cell with a regulatory mechanism for the control of tissue degradation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nesbitt, S A -- Horton, M A -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1997 Apr 11;276(5310):266-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bone and Mineral Centre, Department of Medicine, University College London Medical School, University College London, London WIN 8AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9092478" target="_blank"〉PubMed〈/a〉
    Keywords: Bone Matrix/*metabolism ; *Bone Resorption ; Cell Membrane/metabolism/ultrastructure ; Collagen/*metabolism ; Dentin/metabolism ; *Endocytosis ; Humans ; Microscopy, Confocal ; Osteoclasts/*metabolism/ultrastructure ; Tumor Cells, Cultured
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    Caspase-3-generated fragment of gelsolin: effector of morphological change in apoptosis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-10
    Description: The caspase-3 (CPP32, apopain, YAMA) family of cysteinyl proteases has been implicated as key mediators of apoptosis in mammalian cells. Gelsolin was identified as a substrate for caspase-3 by screening the translation products of small complementary DNA pools for sensitivity to cleavage by caspase-3. Gelsolin was cleaved in vivo in a caspase-dependent manner in cells stimulated by Fas. Caspase-cleaved gelsolin severed actin filaments in vitro in a Ca2+-independent manner. Expression of the gelsolin cleavage product in multiple cell types caused the cells to round up, detach from the plate, and undergo nuclear fragmentation. Neutrophils isolated from mice lacking gelsolin had delayed onset of both blebbing and DNA fragmentation, following apoptosis induction, compared with wild-type neutrophils. Thus, cleaved gelsolin may be one physiological effector of morphologic change during apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kothakota, S -- Azuma, T -- Reinhard, C -- Klippel, A -- Tang, J -- Chu, K -- McGarry, T J -- Kirschner, M W -- Koths, K -- Kwiatkowski, D J -- Williams, L T -- P01 HL48743/HL/NHLBI NIH HHS/ -- R01 HL54188/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):294-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chiron Corporation, Emeryville, CA 94608, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323209" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; Antigens, CD95/physiology ; *Apoptosis ; Caspase 3 ; *Caspases ; Cell Line ; *Cell Size ; Cycloheximide/pharmacology ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Cytoskeleton/metabolism ; DNA Fragmentation ; Gelsolin/*metabolism ; Humans ; Mice ; Neutrophils/cytology/metabolism ; Recombinant Proteins/metabolism ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/pharmacology
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    Constitutive transcriptional activation by a beta-catenin-Tcf complex in APC-/- colon carcinoma (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-21
    Description: The adenomatous polyposis coli (APC) tumor suppressor protein binds to beta-catenin, a protein recently shown to interact with Tcf and Lef transcription factors. The gene encoding hTcf-4, a Tcf family member that is expressed in colonic epithelium, was cloned and characterized. hTcf-4 transactivates transcription only when associated with beta-catenin. Nuclei of APC-/- colon carcinoma cells were found to contain a stable beta-catenin-hTcf-4 complex that was constitutively active, as measured by transcription of a Tcf reporter gene. Reintroduction of APC removed beta-catenin from hTcf-4 and abrogated the transcriptional transactivation. Constitutive transcription of Tcf target genes, caused by loss of APC function, may be a crucial event in the early transformation of colonic epithelium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korinek, V -- Barker, N -- Morin, P J -- van Wichen, D -- de Weger, R -- Kinzler, K W -- Vogelstein, B -- Clevers, H -- CA57345/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1784-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University Hospital, Post Office Box 85500, 3508 GA Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9065401" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Amino Acid Sequence ; Animals ; Cell Line ; Cell Transformation, Neoplastic ; Cloning, Molecular ; Colon/metabolism ; Colonic Neoplasms/*genetics/metabolism ; Cytoskeletal Proteins/genetics/*metabolism ; Gene Expression Regulation, Neoplastic ; *Genes, APC ; Genes, Reporter ; Humans ; Intestinal Mucosa/metabolism ; Mice ; Molecular Sequence Data ; Signal Transduction ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/chemistry/genetics/*metabolism ; *Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; beta Catenin
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    Alternative cleavage of Alzheimer-associated presenilins during apoptosis by a caspase-3 family protease (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-18
    Description: Most cases of early-onset familial Alzheimer's disease (FAD) are caused by mutations in the genes encoding the presenilin 1 (PS1) and PS2 proteins, both of which undergo regulated endoproteolytic processing. During apoptosis, PS1 and PS2 were shown to be cleaved at sites distal to their normal cleavage sites by a caspase-3 family protease. In cells expressing PS2 containing the asparagine-141 FAD mutant, the ratio of alternative to normal PS2 cleavage fragments was increased relative to wild-type PS2-expressing cells, suggesting a potential role for apoptosis-associated cleavage of presenilins in the pathogenesis of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, T W -- Pettingell, W H -- Jung, Y K -- Kovacs, D M -- Tanzi, R E -- New York, N.Y. -- Science. 1997 Jul 18;277(5324):373-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetics and Aging Unit, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9219695" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics/metabolism/pathology ; Amino Acid Chloromethyl Ketones/pharmacology ; Amino Acid Substitution ; Animals ; *Apoptosis ; Caspase 3 ; *Caspases ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Enzyme Activation ; Etoposide/pharmacology ; Membrane Proteins/chemistry/genetics/*metabolism ; Mutation ; Oligopeptides/pharmacology ; Phosphorylation ; Presenilin-1 ; Presenilin-2 ; Rats ; Staurosporine/pharmacology ; Tumor Cells, Cultured
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    Control of TRAIL-induced apoptosis by a family of signaling and decoy receptors (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-08
    Description: TRAIL (also called Apo2L) belongs to the tumor necrosis factor family, activates rapid apoptosis in tumor cells, and binds to the death-signaling receptor DR4. Two additional TRAIL receptors were identified. The receptor designated death receptor 5 (DR5) contained a cytoplasmic death domain and induced apoptosis much like DR4. The receptor designated decoy receptor 1 (DcR1) displayed properties of a glycophospholipid-anchored cell surface protein. DcR1 acted as a decoy receptor that inhibited TRAIL signaling. Thus, a cell surface mechanism exists for the regulation of cellular responsiveness to pro-apoptotic stimuli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheridan, J P -- Marsters, S A -- Pitti, R M -- Gurney, A -- Skubatch, M -- Baldwin, D -- Ramakrishnan, L -- Gray, C L -- Baker, K -- Wood, W I -- Goddard, A D -- Godowski, P -- Ashkenazi, A -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):818-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, Genentech, South San Francisco, CA 94080-4918, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9242611" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Apoptosis ; Apoptosis Regulatory Proteins ; Cell Membrane/metabolism ; Cells, Cultured ; GPI-Linked Proteins ; Glycosylphosphatidylinositols/metabolism ; HeLa Cells ; Humans ; Ligands ; Membrane Glycoproteins/*metabolism ; Molecular Sequence Data ; NF-kappa B/metabolism ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Signal Transduction ; TNF-Related Apoptosis-Inducing Ligand ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor Decoy Receptors ; Tumor Necrosis Factor-alpha/*metabolism
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    The product of the proto-oncogene c-cbl: a negative regulator of the Syk tyrosine kinase (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-04-18
    Description: Engagement of antigen and immunoglobulin receptors on hematopoietic cells is directly coupled to activation of nonreceptor protein tyrosine kinases (PTKs) that then phosphorylate critical intracellular substrates. In mast cells stimulated through the FcvarepsilonRI receptor, activation of several PTKs including Syk leads to degranulation and release of such mediators of the allergic response as histamine and serotonin. Regulation of Syk function occurred through interaction with the Cbl protein, itself a PTK substrate in this system. Overexpression of Cbl led to inhibition of Syk and suppression of serotonin release from mast cells, demonstrating its ability to inhibit a nonreceptor tyrosine kinase. Complex adaptor proteins such as Cbl can directly regulate the functions of the proteins they bind.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ota, Y -- Samelson, L E -- New York, N.Y. -- Science. 1997 Apr 18;276(5311):418-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-5430, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9103201" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Degranulation ; Enzyme Precursors/antagonists & inhibitors/*metabolism ; Genetic Vectors ; Intracellular Signaling Peptides and Proteins ; Mast Cells/*metabolism ; Mutation ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-cbl ; Rats ; Receptors, IgE/metabolism ; Receptors, IgG/metabolism ; Recombinant Proteins/metabolism ; Serotonin/metabolism ; Signal Transduction ; Tumor Cells, Cultured ; *Ubiquitin-Protein Ligases ; Vaccinia virus
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  • 44
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    Modulation of hepatic gene expression by hepatocyte nuclear factor 1 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-04
    Description: Hepatocyte nuclear factors 1 and 4 (HNF-1 and HNF-4) are liver-enriched transcription factors that function in the regulation of several liver-specific genes. HNF-1 activates genes containing promoters with HNF-1 binding sites. However, this factor negatively regulates its own expression and that of other HNF-4-dependent genes that lack HNF-1 binding sites in their promoter region. This repression is exerted by a direct interaction of HNF-1 with AF2, the main activation domain of HNF-4. The dual functions of gene activation and repression suggest that HNF-1 is a global regulator of the transcriptional network involved in the maintenance of hepatocyte-specific phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ktistaki, E -- Talianidis, I -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):109-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology-Hellas, Post Office Box 1527, 711 10 Heraklion, Crete, Greece.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9204893" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Binding Sites ; COS Cells ; *DNA-Binding Proteins ; *Gene Expression Regulation ; Hepatocyte Nuclear Factor 1 ; Hepatocyte Nuclear Factor 1-alpha ; Hepatocyte Nuclear Factor 1-beta ; Hepatocyte Nuclear Factor 4 ; Humans ; Liver/cytology/*metabolism ; Nuclear Proteins/genetics/metabolism ; Phosphoproteins/genetics/metabolism ; Promoter Regions, Genetic ; RNA, Messenger/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Transcription Factors/*genetics/*metabolism ; Transcriptional Activation ; Tumor Cells, Cultured
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  • 45
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    Identification of a chemokine receptor encoded by human cytomegalovirus as a cofactor for HIV-1 entry (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-06-20
    Description: The human cytomegalovirus encodes a beta-chemokine receptor (US28) that is distantly related to the human chemokine receptors CCR5 and CXCR4, which also serve as cofactors for the entry into cells of human immunodeficiency virus-type 1 (HIV-1). Like CCR5, US28 allowed infection of CD4-positive human cell lines by primary isolates of HIV-1 and HIV-2, as well as fusion of these cell lines with cells expressing the viral envelope proteins. In addition, US28 mediated infection by cell line-adapted HIV-1 for which CXCR4 was an entry cofactor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pleskoff, O -- Treboute, C -- Brelot, A -- Heveker, N -- Seman, M -- Alizon, M -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1874-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Inserm U.332, Institut Cochin de Genetique Moleculaire, 22 rue Mechain, 75014 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9188536" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS-Related Opportunistic Infections/virology ; Amino Acid Sequence ; Cell Fusion ; Chemokines ; Coculture Techniques ; Cytomegalovirus/*genetics/physiology ; Cytomegalovirus Infections/virology ; Giant Cells ; HIV Infections/virology ; HIV-1/*physiology ; HIV-2/*physiology ; HeLa Cells ; Humans ; Membrane Proteins/physiology ; Molecular Sequence Data ; Receptors, CCR2 ; Receptors, CCR5 ; Receptors, CXCR4 ; *Receptors, Chemokine ; Receptors, Cytokine/genetics/*physiology ; Receptors, HIV/genetics/*physiology ; Transfection ; Tumor Cells, Cultured ; Viral Proteins/genetics/*physiology
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    Cystic fibrosis transmembrane conductance regulator and adenosine triphosphate (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abraham, E H -- Okunieff, P -- Scala, S -- Vos, P -- Oosterveld, M J -- Chen, A Y -- Shrivastav, B -- New York, N.Y. -- Science. 1997 Feb 28;275(5304):1324-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9064787" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/metabolism ; Adenosine Triphosphate/*metabolism ; Biological Transport ; Cell Membrane/*metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator/*metabolism ; Humans ; P-Glycoprotein/metabolism ; Tumor Cells, Cultured
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  • 47
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    A mammalian telomerase-associated protein (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-02-14
    Description: The telomerase ribonucleoprotein catalyzes the addition of new telomeres onto chromosome ends. A gene encoding a mammalian telomerase homolog called TP1 (telomerase-associated protein 1) was identified and cloned. TP1 exhibited extensive amino acid similarity to the Tetrahymena telomerase protein p80 and was shown to interact specifically with mammalian telomerase RNA. Antiserum to TP1 immunoprecipitated telomerase activity from cell extracts, suggesting that TP1 is associated with telomerase in vivo. The identification of TP1 suggests that telomerase-associated proteins are conserved from ciliates to humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harrington, L -- McPhail, T -- Mar, V -- Zhou, W -- Oulton, R -- Bass, M B -- Arruda, I -- Robinson, M O -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):973-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Arruda, Ontario Cancer Institute-Amgen Institute, Department of Medical Biophysics, University of Toronto, 620 University Avenue, Toronto, Ontario M5G 2C1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020079" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Carrier Proteins/*chemistry/genetics/immunology/*metabolism ; Cell Line ; Cloning, Molecular ; DNA, Complementary/genetics ; Humans ; Mice ; Molecular Sequence Data ; Precipitin Tests ; RNA/*metabolism ; RNA, Messenger/genetics/metabolism ; Sequence Homology, Amino Acid ; Telomerase/*chemistry/genetics/metabolism ; Tetrahymena/chemistry/genetics ; Transfection ; Tumor Cells, Cultured
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  • 48
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    Requirement for GD3 ganglioside in CD95- and ceramide-induced apoptosis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-12
    Description: Gangliosides participate in development and tissue differentiation. Cross-linking of the apoptosis-inducing CD95 protein (also called Fas or APO-1) in lymphoid and myeloid tumor cells triggered GD3 ganglioside synthesis and transient accumulation. CD95-induced GD3 accumulation depended on integral receptor "death domains" and on activation of a family of cysteine proteases called caspases. Cell-permeating ceramides, which are potent inducers of apoptosis, also triggered GD3 synthesis. GD3 disrupted mitochondrial transmembrane potential (DeltaPsim), and induced apoptosis, in a caspase-independent fashion. Transient overexpression of the GD3 synthase gene directly triggered apoptosis. Pharmacological inhibition of GD3 synthesis and exposure to GD3 synthase antisense oligodeoxynucleotides prevented CD95-induced apoptosis. Thus, GD3 ganglioside mediates the propagation of CD95-generated apoptotic signals in hematopoietic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Maria, R -- Lenti, L -- Malisan, F -- d'Agostino, F -- Tomassini, B -- Zeuner, A -- Rippo, M R -- Testi, R -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1652-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Medicine and Biochemical Sciences, University of Rome "Tor Vergata," 00133 Rome, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9287216" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD95/metabolism/*physiology ; *Apoptosis ; Ceramides/pharmacology/*physiology ; Cysteine Endopeptidases/metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Enzyme Inhibitors/pharmacology ; Gangliosides/biosynthesis/*metabolism/pharmacology ; Golgi Apparatus/metabolism ; Humans ; Membrane Potentials ; Mitochondria/physiology ; Morpholines/pharmacology ; Oligonucleotides, Antisense/pharmacology ; Sialyltransferases/genetics/metabolism ; Signal Transduction ; Transfection ; Tumor Cells, Cultured
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    Somatic frameshift mutations in the BAX gene in colon cancers of the microsatellite mutator phenotype (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-14
    Description: Cancers of the microsatellite mutator phenotype (MMP) show exaggerated genomic instability at simple repeat sequences. More than 50 percent (21 out of 41) of human MMP+ colon adenocarcinomas examined were found to have frameshift mutations in a tract of eight deoxyguanosines [(G)8] within BAX, a gene that promotes apoptosis. These mutations were absent in MMP- tumors and were significantly less frequent in (G)8 repeats from other genes. Frameshift mutations were present in both BAX alleles in some MMP+ colon tumor cell lines and in primary tumors. These results suggest that inactivating BAX mutations are selected for during the progression of colorectal MMP+ tumors and that the wild-type BAX gene plays a suppressor role in a p53-independent pathway for colorectal carcinogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rampino, N -- Yamamoto, H -- Ionov, Y -- Li, Y -- Sawai, H -- Reed, J C -- Perucho, M -- CA38579/CA/NCI NIH HHS/ -- CA63585/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):967-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Burnham Institute, La Jolla Cancer Research Center, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020077" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/*genetics ; Alleles ; Apoptosis ; Base Sequence ; Colonic Neoplasms/*genetics ; *Frameshift Mutation ; Gene Expression ; *Genes, Tumor Suppressor ; Humans ; Microsatellite Repeats/*genetics ; Molecular Sequence Data ; Mutation ; Phenotype ; Polymerase Chain Reaction ; Proto-Oncogene Proteins/*genetics ; *Proto-Oncogene Proteins c-bcl-2 ; Sequence Deletion ; Tumor Cells, Cultured ; bcl-2-Associated X Protein
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    Molecules give new insights into deadliest brain cancers (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1226.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brevican ; Carrier Proteins/genetics/*physiology ; Chloride Channels/*physiology ; Chondroitin Sulfate Proteoglycans ; Glioma/*metabolism/*pathology/therapy ; Humans ; Lectins, C-Type ; Neoplasm Invasiveness ; Nerve Tissue Proteins/genetics/*physiology ; Neuroglia/metabolism ; Rats ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Activation of beta-catenin-Tcf signaling in colon cancer by mutations in beta-catenin or APC (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-21
    Description: Inactivation of the adenomatous polyposis coli (APC) tumor suppressor gene initiates colorectal neoplasia. One of the biochemical activities associated with the APC protein is down-regulation of transcriptional activation mediated by beta-catenin and T cell transcription factor 4 (Tcf-4). The protein products of mutant APC genes present in colorectal tumors were found to be defective in this activity. Furthermore, colorectal tumors with intact APC genes were found to contain activating mutations of beta-catenin that altered functionally significant phosphorylation sites. These results indicate that regulation of beta-catenin is critical to APC's tumor suppressive effect and that this regulation can be circumvented by mutations in either APC or beta-catenin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morin, P J -- Sparks, A B -- Korinek, V -- Barker, N -- Clevers, H -- Vogelstein, B -- Kinzler, K W -- CA57345/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1787-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Johns Hopkins Oncology Center, 424 North Bond Street, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9065402" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Colonic Neoplasms/*genetics/metabolism ; Cytoskeletal Proteins/*genetics/*metabolism ; Gene Expression Regulation, Neoplastic ; *Genes, APC ; Genes, Reporter ; Germ-Line Mutation ; Humans ; Mutation ; Phosphorylation ; Signal Transduction ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/*metabolism ; *Transcription, Genetic ; Transfection ; Tumor Cells, Cultured ; beta Catenin
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    Curing rat glioblastoma: immunotherapy or graft rejection? (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beutler, A S -- Banck, M S -- Aguzzi, A -- New York, N.Y. -- Science. 1997 Apr 4;276(5309):20-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122700" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Glioblastoma/*immunology/*therapy ; *Graft Rejection ; Histocompatibility Antigens/*immunology ; Insulin-Like Growth Factor I/*genetics ; Major Histocompatibility Complex ; Neoplasm Transplantation ; RNA, Antisense/*therapeutic use ; Rats ; Transplantation, Homologous ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Synergy paper questioned at toxicology meeting (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, J -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1879.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122688" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chlordan/metabolism/pharmacology ; Dieldrin/metabolism/pharmacology ; Drug Synergism ; Endosulfan/metabolism/pharmacology ; Estrogens, Non-Steroidal/metabolism/*pharmacology ; Female ; Humans ; Insecticides/metabolism/*pharmacology ; Receptors, Estrogen/*drug effects/metabolism ; Reproducibility of Results ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Angiogenic and HIV-inhibitory functions of KSHV-encoded chemokines (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-10
    Description: Unique among known human herpesviruses, Kaposi's sarcoma-associated herpesvirus (KSHV or HHV-8) encodes chemokine-like proteins (vMIP-I and vMIP-II). vMIP-II was shown to block infection of human immunodeficiency virus-type 1 (HIV-1) on a CD4-positive cell line expressing CCR3 and to a lesser extent on one expressing CCR5, whereas both vMIP-I and vMIP-II partially inhibited HIV infection of peripheral blood mononuclear cells. Like eotaxin, vMIP-II activated and chemoattracted human eosinophils by way of CCR3. vMIP-I and vMIP-II, but not cellular MIP-1alpha or RANTES, were highly angiogenic in the chorioallantoic assay, suggesting a possible pathogenic role in Kaposi's sarcoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boshoff, C -- Endo, Y -- Collins, P D -- Takeuchi, Y -- Reeves, J D -- Schweickart, V L -- Siani, M A -- Sasaki, T -- Williams, T J -- Gray, P W -- Moore, P S -- Chang, Y -- Weiss, R A -- CA 67391/CA/NCI NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):290-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cancer Research, Chester Beatty Laboratories, London SW3 6JB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323208" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/virology ; Chemokines/genetics/metabolism/pharmacology/*physiology ; Chemotaxis, Leukocyte ; Chick Embryo ; Eosinophils/physiology ; HIV-1/*physiology ; Herpesvirus 8, Human/*genetics/physiology ; Humans ; Leukocytes, Mononuclear/virology ; Macrophage Inflammatory Proteins/genetics/metabolism/pharmacology/*physiology ; Neovascularization, Pathologic/*etiology ; Neutrophils/physiology ; Receptors, CCR3 ; *Receptors, Chemokine ; Receptors, Cytokine/agonists/metabolism ; Receptors, HIV/metabolism ; Tumor Cells, Cultured ; *Viral Proteins ; Virus Replication
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    A critical role for tapasin in the assembly and function of multimeric MHC class I-TAP complexes (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-29
    Description: Newly assembled major histocompatibility complex (MHC) class I molecules, together with the endoplasmic reticulum chaperone calreticulin, interact with the transporter associated with antigen processing (TAP) through a molecule called tapasin. The molecular cloning of tapasin revealed it to be a transmembrane glycoprotein encoded by an MHC-linked gene. It is a member of the immunoglobulin superfamily with a probable cytoplasmic endoplasmic reticulum retention signal. Up to four MHC class I-tapasin complexes were found to bind to each TAP molecule. Expression of tapasin in a negative mutant human cell line (220) restored class I-TAP association and normal class I cell surface expression. Tapasin expression also corrected the defective recognition of virus-infected 220 cells by class I-restricted cytotoxic T cells, establishing a critical functional role for tapasin in MHC class I-restricted antigen processing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ortmann, B -- Copeman, J -- Lehner, P J -- Sadasivan, B -- Herberg, J A -- Grandea, A G -- Riddell, S R -- Tampe, R -- Spies, T -- Trowsdale, J -- Cresswell, P -- AI30581/AI/NIAID NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1997 Aug 29;277(5330):1306-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine, 310 Cedar Street, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9271576" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/*metabolism ; Amino Acid Sequence ; Antigen Presentation ; Antiporters/chemistry/genetics/*metabolism ; Calcium-Binding Proteins/metabolism ; Calreticulin ; Cell Line ; Cell Line, Transformed ; Chromosome Mapping ; Chromosomes, Human, Pair 6 ; Cloning, Molecular ; Dimerization ; Endoplasmic Reticulum/metabolism ; Genetic Linkage ; HLA Antigens/*metabolism ; Histocompatibility Antigens Class I/*metabolism ; Humans ; Immunoglobulin G/chemistry ; Immunoglobulins/chemistry/genetics/*metabolism ; Major Histocompatibility Complex/genetics ; Membrane Transport Proteins ; Molecular Sequence Data ; Ribonucleoproteins/metabolism ; Sequence Homology, Amino Acid ; T-Lymphocytes, Cytotoxic ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    An antagonist decoy receptor and a death domain-containing receptor for TRAIL (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-08
    Description: TRAIL, also called Apo2L, is a cytotoxic protein that induces apoptosis of many transformed cell lines but not of normal tissues, even though its death domain-containing receptor, DR4, is expressed on both cell types. An antagonist decoy receptor (designated as TRID for TRAIL receptor without an intracellular domain) that may explain the resistant phenotype of normal tissues was identified. TRID is a distinct gene product with an extracellular TRAIL-binding domain and a transmembrane domain but no intracellular signaling domain. TRID transcripts were detected in many normal human tissues but not in most cancer cell lines examined. Ectopic expression of TRID protected mammalian cells from TRAIL-induced apoptosis, which is consistent with a protective role. Another death domain-containing receptor for TRAIL (designated as death receptor-5), which preferentially engaged a FLICE (caspase-8)-related death protease, was also identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, G -- Ni, J -- Wei, Y F -- Yu, G -- Gentz, R -- Dixit, V M -- ES08111/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):815-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9242610" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Caspase 10 ; Caspase 8 ; Caspase 9 ; *Caspases ; Cell Line, Transformed ; Cysteine Endopeptidases/metabolism ; GPI-Linked Proteins ; HeLa Cells ; Humans ; Ligands ; Membrane Glycoproteins/*metabolism ; Molecular Sequence Data ; Protein Sorting Signals ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Sequence Alignment ; Signal Transduction ; TNF-Related Apoptosis-Inducing Ligand ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor Decoy Receptors ; Tumor Necrosis Factor-alpha/*metabolism
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    The receptor for the cytotoxic ligand TRAIL (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-04
    Description: TRAIL (also known as Apo-2L) is a member of the tumor necrosis factor (TNF) ligand family that rapidly induces apoptosis in a variety of transformed cell lines. The human receptor for TRAIL was found to be an undescribed member of the TNF-receptor family (designated death receptor-4, DR4) that contains a cytoplasmic "death domain" capable of engaging the cell suicide apparatus but not the nuclear factor kappa B pathway in the system studied. Unlike Fas, TNFR-1, and DR3, DR4 could not use FADD to transmit the death signal, suggesting the use of distinct proximal signaling machinery. Thus, the DR4-TRAIL axis defines another receptor-ligand pair involved in regulating cell suicide and tissue homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, G -- O'Rourke, K -- Chinnaiyan, A M -- Gentz, R -- Ebner, R -- Ni, J -- Dixit, V M -- DAMD17-96-1-6085/DA/NIDA NIH HHS/ -- ES08111/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1997 Apr 4;276(5309):111-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9082980" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; *Apoptosis ; Apoptosis Regulatory Proteins ; Carrier Proteins/metabolism ; Cell Line ; Fas-Associated Death Domain Protein ; Humans ; Ligands ; Membrane Glycoproteins/*metabolism ; Molecular Sequence Data ; NF-kappa B/metabolism ; Proteins/metabolism ; RNA, Messenger/genetics/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 1 ; TNF-Related Apoptosis-Inducing Ligand ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Beta-catenin as oncogene: the smoking gun (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peifer, M -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1752-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-3280, USA. peifer@unc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122680" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Animals ; Apoptosis ; Cell Division ; Cell Movement ; Colon/cytology/metabolism ; Colonic Neoplasms/*genetics/metabolism ; Cytoskeletal Proteins/*genetics/*metabolism ; DNA-Binding Proteins/metabolism ; *Drosophila Proteins ; Gene Expression Regulation, Neoplastic ; Genes, APC ; Humans ; Insect Proteins/metabolism ; Intestinal Mucosa/cytology/metabolism ; Lymphoid Enhancer-Binding Factor 1 ; Melanoma/*genetics/metabolism ; Mutation ; *Oncogenes ; *Repressor Proteins ; Signal Transduction ; *Trans-Activators ; Transcription Factors/metabolism ; Tumor Cells, Cultured ; beta Catenin
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    Potential involvement of Fas and its ligand in the pathogenesis of Hashimoto's thyroiditis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-14
    Description: The mechanisms responsible for thyrocyte destruction in Hashimoto's thyroiditis (HT) are poorly understood. Thyrocytes from HT glands, but not from nonautoimmune thyroids, expressed Fas. Interleukin-1beta (IL-1beta), abundantly produced in HT glands, induced Fas expression in normal thyrocytes, and cross-linking of Fas resulted in massive thyrocyte apoptosis. The ligand for Fas (FasL) was shown to be constitutively expressed both in normal and HT thyrocytes and was able to kill Fas-sensitive targets. Exposure to IL-1beta induced thyrocyte apoptosis, which was prevented by antibodies that block Fas, suggesting that IL-1beta-induced Fas expression serves as a limiting factor for thyrocyte destruction. Thus, Fas-FasL interactions among HT thyrocytes may contribute to clinical hypothyroidism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giordano, C -- Stassi, G -- De Maria, R -- Todaro, M -- Richiusa, P -- Papoff, G -- Ruberti, G -- Bagnasco, M -- Testi, R -- Galluzzo, A -- A.066/Telethon/Italy -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):960-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, Endocrinology Section, Institute of Clinica Medica, University of Palermo, Palermo, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020075" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal/immunology ; Antigens, CD95/biosynthesis/immunology/*metabolism ; *Apoptosis ; Cells, Cultured ; Cytokines/pharmacology ; Fas Ligand Protein ; Humans ; Immunoenzyme Techniques ; Interleukin-1/pharmacology ; Membrane Glycoproteins/biosynthesis/*metabolism ; Nucleic Acid Synthesis Inhibitors/pharmacology ; Polymerase Chain Reaction ; Protein Synthesis Inhibitors/pharmacology ; RNA, Messenger/genetics/metabolism ; Recombinant Proteins/pharmacology ; Thyroid Gland/*metabolism/pathology ; Thyroiditis, Autoimmune/*etiology/metabolism/pathology ; Tumor Cells, Cultured
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    Inhibition of phosphatases and increased Ca2+ channel activity by inositol hexakisphosphate (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-23
    Description: Inositol hexakisphosphate (InsP6), the dominant inositol phosphate in insulin-secreting pancreatic beta cells, inhibited the serine-threonine protein phosphatases type 1, type 2A, and type 3 in a concentration-dependent manner. The activity of voltage-gated L-type calcium channels is increased in cells treated with inhibitors of serine-threonine protein phosphatases. Thus, the increased calcium channel activity obtained in the presence of InsP6 might result from the inhibition of phosphatase activity. Glucose elicited a transient increase in InsP6 concentration, which indicates that this inositol polyphosphate may modulate calcium influx over the plasma membrane and serve as a signal in the pancreatic beta cell stimulus-secretion coupling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Larsson, O -- Barker, C J -- Sjoholm, A -- Carlqvist, H -- Michell, R H -- Bertorello, A -- Nilsson, T -- Honkanen, R E -- Mayr, G W -- Zwiller, J -- Berggren, P O -- New York, N.Y. -- Science. 1997 Oct 17;278(5337):471-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rolf Luft Center for Diabetes Research, Department of Molecular Medicine, Karolinska Institute, S-171 76 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9334307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels/drug effects/*metabolism ; Cell Membrane/metabolism ; Cricetinae ; Dose-Response Relationship, Drug ; Glucose/pharmacology ; Inositol/pharmacology ; Inositol Phosphates/pharmacology ; Ion Channel Gating ; Islets of Langerhans/drug effects/*metabolism ; Patch-Clamp Techniques ; Phosphoprotein Phosphatases/*antagonists & inhibitors ; Phytic Acid/*pharmacology ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Differing roles found for estrogen's two receptors (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1997 Sep 5;277(5331):1439.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9304214" target="_blank"〉PubMed〈/a〉
    Keywords: Enhancer Elements, Genetic ; Estrogen Antagonists/metabolism/pharmacology ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Estrogens/metabolism/pharmacology ; Gene Expression Regulation ; Genes, Reporter ; Humans ; Ligands ; Receptors, Estrogen/genetics/*physiology ; Regulatory Sequences, Nucleic Acid ; Transcription Factor AP-1/metabolism ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Phosphorylation of the translational repressor PHAS-I by the mammalian target of rapamycin (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-04
    Description: The immunosuppressant rapamycin interferes with G1-phase progression in lymphoid and other cell types by inhibiting the function of the mammalian target of rapamycin (mTOR). mTOR was determined to be a terminal kinase in a signaling pathway that couples mitogenic stimulation to the phosphorylation of the eukaryotic initiation factor (eIF)-4E-binding protein, PHAS-I. The rapamycin-sensitive protein kinase activity of mTOR was required for phosphorylation of PHAS-I in insulin-stimulated human embryonic kidney cells. mTOR phosphorylated PHAS-I on serine and threonine residues in vitro, and these modifications inhibited the binding of PHAS-I to eIF-4E. These studies define a role for mTOR in translational control and offer further insights into the mechanism whereby rapamycin inhibits G1-phase progression in mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunn, G J -- Hudson, C C -- Sekulic, A -- Williams, J M -- Hosoi, H -- Houghton, P J -- Lawrence, J C Jr -- Abraham, R T -- AR41189/AR/NIAMS NIH HHS/ -- DK28312/DK/NIDDK NIH HHS/ -- DK50628/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):99-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9204908" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Androstadienes/pharmacology ; Animals ; Carrier Proteins/pharmacology ; Cell Line ; DNA-Binding Proteins/pharmacology ; Eukaryotic Initiation Factor-4E ; G1 Phase ; Heat-Shock Proteins/pharmacology ; Humans ; Insulin/pharmacology ; Peptide Initiation Factors/metabolism ; Phosphoproteins/genetics/*metabolism ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/antagonists & inhibitors/*metabolism ; Polyenes/*pharmacology ; *Protein Kinases ; Rats ; Recombinant Proteins/metabolism ; Repressor Proteins/genetics/*metabolism ; Signal Transduction ; Sirolimus ; TOR Serine-Threonine Kinases ; Tacrolimus Binding Proteins ; 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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    New tumor suppressor found--twice (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1876-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122687" target="_blank"〉PubMed〈/a〉
    Keywords: Brain Neoplasms/genetics ; Breast Neoplasms/genetics ; Chromosome Mapping ; *Chromosomes, Human, Pair 10 ; Female ; Gene Deletion ; *Genes, Tumor Suppressor ; Glioma/genetics ; Humans ; Male ; Microfilament Proteins/chemistry/metabolism ; Neoplasms/*genetics ; Patents as Topic ; Prostatic Neoplasms/genetics ; Protein Tyrosine Phosphatases/chemistry/*genetics/metabolism/physiology ; Publishing ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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    Cysteine and glutathione secretion in response to protein disulfide bond formation in the ER (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-12
    Description: Protein folding in the endoplasmic reticulum (ER) often involves the formation of disulfide bonds. The oxidizing conditions required within this organelle were shown to be maintained through the release of small thiols, mainly cysteine and glutathione. Thiol secretion was stimulated when proteins rich in disulfide bonds were translocated into the ER, and secretion was prevented by the inhibition of protein synthesis. Endogenously generated cysteine and glutathione counteracted thiol-mediated retention in the ER and altered the extracellular redox. The secretion of thiols might link disulfide bond formation in the ER to intra- and intercellular redox signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carelli, S -- Ceriotti, A -- Cabibbo, A -- Fassina, G -- Ruvo, M -- Sitia, R -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1681-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DIBIT, Istituto Scientifico San Raffaele, Milano, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9287224" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzopyrans/metabolism ; Brefeldin A ; Cycloheximide/pharmacology ; Cyclopentanes/pharmacology ; Cysteine/*secretion ; Cystine/secretion ; Disulfides/*metabolism ; Endoplasmic Reticulum/*metabolism ; Exocytosis ; Glutathione/analogs & derivatives/*secretion ; Glutathione Disulfide ; Golgi Apparatus/metabolism ; Hemagglutinin Glycoproteins, Influenza Virus/biosynthesis ; Immunoglobulin M/biosynthesis ; Immunoglobulin lambda-Chains/metabolism ; Oocytes ; Oxidation-Reduction ; Protein Synthesis Inhibitors/pharmacology ; Proteins/*metabolism ; Temperature ; Tumor Cells, Cultured ; Xenopus laevis
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    PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-28
    Description: Mapping of homozygous deletions on human chromosome 10q23 has led to the isolation of a candidate tumor suppressor gene, PTEN, that appears to be mutated at considerable frequency in human cancers. In preliminary screens, mutations of PTEN were detected in 31% (13/42) of glioblastoma cell lines and xenografts, 100% (4/4) of prostate cancer cell lines, 6% (4/65) of breast cancer cell lines and xenografts, and 17% (3/18) of primary glioblastomas. The predicted PTEN product has a protein tyrosine phosphatase domain and extensive homology to tensin, a protein that interacts with actin filaments at focal adhesions. These homologies suggest that PTEN may suppress tumor cell growth by antagonizing protein tyrosine kinases and may regulate tumor cell invasion and metastasis through interactions at focal adhesions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, J -- Yen, C -- Liaw, D -- Podsypanina, K -- Bose, S -- Wang, S I -- Puc, J -- Miliaresis, C -- Rodgers, L -- McCombie, R -- Bigner, S H -- Giovanella, B C -- Ittmann, M -- Tycko, B -- Hibshoosh, H -- Wigler, M H -- Parsons, R -- 5R35 CA39829/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1943-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, College of Physicians & Surgeons, Columbia University, 630 West 168 Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072974" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Brain Neoplasms/genetics ; Breast Neoplasms/genetics ; Chromosome Mapping ; *Chromosomes, Human, Pair 10 ; Female ; Frameshift Mutation ; *Genes, Tumor Suppressor ; Glioblastoma/genetics ; Humans ; Male ; Microfilament Proteins/chemistry ; Molecular Sequence Data ; *Mutation ; Neoplasm Transplantation ; Neoplasms/*genetics ; PTEN Phosphohydrolase ; *Phosphoric Monoester Hydrolases ; Phosphotyrosine/metabolism ; Prostatic Neoplasms/genetics ; Protein Tyrosine Phosphatases/chemistry/*genetics/physiology ; Protein-Tyrosine Kinases/antagonists & inhibitors ; Sequence Deletion ; Sequence Homology, Amino Acid ; Transplantation, Heterologous ; Tumor Cells, Cultured ; *Tumor Suppressor Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Human DNA-(cytosine-5) methyltransferase-PCNA complex as a target for p21WAF1 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-26
    Description: DNA-(cytosine-5) methyltransferase (MCMT) methylates newly replicated mammalian DNA, but the factors regulating this activity are unknown. Here, MCMT is shown to bind proliferating cell nuclear antigen (PCNA), an auxiliary factor for DNA replication and repair. Binding of PCNA requires amino acids 163 to 174 of MCMT, occurs in intact cells at foci of newly replicated DNA, and does not alter MCMT activity. A peptide derived from the cell cycle regulator p21(WAF1) can disrupt the MCMT-PCNA interaction, which suggests that p21(WAF1) may regulate methylation by blocking access of MCMT to PCNA. MCMT and p21(WAF1) may be linked in a regulatory pathway, because the extents of their expression are inversely related in both SV40-transformed and nontransformed cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chuang, L S -- Ian, H I -- Koh, T W -- Ng, H H -- Xu, G -- Li, B F -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):1996-2000.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chemical Carcinogenesis Laboratory, Institute of Molecular and Cell Biology, National University of Singapore, Kent Ridge Crescent, Singapore 119260, Republic of Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9302295" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Line, Transformed ; Cell Nucleus/metabolism ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/chemistry/*metabolism ; DNA (Cytosine-5-)-Methyltransferase/*metabolism ; DNA Damage ; *DNA Methylation ; DNA Repair ; DNA Replication ; Humans ; Molecular Sequence Data ; Peptides/pharmacology ; Proliferating Cell Nuclear Antigen/*metabolism ; Recombinant Fusion Proteins/metabolism/pharmacology ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Specific inhibition of Stat3 signal transduction by PIAS3 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: The signal transducer and activator of transcription-3 (Stat3) protein is activated by the interleukin 6 (IL-6) family of cytokines, epidermal growth factor, and leptin. A protein named PIAS3 (protein inhibitor of activated STAT) that binds to Stat3 was isolated and characterized. The association of PIAS3 with Stat3 in vivo was only observed in cells stimulated with ligands that cause the activation of Stat3. PIAS3 blocked the DNA-binding activity of Stat3 and inhibited Stat3-mediated gene activation. Although Stat1 is also phosphorylated in response to IL-6, PIAS3 did not interact with Stat1 or affect its DNA-binding or transcriptional activity. The results indicate that PIAS3 is a specific inhibitor of Stat3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chung, C D -- Liao, J -- Liu, B -- Rao, X -- Jay, P -- Berta, P -- Shuai, K -- AI39612/AI/NIAID NIH HHS/ -- T32CA09056/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Dec 5;278(5344):1803-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9388184" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Carrier Proteins/chemistry/genetics/*metabolism/pharmacology ; Cell Line ; DNA/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Gene Expression Regulation ; Humans ; Interferon Regulatory Factor-1 ; Interferon-alpha/pharmacology ; Interleukin-6/pharmacology ; *Intracellular Signaling Peptides and Proteins ; Mice ; Molecular Sequence Data ; NF-kappa B/metabolism ; Phosphoproteins/genetics ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Inhibitors of Activated STAT ; Recombinant Fusion Proteins/pharmacology ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; *Signal Transduction ; Trans-Activators/*metabolism ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Transient expression of a mutator phenotype in cancer cells (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Loeb, L A -- New York, N.Y. -- Science. 1997 Sep 5;277(5331):1449-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Washington, Seattle, WA 98195-7705, USA. laloeb@u.washington.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9304215" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division ; DNA Repair ; Disease Progression ; Humans ; Microsatellite Repeats/*genetics ; *Mutation ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neoplasms/*genetics/pathology ; Neovascularization, Pathologic ; Phenotype ; Tumor Cells, Cultured
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  • 69
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    Measuring serotonin distribution in live cells with three-photon excitation (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-24
    Description: Tryptophan and serotonin were imaged with infrared illumination by three-photon excitation (3PE) of their native ultraviolet (UV) fluorescence. This technique, established by 3PE cross section measurements of tryptophan and the monoamines serotonin and dopamine, circumvents the limitations imposed by photodamage, scattering, and indiscriminate background encountered in other UV microscopies. Three-dimensionally resolved images are presented along with measurements of the serotonin concentration ( approximately 50 mM) and content (up to approximately 5 x 10(8) molecules) of individual secretory granules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maiti, S -- Shear, J B -- Williams, R M -- Zipfel, W R -- Webb, W W -- RR04224/RR/NCRR NIH HHS/ -- RR07719/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 24;275(5299):530-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Applied and Engineering Physics, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999797" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival ; Cytoplasmic Granules/*chemistry ; Dopamine/analysis ; Lasers ; Microscopy, Fluorescence/instrumentation/*methods ; Photochemistry ; *Photons ; Rats ; Serotonin/*analysis ; Tryptophan/analysis ; Tumor Cells, Cultured ; Ultraviolet Rays
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Potency of combined estrogenic pesticides (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramamoorthy, K -- Wang, F -- Chen, I C -- Safe, S -- Norris, J D -- McDonnell, D P -- Gaido, K W -- Bocchinfuso, W P -- Korach, K S -- New York, N.Y. -- Science. 1997 Jan 17;275(5298):405-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dieldrin/metabolism/*pharmacology ; Drug Interactions ; Drug Synergism ; Estrogens, Non-Steroidal/metabolism/*pharmacology ; Female ; Humans ; Insecticides/metabolism/*pharmacology ; Mice ; Receptors, Estrogen/metabolism ; Toxaphene/metabolism/*pharmacology ; Tumor Cells, Cultured
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    Tumor infarction in mice by antibody-directed targeting of tissue factor to tumor vasculature (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-24
    Description: Selective occlusion of tumor vasculature was tested as a therapy for solid tumors in a mouse model. The formation of blood clots (thrombosis) within the tumor vessels was initiated by targeting the cell surface domain of human tissue factor, by means of a bispecific antibody, to an experimentally induced marker on tumor vascular endothelial cells. This truncated form of tissue factor (tTF) had limited ability to initiate thrombosis when free in the circulation, but became an effective and selective thrombogen when targeted to tumor endothelial cells. Intravenous administration of the antibody-tTF complex to mice with large neuroblastomas resulted in complete tumor regressions in 38 percent of the mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, X -- Molema, G -- King, S -- Watkins, L -- Edgington, T S -- Thorpe, P E -- P01-HL16411/HL/NHLBI NIH HHS/ -- R01-CA54168/CA/NCI NIH HHS/ -- R01-CA59569/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 24;275(5299):547-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, TX 75235, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999802" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; *Blood Coagulation ; Endothelium, Vascular/immunology ; Histocompatibility Antigens Class II/immunology/metabolism ; Humans ; Immunoconjugates/administration & dosage/metabolism/*therapeutic use ; Injections, Intravenous ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neuroblastoma/*blood supply/*drug therapy/pathology ; Thromboplastin/administration & dosage/metabolism/*therapeutic use ; Tumor Cells, Cultured
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    Cancer chemopreventive activity of resveratrol, a natural product derived from grapes (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-10
    Description: Resveratrol, a phytoalexin found in grapes and other food products, was purified and shown to have cancer chemopreventive activity in assays representing three major stages of carcinogenesis. Resveratrol was found to act as an antioxidant and antimutagen and to induce phase II drug-metabolizing enzymes (anti-initiation activity); it mediated anti-inflammatory effects and inhibited cyclooxygenase and hydroperoxidase functions (antipromotion activity); and it induced human promyelocytic leukemia cell differentiation (antiprogression activity). In addition, it inhibited the development of preneoplastic lesions in carcinogen-treated mouse mammary glands in culture and inhibited tumorigenesis in a mouse skin cancer model. These data suggest that resveratrol, a common constituent of the human diet, merits investigation as a potential cancer chemopreventive agent in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jang, M -- Cai, L -- Udeani, G O -- Slowing, K V -- Thomas, C F -- Beecher, C W -- Fong, H H -- Farnsworth, N R -- Kinghorn, A D -- Mehta, R G -- Moon, R C -- Pezzuto, J M -- P01 CA48112/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):218-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, University of Illinois at Chicago, Chicago, IL 60612, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8985016" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology/therapeutic use ; Anticarcinogenic Agents/*pharmacology/therapeutic use ; Antimutagenic Agents/pharmacology ; Carcinogens ; Cell Differentiation/drug effects ; Cyclooxygenase 1 ; Cyclooxygenase Inhibitors/pharmacology/therapeutic use ; Female ; Fruit/*chemistry ; Humans ; Inflammation/drug therapy ; Isoenzymes/metabolism ; Mammary Neoplasms, Experimental/chemically induced/prevention & control ; Membrane Proteins ; Mice ; Neoplasms, Experimental/*prevention & control ; Peroxidases/antagonists & inhibitors ; Precancerous Conditions/prevention & control ; Prostaglandin-Endoperoxide Synthases/metabolism ; Rats ; Rats, Wistar ; Skin Neoplasms/chemically induced/prevention & control ; Stilbenes/*pharmacology/therapeutic use ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 73
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    Elementary calcium-release units induced by inositol trisphosphate (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-13
    Description: The extent to which inositol 1,4,5-trisphosphate (InsP3)-induced calcium signals are localized is a critical parameter for understanding the mechanism of effector activation. The spatial characteristics of InsP3-mediated calcium signals were determined by targeting a dextran-based calcium indicator to intracellular membranes through the in situ addition of a geranylgeranyl lipid group. Elementary calcium-release events observed with this indicator typically lasted less than 33 milliseconds, had diameters less than 2 micrometers, and were uncoupled from each other by the calcium buffer EGTA. Cellwide calcium transients are likely to result from synchronized triggering of such local release events, suggesting that calcium-dependent effector proteins could be selectively activated by localization near sites of local calcium release.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horne, J H -- Meyer, T -- GM-51457/GM/NIGMS NIH HHS/ -- P01-HL-47053/HL/NHLBI NIH HHS/ -- R01-GM-48113/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1690-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9180077" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/metabolism ; Cytosol/metabolism ; Egtazic Acid/pharmacology ; Electroporation ; Fluorescent Dyes ; Inositol 1,4,5-Trisphosphate/*pharmacology ; Intracellular Membranes/*metabolism ; Kinetics ; Microscopy, Confocal ; Microscopy, Fluorescence ; Organic Chemicals ; Peptides/metabolism ; Rats ; Signal Transduction ; Tumor Cells, Cultured
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    Negative regulation by HLA-DO of MHC class II-restricted antigen processing (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-06
    Description: HLA-DM is a major histocompatibility complex (MHC) class II-like molecule that facilitates antigen processing by catalyzing the exchange of invariant chain-derived peptides (CLIP) from class II molecules for antigenic peptides. HLA-DO is a second class II-like molecule that physically associates with HLA-DM in B cells. HLA-DO was shown to block HLA-DM function. Purified HLA-DM-DO complexes could not promote peptide exchange in vitro. Expression of HLA-DO in a class II+ and DM+, DO- human T cell line caused the accumulation of class II-CLIP complexes, indicating that HLA-DO blocked DM function in vivo and suggesting that HLA-DO is an important modulator of class II-restricted antigen processing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Denzin, L K -- Sant'Angelo, D B -- Hammond, C -- Surman, M J -- Cresswell, P -- AI14579/AI/NIAID NIH HHS/ -- AI23081/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):106-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, 310 Cedar Street, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311912" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Antigen Presentation ; Antigens, Differentiation, B-Lymphocyte/metabolism ; B-Lymphocytes/*immunology ; HLA-D Antigens/*metabolism ; HLA-DR3 Antigen/metabolism ; Histocompatibility Antigens Class II/metabolism ; Humans ; Molecular Sequence Data ; *Nuclear Proteins ; T-Lymphocytes/*immunology ; Trans-Activators/genetics ; Transfection ; Tumor Cells, Cultured
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    AIB1, a steroid receptor coactivator amplified in breast and ovarian cancer (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-08-15
    Description: Members of the recently recognized SRC-1 family of transcriptional coactivators interact with steroid hormone receptors to enhance ligand-dependent transcription. AIB1, a member of the SRC-1 family, was cloned during a search on the long arm of chromosome 20 for genes whose expression and copy number were elevated in human breast cancers. AIB1 amplification and overexpression were observed in four of five estrogen receptor-positive breast and ovarian cancer cell lines. Subsequent evaluation of 105 unselected specimens of primary breast cancer found AIB1 amplification in approximately 10 percent and high expression in 64 percent of the primary tumors analyzed. AIB1 protein interacted with estrogen receptors in a ligand-dependent fashion, and transfection of AIB1 resulted in enhancement of estrogen-dependent transcription. These observations identify AIB1 as a nuclear receptor coactivator whose altered expression may contribute to development of steroid-dependent cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anzick, S L -- Kononen, J -- Walker, R L -- Azorsa, D O -- Tanner, M M -- Guan, X Y -- Sauter, G -- Kallioniemi, O P -- Trent, J M -- Meltzer, P S -- New York, N.Y. -- Science. 1997 Aug 15;277(5328):965-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cancer Genetics, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9252329" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Breast/metabolism ; Breast Neoplasms/*genetics/metabolism ; Chromosomes, Human, Pair 20 ; Cloning, Molecular ; Estradiol/metabolism/pharmacology ; Female ; *Gene Amplification ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Histone Acetyltransferases ; Humans ; In Situ Hybridization, Fluorescence ; Ligands ; Molecular Sequence Data ; Neoplasms, Hormone-Dependent/*genetics/metabolism ; Nuclear Receptor Coactivator 1 ; Nuclear Receptor Coactivator 2 ; Ovarian Neoplasms/*genetics/metabolism ; Receptors, Estrogen/genetics/*metabolism ; Transcription Factors/genetics ; Transcriptional Activation ; 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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    An information-intensive approach to the molecular pharmacology of cancer (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-17
    Description: Since 1990, the National Cancer Institute (NCI) has screened more than 60,000 compounds against a panel of 60 human cancer cell lines. The 50-percent growth-inhibitory concentration (GI50) for any single cell line is simply an index of cytotoxicity or cytostasis, but the patterns of 60 such GI50 values encode unexpectedly rich, detailed information on mechanisms of drug action and drug resistance. Each compound's pattern is like a fingerprint, essentially unique among the many billions of distinguishable possibilities. These activity patterns are being used in conjunction with molecular structural features of the tested agents to explore the NCI's database of more than 460,000 compounds, and they are providing insight into potential target molecules and modulators of activity in the 60 cell lines. For example, the information is being used to search for candidate anticancer drugs that are not dependent on intact p53 suppressor gene function for their activity. It remains to be seen how effective this information-intensive strategy will be at generating new clinically active agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weinstein, J N -- Myers, T G -- O'Connor, P M -- Friend, S H -- Fornace, A J Jr -- Kohn, K W -- Fojo, T -- Bates, S E -- Rubinstein, L V -- Anderson, N L -- Buolamwini, J K -- van Osdol, W W -- Monks, A P -- Scudiero, D A -- Sausville, E A -- Zaharevitz, D W -- Bunow, B -- Viswanadhan, V N -- Johnson, G S -- Wittes, R E -- Paull, K D -- New York, N.Y. -- Science. 1997 Jan 17;275(5298):343-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Pharmacology (LMP), Division of Basic Science, National Cancer Institute (NCI), National Institutes of Health, Bethesda, MD 20892, USA. weinstein@dtpax2.ncifcrf.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8994024" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Antineoplastic Agents/chemistry/*pharmacology ; Cluster Analysis ; *Computational Biology ; Computer Communication Networks ; *Databases, Factual ; *Drug Screening Assays, Antitumor ; Genes, p53 ; Humans ; Molecular Structure ; Mutation ; Software ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Counterfeit chromosomes for humans (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roush, W -- New York, N.Y. -- Science. 1997 Apr 4;276(5309):38-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122708" target="_blank"〉PubMed〈/a〉
    Keywords: Base Composition ; Chromosomes, Artificial, Yeast ; *Chromosomes, Human/genetics ; DNA Replication ; DNA, Satellite ; Gene Transfer Techniques ; Genetic Techniques ; Humans ; Replication Origin ; Telomere/genetics ; Tumor Cells, Cultured
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    Endosomal targeting by the cytoplasmic tail of membrane immunoglobulin (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-04-18
    Description: Membrane-bound immunoglobulin (mIg) of the IgG, IgA, and IgE classes have conserved cytoplasmic tails. To investigate the function of these tails, a B cell line was transfected with truncated or mutated gamma2a heavy chains. Transport to the endosomal compartment of antigen bound by the B cell antigen receptor did not occur in the absence of the cytoplasmic tail; and one or two mutations, respectively, in the Tyr-X-X-Met motif of the tail partially or completely interrupted the process. Experiments with chimeric antigen receptors confirmed these findings. Thus, a role for the cytoplasmic tail of mIg heavy chains in endosomal targeting of antigen is revealed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiser, P -- Muller, R -- Braun, U -- Reth, M -- New York, N.Y. -- Science. 1997 Apr 18;276(5311):407-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Immunbiologie, Stubeweg 51, D-79108 Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9103197" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; B-Lymphocytes/*immunology ; Biological Transport ; Cytoplasm ; Dimerization ; Endosomes/*immunology ; Immunoglobulin gamma-Chains/chemistry/genetics/*metabolism ; Immunologic Memory ; Mice ; Mutation ; Receptors, Antigen, B-Cell/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Transfection ; Tumor Cells, Cultured
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  • 79
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    First p53 relative may be a new tumor suppressor (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dickman, S -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1605-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9312855" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Division ; Chromosome Mapping ; Chromosomes, Human, Pair 1 ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/biosynthesis ; DNA-Binding Proteins/*genetics/physiology ; *Genes, Tumor Suppressor ; *Genes, p53 ; Genomic Imprinting ; Humans ; Mice ; Neuroblastoma/*genetics ; Nuclear Proteins/*genetics/physiology ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/physiology ; Tumor Suppressor Proteins
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  • 80
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    Stabilization of beta-catenin by genetic defects in melanoma cell lines (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-03-21
    Description: Signal transduction by beta-catenin involves its posttranslational stabilization and downstream coupling to the Lef and Tcf transcription factors. Abnormally high amounts of beta-catenin were detected in 7 of 26 human melanoma cell lines. Unusual messenger RNA splicing and missense mutations in the beta-catenin gene (CTNNB1) that result in stabilization of the protein were identified in six of the lines, and the adenomatous polyposis coli tumor suppressor protein (APC) was altered or missing in two others. In the APC-deficient cells, ectopic expression of wild-type APC eliminated the excess beta-catenin. Cells with stabilized beta-catenin contained a constitutive beta-catenin-Lef-1 complex. Thus, genetic defects that result in up-regulation of beta-catenin may play a role in melanoma progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rubinfeld, B -- Robbins, P -- El-Gamil, M -- Albert, I -- Porfiri, E -- Polakis, P -- 1R43CA69931/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1790-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Onyx Pharmaceuticals, 3031 Research Drive, Richmond, CA 94806, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9065403" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Animals ; Cell Line ; Cytoskeletal Proteins/chemistry/*genetics/metabolism ; DNA-Binding Proteins/metabolism ; *Gene Expression Regulation, Neoplastic ; *Genes, APC ; Humans ; Lymphoid Enhancer-Binding Factor 1 ; Melanoma/*genetics/metabolism ; Mice ; Mutation ; Point Mutation ; RNA Splicing ; RNA, Messenger/genetics ; RNA, Neoplasm/genetics ; *Trans-Activators ; Transcription Factors/metabolism ; Transfection ; Tumor Cells, Cultured ; Up-Regulation ; beta Catenin
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    Gene expression profiles in normal and cancer cells (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-05-23
    Description: As a step toward understanding the complex differences between normal and cancer cells in humans, gene expression patterns were examined in gastrointestinal tumors. More than 300,000 transcripts derived from at least 45,000 different genes were analyzed. Although extensive similarity was noted between the expression profiles, more than 500 transcripts that were expressed at significantly different levels in normal and neoplastic cells were identified. These data provide insight into the extent of expression differences underlying malignancy and reveal genes that may prove useful as diagnostic or prognostic markers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, L -- Zhou, W -- Velculescu, V E -- Kern, S E -- Hruban, R H -- Hamilton, S R -- Vogelstein, B -- Kinzler, K W -- CA57345/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 May 23;276(5316):1268-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, The Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9157888" target="_blank"〉PubMed〈/a〉
    Keywords: Colorectal Neoplasms/genetics ; Computer Simulation ; *Digestive System Physiological Phenomena ; Gastrointestinal Neoplasms/*genetics ; *Gene Expression ; Humans ; Reference Values ; Tumor Cells, Cultured
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  • 82
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    Differential ligand activation of estrogen receptors ERalpha and ERbeta at AP1 sites (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-05
    Description: The transactivation properties of the two estrogen receptors, ERalpha and ERbeta, were examined with different ligands in the context of an estrogen response element and an AP1 element. ERalpha and ERbeta were shown to signal in opposite ways when complexed with the natural hormone estradiol from an AP1 site: with ERalpha, 17beta-estradiol activated transcription, whereas with ERbeta, 17beta-estradiol inhibited transcription. Moreover, the antiestrogens tamoxifen, raloxifene, and Imperial Chemical Industries 164384 were potent transcriptional activators with ERbeta at an AP1 site. Thus, the two ERs signal in different ways depending on ligand and response element. This suggests that ERalpha and ERbeta may play different roles in gene regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paech, K -- Webb, P -- Kuiper, G G -- Nilsson, S -- Gustafsson, J -- Kushner, P J -- Scanlan, T S -- GM 50672/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 5;277(5331):1508-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmaceutical Chemistry, University of California, San Francisco, CA 94143-0446, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9278514" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/metabolism ; Cell Line ; Diethylstilbestrol/metabolism/pharmacology ; *Enhancer Elements, Genetic ; Estradiol/analogs & derivatives/metabolism/pharmacology ; Estrogen Antagonists/*pharmacology ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Estrogens/*pharmacology ; Female ; HeLa Cells ; Humans ; Ligands ; Piperidines/metabolism/pharmacology ; Polyunsaturated Alkamides ; Raloxifene Hydrochloride ; Rats ; Receptors, Estrogen/*metabolism ; Tamoxifen/metabolism/pharmacology ; Transcription Factor AP-1/*genetics ; *Transcriptional Activation/drug effects ; Transfection ; Tumor Cells, Cultured ; Uterus/metabolism
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  • 83
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    Repression of c-myc transcription by Blimp-1, an inducer of terminal B cell differentiation (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-25
    Description: Transcription of c-myc in plasma cells, which are terminally differentiated B cells, is repressed by plasmacytoma repressor factor. This factor was identified as Blimp-1, known for its ability to induce B cell differentiation. Blimp-1 repressed c-myc promoter activity in a binding site-dependent manner. Treatment of BCL1 lymphoma cells with interleukin-2 (IL-2) plus IL-5 induced Blimp-1 and caused a subsequent decline in c-Myc protein. Ectopic expression of Blimp-1 in Abelson-transformed precursor B cells repressed endogenous c-Myc and caused apoptosis; Blimp-1-induced death was partially overcome by ectopic expression of c-Myc. Thus, repression of c-myc is a component of the Blimp-1 program of terminal B cell differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Y -- Wong, K -- Calame, K -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):596-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9110979" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; B-Lymphocytes/*cytology/metabolism ; Binding Sites ; Cell Differentiation ; Cell Line ; Gene Expression Regulation ; *Genes, myc ; Interleukin-2/pharmacology ; Interleukin-5/pharmacology ; Mice ; Mutagenesis, Site-Directed ; Plasmacytoma ; Promoter Regions, Genetic ; *Repressor Proteins ; Transcription Factors/genetics/*metabolism ; *Transcription, Genetic ; Transfection ; Tumor Cells, Cultured ; Zinc Fingers
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    How TRAIL kills cancer cells, but not normal cells (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gura, T -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):768.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9273698" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Binding Sites ; Databases, Factual ; GPI-Linked Proteins ; Humans ; Membrane Glycoproteins/*metabolism/therapeutic use ; Neoplasms/*metabolism/pathology ; Rats ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor/chemistry/*metabolism ; TNF-Related Apoptosis-Inducing Ligand ; Tumor Cells, Cultured ; Tumor Necrosis Factor Decoy Receptors ; Tumor Necrosis Factor-alpha/*metabolism/therapeutic use
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    Interaction of CED-4 with CED-3 and CED-9: a molecular framework for cell death (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-21
    Description: Previous genetic studies of the nematode Caenorhabditis elegans identified three important components of the cell death machinery. CED-3 and CED-4 function to kill cells, whereas CED-9 protects cells from death. Here CED-9 and its mammalian homolog Bcl-xL (a member of the Bcl-2 family of cell death regulators) were both found to interact with and inhibit the function of CED-4. In addition, analysis revealed that CED-4 can simultaneously interact with CED-3 and its mammalian counterparts interleukin-1beta-converting enzyme (ICE) and FLICE. Thus, CED-4 plays a central role in the cell death pathway, biochemically linking CED-9 and the Bcl-2 family to CED-3 and the ICE family of pro-apoptotic cysteine proteases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chinnaiyan, A M -- O'Rourke, K -- Lane, B R -- Dixit, V M -- 7863/PHS HHS/ -- New York, N.Y. -- Science. 1997 Feb 21;275(5303):1122-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Michigan Medical School, Department of Pathology, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9027312" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Caenorhabditis elegans/*cytology/genetics/metabolism ; *Caenorhabditis elegans Proteins ; Calcium-Binding Proteins/genetics/*metabolism ; Caspase 1 ; Caspase 8 ; Caspase 9 ; *Caspases ; Cell Line ; Cysteine Endopeptidases/genetics/*metabolism ; Genes, Helminth ; Helminth Proteins/genetics/*metabolism ; Humans ; Mutation ; Proto-Oncogene Proteins/genetics/*metabolism ; *Proto-Oncogene Proteins c-bcl-2 ; Transfection ; Tumor Cells, Cultured ; bcl-X Protein
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