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  • United States  (930)
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  • American Association for the Advancement of Science (AAAS)  (1,717)
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  • 1990-1994  (1,717)
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  • American Association for the Advancement of Science (AAAS)  (1,717)
  • American Association of Petroleum Geologists (AAPG)
  • Springer Nature
  • Springer  (50)
  • Wiley-Blackwell  (6)
Years
Year
  • 1
    Publication Date: 1994-02-25
    Description: Activation of the serine-threonine kinase p34cdc2 at an inappropriate time during the cell cycle leads to cell death that resembles apoptosis. Premature activation of p34cdc2 was shown to be required for apoptosis induced by a lymphocyte granule protease. The kinase was rapidly activated and tyrosine dephosphorylated at the initiation of apoptosis. DNA fragmentation and nuclear collapse could be prevented by blocking p34cdc2 activity with excess peptide substrate, or by inactivating p34cdc2 in a temperature-sensitive mutant. Premature p34cdc2 activation may be a general mechanism by which cells induced to undergo apoptosis initiate the disruption of the nucleus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shi, L -- Nishioka, W K -- Th'ng, J -- Bradbury, E M -- Litchfield, D W -- Greenberg, A H -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1143-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8108732" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Apoptosis ; CDC2 Protein Kinase/*metabolism ; DNA Damage ; Deoxyribonucleases/pharmacology ; Enzyme Activation ; Enzyme Induction ; Membrane Glycoproteins/pharmacology ; Mice ; Mitosis ; Molecular Sequence Data ; Perforin ; Phosphorylation ; Pore Forming Cytotoxic Proteins ; Serine Endopeptidases/pharmacology ; 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
    Publication Date: 1994-01-07
    Description: Coexpression of the human Met receptor and its ligand, hepatocyte growth factor/scatter factor (HGF/SF), in NIH 3T3 fibroblasts causes the cells to become tumorigenic in nude mice. The resultant tumors display lumen-like morphology, contain carcinoma-like focal areas with intercellular junctions resembling desmosomes, and coexpress epithelial (cytokeratin) and mesenchymal (vimentin) cytoskeletal markers. The tumor cells also display enhanced expression of desmosomal and tight-junction proteins. The apparent mesenchymal to epithelial conversion of the tumor cells mimics the conversion that occurs during embryonic kidney development, suggesting that Met-HGF/SF signaling plays a role in this process as well as in tumors that express both epithelial and mesenchymal markers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsarfaty, I -- Rong, S -- Resau, J H -- Rulong, S -- da Silva, P P -- Vande Woude, G F -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Jan 7;263(5143):98-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute (NCI)-Frederick Cancer Research and Development Center, MD 21702-1201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7505952" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; *Cell Transformation, Neoplastic ; Desmosomes/ultrastructure ; Epithelial Cells ; Hepatocyte Growth Factor/metabolism/pharmacology ; Keratins/biosynthesis ; Kidney/embryology/metabolism ; Mesoderm/cytology ; Mice ; Mice, Nude ; Neoplasms, Experimental/metabolism/*pathology ; Proto-Oncogene Proteins/genetics/*metabolism ; Proto-Oncogene Proteins c-met ; *Proto-Oncogenes ; Receptor Protein-Tyrosine Kinases/genetics/*metabolism ; Signal Transduction ; Transfection ; Vimentin/biosynthesis
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-03-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, C -- New York, N.Y. -- Science. 1994 Mar 4;263(5151):1216.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8122099" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; *Clinical Trials as Topic ; Female ; Humans ; Informed Consent ; *Institute of Medicine (U.S.) ; National Institutes of Health (U.S.) ; *Pregnancy ; *Pregnant Women ; Research Subjects ; United States ; *Women's Health
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kinoshita, J -- Mervis, J -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1187.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973699" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; *Gene Library ; *Genome, Plant ; International Cooperation ; Japan ; Oryza/*genetics ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-02-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, C -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1080, 1082.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8108722" target="_blank"〉PubMed〈/a〉
    Keywords: Budgets ; Clinical Trials as Topic ; Databases, Factual ; Humans ; Medical Records ; *Outcome Assessment (Health Care)/economics ; Retrospective Studies ; Treatment Outcome ; United States ; *United States Agency for Healthcare Research and Quality/economics
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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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-08-26
    Description: The interaction of B7-related molecules on antigen-presenting cells with CD28 or CTLA-4 antigens on T cells provides a second signal for T cell activation. Selection inhibition of the B7-CD28 or B7-CTLA-4 interactions produces antigen-specific T cell unresponsiveness in vitro and suppresses immune function in vivo. To determine whether selective inhibition of the B7-CD28 or B7-CTLA-4 interactions could suppress spontaneous autoimmune disease, a B7-binding protein was generated by genetic fusion of the extracellular domain of murine CTLA-4 to the Fc portion of a mouse immunoglobulin G2a monoclonal antibody (muCTLA4Ig). In lupus-prone NZB/NZW filial generation (F1) mice, treatment with muCTLA4Ig blocked autoantibody production and prolonged life, even when treatment was delayed until the most advanced stage of clinical illness. These findings suggest a possible role for human CTLA4Ig in the treatment of autoimmune diseases in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finck, B K -- Linsley, P S -- Wofsy, D -- New York, N.Y. -- Science. 1994 Aug 26;265(5176):1225-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7520604" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antibodies, Antinuclear/biosynthesis ; Antibodies, Monoclonal ; Antigens, CD ; Antigens, CD80/metabolism ; Antigens, Differentiation/immunology/metabolism/*therapeutic use ; B-Lymphocytes/immunology ; CTLA-4 Antigen ; Female ; Humans ; *Immunoconjugates ; Immunotherapy ; Lupus Erythematosus, Systemic/immunology/*therapy ; Mice ; Mice, Inbred NZB ; Mice, Inbred Strains ; Recombinant Fusion Proteins/therapeutic use ; T-Lymphocytes/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-02-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, C -- New York, N.Y. -- Science. 1994 Feb 18;263(5149):909-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8310287" target="_blank"〉PubMed〈/a〉
    Keywords: *Biotechnology ; *Federal Government ; *Genes ; Internationality ; *National Institutes of Health (U.S.) ; *Patents as Topic ; United States
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-01-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Valigra, L -- New York, N.Y. -- Science. 1994 Jan 14;263(5144):168-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8284666" target="_blank"〉PubMed〈/a〉
    Keywords: *Biotechnology ; *International Cooperation ; Japan ; *Research ; United States
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  • 9
    Publication Date: 1994-10-14
    Description: Mice deficient for the gene encoding alpha-calcium-calmodulin-dependent kinase II (alpha-CaMKII knockout mice) provide a promising tool to link behavioral and cellular abnormalities with a specific molecular lesion. The heterozygous mouse exhibited a well-circumscribed syndrome of behavioral abnormalities, consisting primarily of a decreased fear response and an increase in defensive aggression, in the absence of any measured cognitive deficits. Unlike the heterozygote, the homozygote displayed abnormal behavior in all paradigms tested. At the cellular level, both extracellular and whole-cell patch clamp recordings indicated that serotonin release in putative serotonergic neurons of the dorsal raphe was reduced. Thus, alpha-CaMKII knockout mice, in particular the heterozygote, may provide a model for studying the molecular and cellular basis underlying emotional disorders involving fear and aggression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, C -- Rainnie, D G -- Greene, R W -- Tonegawa, S -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):291-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Center for Cancer Research, Cambridge, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939668" target="_blank"〉PubMed〈/a〉
    Keywords: *Aggression ; Animals ; Behavior, Animal ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/deficiency/genetics/*physiology ; *Fear ; Fluoxetine/pharmacology ; Gene Dosage ; Heterozygote ; Homozygote ; In Vitro Techniques ; Membrane Potentials ; Mice ; Mice, Knockout ; Mutation ; Neurons/metabolism ; Patch-Clamp Techniques ; Raphe Nuclei/metabolism ; Serotonin/metabolism/pharmacology ; Synaptic Transmission/drug effects
    Print ISSN: 0036-8075
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-03-04
    Description: Conversion of external signals into proliferative responses may be mediated by interactions between signaling pathways that control cell proliferation. Interactions between G alpha s, the alpha subunit of the heterotrimeric guanine nucleotide binding protein that stimulates adenylyl cyclase, and Ras, an important element in growth factor signaling, were studied. Expression of activated G alpha s in NIH 3T3 cells increased intracellular concentrations of adenosine 3',5'-monophosphate (cAMP) and inhibited H-Ras-stimulated DNA synthesis and mitogen-activated protein kinase activity. Activated G alpha s and 8-Br-cAMP suppressed H-Ras-induced transformation of NIH 3T3 cells. Apparently, G alpha s inhibits proliferative signals from Ras by stimulating cAMP production and activating protein kinase A.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, J -- Iyengar, R -- CA-44998/CA/NCI NIH HHS/ -- DK-38761/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 4;263(5151):1278-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Mount Sinai School of Medicine, City University of New York, NY 10029.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8122111" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Animals ; Cell Division ; Cell Line ; *Cell Transformation, Neoplastic ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Enzyme Activation ; GTP-Binding Proteins/genetics/*physiology ; *Genes, ras ; Mice ; Mitogen-Activated Protein Kinase 1 ; Mutagenesis, Site-Directed ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Protein-Tyrosine Kinases/antagonists & inhibitors/metabolism ; Signal Transduction ; Transfection
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  • 11
    Publication Date: 1994-03-11
    Description: The gamma chain of the interleukin-2 (IL-2) receptor is shared with the functional IL-4 receptor and is causatively related to X-linked severe combined immunodeficiency (XSCID), which is ascribed to a profound T cell defect. Studies with monoclonal antibodies specific for the IL-2 receptor gamma chain showed that the gamma chain participates in the functional high-affinity receptor complexes for IL-7 that are involved in the differentiation of T and B cells. Participation of the gamma subunit in more than one receptor may enable the elucidation of the mechanisms of XSCID development and lymphocyte differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, M -- Takeshita, T -- Higuchi, M -- Nakamura, M -- Sudo, T -- Nishikawa, S -- Sugamura, K -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1453-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Tohoku University School of Medicine, Sendai, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128231" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; B-Lymphocytes/*immunology ; Cell Line ; Cells, Cultured ; Female ; Genetic Linkage ; Interleukin-7/*metabolism/pharmacology ; Mice ; Mice, Inbred C57BL ; Receptors, Interleukin/*metabolism ; Receptors, Interleukin-2/genetics/immunology/*metabolism ; Receptors, Interleukin-7 ; Severe Combined Immunodeficiency/genetics/immunology ; T-Lymphocytes/*immunology ; X Chromosome
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
    Publication Date: 1994-08-26
    Description: Experimental autoimmune encephalomyelitis (EAE) is a cell-mediated autoimmune disease that serves as an animal model for multiple sclerosis. Oral administration of myelin basic protein (MBP) suppresses EAE by inducing peripheral tolerance. T cell clones were isolated from the mesenteric lymph nodes of SJL mice that had been orally tolerized to MBP. These clones were CD4+ and were structurally identical to T helper cell type 1 (TH1) encephalitogenic CD4+ clones in T cell receptor usage, major histocompatibility complex restriction, and epitope recognition. However, they produced transforming growth factor-beta with various amounts of interleukin-4 and interleukin-10 and suppressed EAE induced with either MBP or proteolipid protein. Thus, mucosally derived TH2-like clones induced by oral antigen can actively regulate immune responses in vivo and may represent a different subset of T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Y -- Kuchroo, V K -- Inobe, J -- Hafler, D A -- Weiner, H L -- AR/A143220/AR/NIAMS NIH HHS/ -- NS29352/NS/NINDS NIH HHS/ -- NS30843/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 26;265(5176):1237-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7520605" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Amino Acid Sequence ; Animals ; CD4-Positive T-Lymphocytes/*immunology ; Clone Cells ; Encephalomyelitis, Autoimmune, Experimental/*immunology ; Epitopes/immunology ; *Immune Tolerance ; Interleukin-10/biosynthesis ; Interleukin-4/biosynthesis ; Lymph Nodes/immunology ; Major Histocompatibility Complex ; Mesentery/immunology ; Mice ; Molecular Sequence Data ; Myelin Basic Protein/administration & dosage/*immunology ; Myelin Proteins/immunology ; Myelin Proteolipid Protein ; Receptors, Antigen, T-Cell/immunology ; Transforming Growth Factor beta/biosynthesis
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
    Publication Date: 1994-09-23
    Description: Indirect evidence implicates gamma delta T cells in the cross-regulation of CD4 alpha beta T cell responses. Adoptive transfer of small numbers of gamma delta T cells from ovalbumin (OVA)-tolerant mice selectively suppressed TH2-dependent immunoglobulin E (IgE) antibody production without affecting parallel IgG responses. Challenge of these gamma delta T cells in vitro with specific antigen resulted in production of high levels of interferon gamma. The effects of the gamma delta T cells may be mediated by direct inhibition of OVA-specific CD4+ TH2 cell proliferation or selection for specific CD4 TH2 cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McMenamin, C -- Pimm, C -- McKersey, M -- Holt, P G -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1869-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology, Institute for Child Health Research, West Perth, Western Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7916481" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/*immunology ; Dose-Response Relationship, Immunologic ; *Immune Tolerance ; Immunoglobulin E/*biosynthesis ; Immunoglobulin G/biosynthesis ; Immunotherapy, Adoptive ; Interferon-gamma/biosynthesis ; Interleukin-2/biosynthesis ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Ovalbumin/immunology ; Receptors, Antigen, T-Cell, gamma-delta/*immunology ; T-Lymphocyte Subsets/*immunology ; Transforming Growth Factor beta/biosynthesis
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  • 14
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-18
    Description: A diverse set of circadian clock mutants was isolated in a cyanobacterial strain that carries a bacterial luciferase reporter gene attached to a clock-controlled promoter. Among 150,000 clones of chemically mutagenized bioluminescent cells, 12 mutants were isolated that exhibit a broad spectrum of periods (between 16 and 60 hours), and 5 mutants were found that show a variety of unusual patterns, including arrhythmia. These mutations appear to be clock-specific. Moreover, it was demonstrated that in this cyanobacterium it is possible to clone mutant genes by complementation, which provides a means to genetically dissect the circadian mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, T -- Tsinoremas, N F -- Golden, S S -- Johnson, C H -- Kutsuna, S -- Ishiura, M -- GM37040/GM/NIGMS NIH HHS/ -- MH43836/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1233-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute for Basic Biology, Okazaki, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973706" target="_blank"〉PubMed〈/a〉
    Keywords: Circadian Rhythm/*genetics ; Cloning, Molecular ; Cyanobacteria/*genetics/growth & development/physiology ; Darkness ; *Genes, Bacterial ; Genetic Complementation Test ; Light ; Luminescent Measurements ; Mutagenesis ; Mutation ; Temperature
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  • 15
    Publication Date: 1994-09-02
    Description: As a step toward developing poliovirus as a vaccine vector, poliovirus recombinants were constructed by fusing exogenous peptides (up to 400 amino acids) and an artificial cleavage site for viral protease 3Cpro to the amino terminus of the viral polyprotein. Viral replication proceeded normally. An extended polyprotein was produced in infected cells and proteolytically processed into the complete array of viral proteins plus the foreign peptide, which was excluded from mature virions. The recombinants retained exogenous sequences through successive rounds of replication in culture and in vivo. Infection of animals with recombinants elicited a humoral immune response to the foreign peptides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andino, R -- Silvera, D -- Suggett, S D -- Achacoso, P L -- Miller, C J -- Baltimore, D -- Feinberg, M B -- AI22346/AI/NIAID NIH HHS/ -- AI35545/AI/NIAID NIH HHS/ -- RR00169/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1448-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California, San Francisco.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073288" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Bacterial/biosynthesis ; Antibodies, Viral/biosynthesis ; Antigens, Bacterial/genetics/immunology ; Antigens, Viral/genetics/immunology ; Base Sequence ; Cloning, Molecular ; *Genetic Engineering ; Genetic Vectors ; HeLa Cells ; Humans ; Macaca fascicularis ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Poliovirus/*genetics/immunology/physiology ; Poliovirus Vaccine, Oral/*genetics ; *Protein Biosynthesis ; Proteins/metabolism ; Recombinant Proteins/biosynthesis/metabolism ; Vaccines, Synthetic/genetics/*immunology ; Virus Replication
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  • 16
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simm, M -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):653.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171314" target="_blank"〉PubMed〈/a〉
    Keywords: Academies and Institutes/*organization & administration ; Aggression ; Behavioral Research ; Dissent and Disputes ; *Genetics, Behavioral ; Germany ; Group Processes ; Humans ; *Molecular Biology ; Mutation ; National Socialism ; *Violence
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  • 17
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-01-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, C -- New York, N.Y. -- Science. 1994 Jan 7;263(5143):20-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8272861" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research ; Federal Government ; *Government Regulation ; *Scientific Misconduct ; United States ; *United States Office of Research Integrity
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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGarey, B M -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):955.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973673" target="_blank"〉PubMed〈/a〉
    Keywords: *Industry ; *National Institutes of Health (U.S.) ; *Research ; United States ; *Universities
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-24
    Description: Glycosyl-phosphatidylinositol (GPI)-anchored proteins have been reported to reside in clusters collected over small membrane invaginations called caveolae. The detection of different GPI-anchored proteins with fluorescently labeled monoclonal antibodies showed that these proteins are not constitutively concentrated in caveolae; they enter these structures independently after cross-linking with polyclonal secondary antibodies. Analysis of the cell surface distribution of the GPI-anchored folate receptor by electron microscopy confirms these observations. Thus, multimerization of GPI-anchored proteins regulates their sequestration in caveolae, but in the absence of agents that promote clustering they are diffusely distributed over the plasma membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mayor, S -- Rothberg, K G -- Maxfield, F R -- DK27083/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1948-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7516582" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Antibodies, Monoclonal ; Antigens, CD/analysis/immunology/metabolism ; Antigens, CD55 ; Antigens, Surface/analysis/immunology/metabolism ; Antigens, Thy-1 ; Carrier Proteins/analysis/immunology/*metabolism ; Caveolin 1 ; *Caveolins ; Cell Membrane/*metabolism/ultrastructure ; Fluorescent Antibody Technique ; Folate Receptors, GPI-Anchored ; Folic Acid/metabolism ; Glycosylphosphatidylinositols/analysis/*metabolism ; Humans ; Immunoglobulin G/metabolism ; Membrane Glycoproteins/analysis/immunology/metabolism ; Membrane Proteins/analysis ; Mice ; Microscopy, Electron ; *Receptors, Cell Surface ; Tumor Cells, Cultured
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-10-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fink, L E -- New York, N.Y. -- Science. 1994 Oct 21;266(5184):350; author reply 350-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7802836" target="_blank"〉PubMed〈/a〉
    Keywords: *Chlorine ; *Environmental Pollutants ; *Hazardous Substances ; Hazardous Waste ; Humans ; Hydrocarbons, Chlorinated ; Risk Assessment ; United States ; United States Environmental Protection Agency
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  • 21
    Publication Date: 1994-11-11
    Description: Signals mediated by the T cell receptor (TCR) are required for thymocyte maturation and selection. To examine the role of TCR zeta chain signals in development, TCR expression was restored in zeta-deficient mice with transgenic zeta chains that partially or completely lacked sequences required for signal transduction. The zeta chain played a role in thymic development by promoting TCR surface expression, but zeta-mediated signals were not essential because TCRs that contained signaling-deficient zeta chains promoted T cell maturation and transduced signals associated with thymic selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shores, E W -- Huang, K -- Tran, T -- Lee, E -- Grinberg, A -- Love, P E -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1047-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematologic Products, Food and Drug Administration, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7526464" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD/analysis/genetics ; Antigens, CD4/analysis ; Antigens, CD5 ; Antigens, CD8/analysis ; Antigens, Differentiation, T-Lymphocyte/analysis ; *DNA-Binding Proteins ; Down-Regulation ; Gene Expression ; *Homeodomain Proteins ; Lectins, C-Type ; Lymph Nodes/immunology ; Membrane Proteins/genetics/*physiology ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Proteins/genetics ; RNA, Messenger/genetics/metabolism ; Receptors, Antigen, T-Cell/genetics/*physiology ; Signal Transduction ; T-Lymphocytes/cytology/*immunology ; Thymus Gland/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 22
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-01-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, C -- New York, N.Y. -- Science. 1994 Jan 21;263(5145):317-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8278802" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Image Enhancement/*standards ; Image Processing, Computer-Assisted/*standards ; National Library of Medicine (U.S.) ; Periodicals as Topic ; Photography ; Publishing/*standards ; Scientific Misconduct ; United States ; United States Food and Drug Administration
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  • 23
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-02-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, C -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):603.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303264" target="_blank"〉PubMed〈/a〉
    Keywords: *Biomedical Research ; Biotechnology/standards ; Federal Government ; *Government Regulation ; *Guidelines as Topic ; Industry/*standards ; Information Dissemination ; *National Institutes of Health (U.S.) ; *Research ; United States
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  • 24
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varmus, H -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1345.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073266" target="_blank"〉PubMed〈/a〉
    Keywords: *Embryo, Mammalian ; *Guidelines as Topic ; Humans ; National Institutes of Health (U.S.) ; *Research ; United States
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  • 25
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-08-12
    Description: The transcription factor nuclear factor-kappa B (NF-kappa B) is critical for the inducible expression of multiple cellular and viral genes involved in inflammation and infection including interleukin-1 (IL-1), IL-6, and adhesion molecules. The anti-inflammatory drugs sodium salicylate and aspirin inhibited the activation of NF-kappa B, which further explains the mechanism of action of these drugs. This inhibition prevented the degradation of the NF-kappa B inhibitor, I kappa B, and therefore NF-kappa B was retained in the cytosol. Sodium salicylate and aspirin also inhibited NF-kappa B-dependent transcription from the Ig kappa enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kopp, E -- Ghosh, S -- R01 AI 33443-01A1/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 12;265(5174):956-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06536.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8052854" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspirin/*pharmacology ; Cell Line ; Enhancer Elements, Genetic ; Gene Expression/drug effects ; Genes, Reporter ; HIV Long Terminal Repeat ; HIV-1/genetics ; Humans ; Immunoglobulin kappa-Chains/genetics ; Lipopolysaccharides/pharmacology ; Mice ; NF-kappa B/*antagonists & inhibitors/metabolism ; Phosphorylation ; Promoter Regions, Genetic ; Protein Biosynthesis/drug effects ; Proto-Oncogene Proteins/metabolism ; Sodium Salicylate/*pharmacology ; T-Lymphocytes/metabolism ; Transcription Factor RelB ; *Transcription Factors ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varmus, H -- New York, N.Y. -- Science. 1994 Jun 17;264(5166):1649.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8209238" target="_blank"〉PubMed〈/a〉
    Keywords: Budgets ; Financing, Government ; National Institutes of Health (U.S.)/*economics ; Research ; *Research Support as Topic ; United States
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  • 27
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-12-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshland, D E Jr -- New York, N.Y. -- Science. 1994 Dec 23;266(5193):1925.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7801114" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Damage ; *DNA Ligases ; *DNA Repair ; DNA Replication ; Humans ; Mutation ; Species Specificity
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  • 28
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-12-02
    Description: Estrogen hormones produce physiological actions within a variety of target sites in the body and during development by activating a specific receptor protein. Hormone responsiveness for the estrogen receptor protein was investigated at different stages of development with the use of gene knockout techniques because no natural genetic mutants have been described. A mutant mouse line without a functional estrogen receptor was created and is being used to assess estrogen responsiveness. Both sexes of these mutant animals are infertile and show a variety of phenotypic changes, some of which are associated with the gonads, mammary glands, reproductive tracts, and skeletal tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korach, K S -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1524-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Receptor Biology Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985022" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Estrogens/*physiology ; Female ; Heterozygote ; Homozygote ; Humans ; Infertility, Female/etiology ; Infertility, Male/etiology ; Male ; Mice ; Mice, Knockout ; Mutation ; Phenotype ; Receptors, Estrogen/genetics/*physiology ; Signal Transduction
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  • 29
    Publication Date: 1994-03-25
    Description: Fas is an apoptosis-signaling receptor molecule on the surface of a number of cell types. Molecular cloning and nucleotide sequence analysis revealed a human Fas messenger RNA variant capable of encoding a soluble Fas molecule lacking the transmembrane domain because of the deletion of an exon encoding this region. The expression of soluble Fas was confirmed by flow cytometry and immunocytochemical analysis. Supernatants from cells transfected with the variant messenger RNA blocked apoptosis induced by the antibody to Fas. Levels of soluble Fas were elevated in patients with systemic lupus erythematosus, and mice injected with soluble Fas displayed autoimmune features.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, J -- Zhou, T -- Liu, C -- Shapiro, J P -- Brauer, M J -- Kiefer, M C -- Barr, P J -- Mountz, J D -- P01 AR03555/AR/NIAMS NIH HHS/ -- P50 AI23694/AI/NIAID NIH HHS/ -- P60 AR20614/AR/NIAMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1759-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Alabama at Birmingham.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7510905" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies/immunology ; Antigens, CD95 ; Antigens, Surface/chemistry/genetics/immunology/*physiology ; *Apoptosis ; Arthritis, Rheumatoid/blood ; Base Sequence ; Cell Line ; Cell Membrane/chemistry ; Humans ; Lupus Erythematosus, Systemic/blood ; Mice ; Molecular Sequence Data ; RNA, Messenger/genetics ; Solubility ; T-Lymphocyte Subsets/immunology ; Transfection
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  • 30
    Publication Date: 1994-11-04
    Description: Transcription terminators recognized by several RNA polymerases include a DNA segment encoding uridine-rich RNA and, for bacterial RNA polymerase, a hairpin loop located immediately upstream. Here, mutationally altered Escherichia coli RNA polymerase enzymes that have different termination efficiencies were used to show that the extent of transcription through the uridine-rich encoding segment is controlled by the substrate concentration of nucleoside triphosphate. This result implies that the rate of elongation determines the probability of transcript release. Moreover, the position of release sites suggests an important spatial relation between the RNA hairpin and the boundary of the terminator.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDowell, J C -- Roberts, J W -- Jin, D J -- Gross, C -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):822-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, NY 14853.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7526463" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; DNA-Directed RNA Polymerases/genetics/*metabolism ; Escherichia coli/enzymology/genetics ; Molecular Sequence Data ; Mutation ; Nucleic Acid Conformation ; Nucleotides/metabolism ; RNA, Bacterial/*genetics/metabolism ; *Terminator Regions, Genetic ; *Transcription, Genetic ; Uridine Triphosphate/metabolism
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-05-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chiu, N -- Barry, T -- Puskin, J -- Nelson, N -- New York, N.Y. -- Science. 1994 May 27;264(5163):1239-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8191276" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Neoplasms, Radiation-Induced/*etiology ; Radon/*adverse effects ; Risk Factors ; United States ; United States Environmental Protection Agency ; Water Pollutants, Radioactive/*adverse effects ; *Water Supply
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  • 32
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-30
    Description: The cellular proto-oncogene c-myc is involved in cell proliferation and transformation but is also implicated in the induction of programmed cell death (apoptosis). The same characteristics have been described for the tumor suppressor gene p53, the most commonly mutated gene in human cancer. In quiescent mouse fibroblasts expressing wild-type p53 protein, activation of c-Myc was found to induce apoptosis and cell cycle reentry, preceded by stabilization of p53. In contrast, in quiescent p53-null fibroblasts, activation of c-Myc induced cell cycle reentry but not apoptosis. These results suggest that p53 mediates apoptosis as a safeguard mechanism to prevent cell proliferation induced by oncogene activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hermeking, H -- Eick, D -- New York, N.Y. -- Science. 1994 Sep 30;265(5181):2091-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Klinische Molekularbiologie und Tumorgenetik Forschungszentrum fur Umwelt und Gesundheit, GSF, Munchen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091232" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; *Apoptosis ; Cell Line ; Estradiol/pharmacology ; G1 Phase ; Gene Expression Regulation ; Genes, myc ; Genes, p53 ; Mice ; Proto-Oncogene Proteins c-myc/*metabolism ; Tamoxifen/analogs & derivatives/pharmacology ; Transfection ; Tumor Suppressor Protein p53/*metabolism
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  • 33
    Publication Date: 1994-04-29
    Description: In a search for genes that regulate circadian rhythms in mammals, the progeny of mice treated with N-ethyl-N-nitrosourea (ENU) were screened for circadian clock mutations. A semidominant mutation, Clock, that lengthens circadian period and abolishes persistence of rhythmicity was identified. Clock segregated as a single gene that mapped to the midportion of mouse chromosome 5, a region syntenic to human chromosome 4. The power of ENU mutagenesis combined with the ability to clone murine genes by map position provides a generally applicable approach to study complex behavior in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3839659/" 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/PMC3839659/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vitaterna, M H -- King, D P -- Chang, A M -- Kornhauser, J M -- Lowrey, P L -- McDonald, J D -- Dove, W F -- Pinto, L H -- Turek, F W -- Takahashi, J S -- P30-CA07175/CA/NCI NIH HHS/ -- R01-DK40493/DK/NIDDK NIH HHS/ -- T32 NS071040/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- etc. -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):719-25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171325" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Chromosomes, Human, Pair 4 ; Circadian Rhythm/*genetics ; Ethylnitrosourea ; Female ; *Genes ; Genotype ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; *Mutagenesis ; Phenotype
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  • 34
    Publication Date: 1994-03-18
    Description: Engagement of antigen receptor complexes induces rapid activation of Src-family kinases and association with phosphatidylinositol-3' kinase (PI-3 kinase). Here it was found that the Src homology 3 (SH3) domain of Lyn and Fyn bound to a proline-rich region (residues 84 to 99) within the 85-kilodalton subunit (p85) of PI-3 kinase. The binding of SH3 to the purified kinase led to a five- to sevenfold increase in the specific activity of PI-3 kinase. Ligand-induced receptor stimulation activated PI-3 kinase, and this activation was blocked by a peptide containing residues 84 to 99 of p85. These data demonstrate a mechanism for PI-3 kinase activation and show that binding of SH3 domains to proline-rich target sequences can regulate enzymatic activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pleiman, C M -- Hertz, W M -- Cambier, J C -- A120519/PHS HHS/ -- A121768/PHS HHS/ -- A129903/PHS HHS/ -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1609-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128248" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/*enzymology ; Enzyme Activation ; Lymphocyte Activation ; Mice ; Molecular Sequence Data ; Peptide Fragments/pharmacology ; Phosphatidylinositol 3-Kinases ; Phosphotransferases (Alcohol Group Acceptor)/chemistry/*metabolism ; Proline/chemistry ; Protein-Tyrosine Kinases/chemistry/*metabolism ; Proto-Oncogene Proteins/chemistry/*metabolism ; Proto-Oncogene Proteins c-fyn ; *src-Family Kinases
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-05-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshland, D E Jr -- New York, N.Y. -- Science. 1994 May 13;264(5161):887.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178141" target="_blank"〉PubMed〈/a〉
    Keywords: Employment ; *Health Care Reform ; *Research ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Borstel, R C -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1144-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7832907" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Anticarcinogenic Agents ; *Antimutagenic Agents ; Carcinogenicity Tests/*statistics & numerical data ; DNA Repair ; Humans ; Mice
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-05-20
    Description: A predictive rule for protein folding is presented that involves two recurrent glycine-based motifs that cap the carboxyl termini of alpha helices. In proteins, helices that terminated in glycine residues were found predominantly in one of these two motifs. These glycine structures had a characteristic pattern of polar and apolar residues. Visual inspection of known helical sequences was sufficient to distinguish the two motifs from each other and from internal glycines that fail to terminate helices. These glycine motifs--in which the local sequence selects between available structures--represent an example of a stereochemical rule for protein folding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aurora, R -- Srinivasan, R -- Rose, G D -- GM 29458/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 May 20;264(5162):1126-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178170" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Glycine/*chemistry ; Hydrogen Bonding ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Oligopeptides/chemistry ; *Protein Folding ; *Protein Structure, Secondary
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mervis, J -- New York, N.Y. -- Science. 1994 Sep 9;265(5178):1516-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8079162" target="_blank"〉PubMed〈/a〉
    Keywords: Budgets ; Facility Design and Construction/*economics ; Financing, Government ; Government Agencies/*economics ; Laboratories/*economics ; National Institutes of Health (U.S.)/*economics ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-02-11
    Description: The TAFII250 subunit of the human transcription factor IID (TFIID) rescues the temperature-sensitive hamster cell line ts13 and overcomes a G1 arrest. Investigation of the transcriptional properties of ts13 nuclear extracts in vitro showed that activation by the site-specific regulators Sp1 and Gal4VP16 is temperature sensitive in ts13 extracts, whereas basal transcription remains unaffected. This transcriptional defect can be rescued by purified human TFIID or by expression of wild-type TAFII250 in ts13 cells. Expression from the cyclin A but not c-fos promoter is temperature sensitive in these mutant cells. Thus, the mutation in TAFII250 appears to have gene-specific effects that may lead to the ts13 cell cycle phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, E H -- Tjian, R -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):811-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303298" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cyclins/genetics ; DNA-Binding Proteins/*genetics/physiology ; Fungal Proteins/physiology ; *G1 Phase ; Genes, fos ; Genetic Complementation Test ; Genetic Vectors ; Histone Acetyltransferases ; Humans ; Mutation ; Nuclear Proteins/*genetics/physiology ; *Promoter Regions, Genetic ; Sp1 Transcription Factor/physiology ; *TATA-Binding Protein Associated Factors ; Temperature ; Trans-Activators/physiology ; Transcription Factor TFIID ; Transcription Factors/pharmacology ; *Transcription, Genetic ; Transfection
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Portier, C J -- Lucier, G W -- Edler, L -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1141-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests/*statistics & numerical data ; Carcinogens/*administration & dosage/toxicity ; DNA Damage ; Dose-Response Relationship, Drug ; Environmental Exposure ; Humans ; Neoplasms/*chemically induced ; Risk Assessment ; Tetrachlorodibenzodioxin/adverse effects ; United States ; United States Environmental Protection Agency
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  • 41
    Publication Date: 1994-04-29
    Description: To facilitate molecular genetic analysis of vertebrate development, haploid genetics was used to construct a recombination map for the zebrafish Danio (Brachydanio) rerio. The map consists of 401 random amplified polymorphic DNAs (RAPDs) and 13 simple sequence repeats spaced at an average interval of 5.8 centimorgans. Strategies that exploit the advantages of haploid genetics and RAPD markers were developed that quickly mapped lethal and visible mutations and that placed cloned genes on the map. This map is useful for the position-based cloning of mutant genes, the characterization of chromosome rearrangements, and the investigation of evolution in vertebrate genomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Postlethwait, J H -- Johnson, S L -- Midson, C N -- Talbot, W S -- Gates, M -- Ballinger, E W -- Africa, D -- Andrews, R -- Carl, T -- Eisen, J S -- 1RO1AI26734/AI/NIAID NIH HHS/ -- HD07470/HD/NICHD NIH HHS/ -- NS23915/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):699-703.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neurosciences, University of Oregon, Eugene 97403.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171321" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Cloning, Molecular ; Female ; Genetic Markers ; Genotype ; Male ; Mutation ; Phenotype ; Polymerase Chain Reaction ; Repetitive Sequences, Nucleic Acid ; Software ; Zebrafish/*genetics
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-03
    Description: Two Arabidopsis thaliana genes, QRT1 and QRT2, are required for pollen separation during normal development. In qrt mutants, the outer walls of the four meiotic products of the pollen mother cell are fused, and pollen grains are released in tetrads. Pollen is viable and fertile, and the cytoplasmic pollen contents are discrete. Pollination with a single tetrad usually yields four seeds, and genetic analysis confirmed that marker loci segregate in a 2:2 ratio within these tetrads. These mutations allow tetrad analysis to be performed in Arabidopsis and define steps in pollen cell wall development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Preuss, D -- Rhee, S Y -- Davis, R W -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1458-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Stanford University, CA 94305-5307.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8197459" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*genetics/physiology/ultrastructure ; Cell Wall/ultrastructure ; Chromosome Mapping ; *Genes, Plant ; Genetic Markers ; Glucuronidase/genetics ; Heterozygote ; Meiosis ; Microscopy, Electron, Scanning ; Mutation ; Phenotype ; Pollen/*physiology/ultrastructure
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-12-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, C -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7992042" target="_blank"〉PubMed〈/a〉
    Keywords: Biology/education ; Education/*standards ; Educational Measurement ; Science/*education ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mervis, J -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):752.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303289" target="_blank"〉PubMed〈/a〉
    Keywords: Financing, Government ; Government Agencies/economics ; National Institutes of Health (U.S.)/economics ; *Research Support as Topic ; Science ; United States
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  • 45
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, F E -- Pan, K M -- Huang, Z -- Baldwin, M -- Fletterick, R J -- Prusiner, S B -- New York, N.Y. -- Science. 1994 Apr 22;264(5158):530-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco 94143-0518.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7909169" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Mice ; Mice, Transgenic ; Models, Biological ; Mutation ; PrPSc Proteins ; Prion Diseases/*metabolism/transmission ; Prions/*biosynthesis/chemistry/genetics/metabolism ; Protein Conformation ; Protein Structure, Secondary
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, C -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1318.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973717" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Financing, Government ; *Genetic Engineering ; Humans ; National Institutes of Health (U.S.)/*economics ; Neoplasms/*genetics ; *Research Support as Topic ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mervis, J -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):744-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303284" target="_blank"〉PubMed〈/a〉
    Keywords: *Budgets ; *Financing, Government ; Government Agencies/economics ; Human Genome Project/economics ; National Institutes of Health (U.S.)/*economics ; *Research Support as Topic ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-01-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mervis, J -- Anderson, C -- Marshall, E -- New York, N.Y. -- Science. 1994 Jan 14;263(5144):164-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8284665" target="_blank"〉PubMed〈/a〉
    Keywords: *Budgets ; Government Agencies/economics ; National Institutes of Health (U.S.)/*economics ; *Research Support as Topic ; United States
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  • 49
    Publication Date: 1994-04-01
    Description: Fetal cardiomyocytes isolated from transgenic mice carrying a fusion gene of the alpha-cardiac myosin heavy chain promoter with a beta-galactosidase reporter were examined for their ability to form stable intracardiac grafts. Embryonic day 15 transgenic cardiomyocytes delivered directly into the myocardium of syngeneic hosts formed stable grafts, as identified by nuclear beta-galactosidase activity. Grafted cardiomyocytes were observed as long as 2 months after implantation, the latest date assayed. Intracardiac graft formation did not induce overtly negative effects on the host myocardium and was not associated with chronic immune rejection. Electron microscopy revealed the presence of nascent intercalated disks connecting the engrafted fetal cardiomyocytes and the host myocardium. These results suggest that intracardiac grafting might provide a useful approach for myocardial repair, provided that the grafted cells can contribute to myocardial function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soonpaa, M H -- Koh, G Y -- Klug, M G -- Field, L J -- HL45453/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):98-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis 46202-4800.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8140423" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Communication ; Cell Differentiation ; Cell Nucleus/metabolism ; *Cell Transplantation ; DNA/biosynthesis ; DNA Primers ; Electrocardiography ; Fetal Heart/*cytology ; *Fetal Tissue Transplantation ; Gap Junctions/physiology/ultrastructure ; Genetic Markers ; Heart/physiology ; Intercellular Junctions/physiology/*ultrastructure ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Myocardium/*cytology/ultrastructure ; beta-Galactosidase/analysis
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fochtmann, L J -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):953.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973669" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; National Institutes of Health (U.S.) ; *Research ; Research Personnel/*economics ; *Research Support as Topic ; United States
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  • 51
    Publication Date: 1994-01-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉St George-Hyslop, P -- McLachlan, D C -- Tsuda, T -- Rogaev, E -- Karlinsky, H -- Lippa, C F -- Pollen, D -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):537.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8290965" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics ; Amyloid beta-Protein Precursor/*genetics ; Apolipoprotein E4 ; Apolipoproteins E/*genetics ; Genotype ; Humans ; Mutation ; Phenotype
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1371-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073270" target="_blank"〉PubMed〈/a〉
    Keywords: Centers for Disease Control and Prevention (U.S.) ; Drug Approval ; Drug Industry ; Humans ; Institute of Medicine (U.S.) ; National Institutes of Health (U.S.) ; *Research ; Research Support as Topic ; United States ; *Vaccines ; World Health Organization
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weissmann, C -- New York, N.Y. -- Science. 1994 Apr 22;264(5158):528-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Molecularbiologie I, Universitat Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7909168" target="_blank"〉PubMed〈/a〉
    Keywords: Aspartic Acid/analogs & derivatives/metabolism ; Fungal Proteins/chemistry/*genetics ; Genes, Fungal ; Glutathione Peroxidase ; Mutation ; PrPSc Proteins ; Prions/chemistry/genetics ; Protein Conformation ; Saccharomyces cerevisiae/*genetics/metabolism ; *Saccharomyces cerevisiae Proteins
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wennberg, J E -- Barry, M J -- New York, N.Y. -- Science. 1994 May 6;264(5160):758-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7513442" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Male ; *Outcome Assessment (Health Care) ; Prostatectomy ; Prostatic Hyperplasia/surgery ; Randomized Controlled Trials as Topic ; United States ; United States Agency for Healthcare Research and Quality
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  • 55
    Publication Date: 1994-04-29
    Description: A gene, reaper (rpr), that appears to play a central control function for the initiation of programmed cell death (apoptosis) in Drosophila was identified. Virtually all programmed cell death that normally occurs during Drosophila embryogenesis was blocked in embryos homozygous for a small deletion that includes the reaper gene. Mutant embryos contained many extra cells and failed to hatch, but many other aspects of development appeared quite normal. Deletions that include reaper also protected embryos from apoptosis caused by x-irradiation and developmental defects. However, high doses of x-rays induced some apoptosis in mutant embryos, and the resulting corpses were phagocytosed by macrophages. These data suggest that the basic cell death program is intact although it was not activated in mutant embryos. The DNA encompassed by the deletion was cloned and the reaper gene was identified on the basis of the ability of cloned DNA to restore apoptosis to cell death defective embryos in germ line transformation experiments. The reaper gene appears to encode a small peptide that shows no homology to known proteins, and reaper messenger RNA is expressed in cells destined to undergo apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, K -- Grether, M E -- Abrams, J M -- Young, L -- Farrell, K -- Steller, H -- 5 F32 NS08536/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):677-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Brain and Cognitive Sciences, Cambridge, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171319" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apoptosis/*genetics ; Base Sequence ; Cloning, Molecular ; DNA Primers ; Drosophila/cytology/embryology/*genetics ; *Drosophila Proteins ; Embryo, Nonmammalian/cytology ; *Genes, Insect ; Models, Genetic ; Molecular Sequence Data ; Mutation ; Nervous System/cytology ; Neurons/cytology ; Peptides/chemistry/*genetics/physiology
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-03-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1678.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8134829" target="_blank"〉PubMed〈/a〉
    Keywords: Hospital Bed Capacity ; *Hospitals, Federal ; *National Institutes of Health (U.S.) ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-07-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Friend, S -- New York, N.Y. -- Science. 1994 Jul 15;265(5170):334-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MGH Cancer Center, Massachusetts General Hospital, Charlestown.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023155" target="_blank"〉PubMed〈/a〉
    Keywords: Crystallization ; Crystallography, X-Ray ; DNA/metabolism ; Genes, p53 ; Hydrogen Bonding ; Mutation ; *Protein Conformation ; Protein Structure, Secondary ; Tumor Suppressor Protein p53/*chemistry/genetics/metabolism
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-03-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1364-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128215" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome/history ; Financing, Government/history ; History, 20th Century ; Humans ; National Institutes of Health (U.S.)/economics/history/*organization & ; administration ; *Research/history ; Research Support as Topic/history ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-22
    Description: A cytoplasmically inherited element, [URE3], allows yeast to use ureidosuccinate in the presence of ammonium ion. Chromosomal mutations in the URE2 gene produce the same phenotype. [URE3] depends for its propagation on the URE2 product (Ure2p), a negative regulator of enzymes of nitrogen metabolism. Saccharomyces cerevisiae strains cured of [URE3] with guanidium chloride were shown to return to the [URE3]-carrying state without its introduction from other cells. Overproduction of Ure2p increased the frequency with which a strain became [URE3] by 100-fold. In analogy to mammalian prions, [URE3] may be an altered form of Ure2p that is inactive for its normal function but can convert normal Ure2p to the altered form. The genetic evidence presented here suggests that protein-based inheritance, involving a protein unrelated to the mammalian prion protein, can occur in a microorganism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickner, R B -- New York, N.Y. -- Science. 1994 Apr 22;264(5158):566-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7909170" target="_blank"〉PubMed〈/a〉
    Keywords: Aspartic Acid/analogs & derivatives/metabolism ; Base Sequence ; Crosses, Genetic ; Fungal Proteins/chemistry/*genetics/metabolism ; Genes, Dominant ; Genes, Fungal ; Genes, Recessive ; Glutathione Peroxidase ; Guanidine ; Guanidines/pharmacology ; Molecular Sequence Data ; Mutation ; Phenotype ; Plasmids ; PrPSc Proteins ; Prions/chemistry/genetics/metabolism ; Saccharomyces cerevisiae/*genetics/metabolism ; *Saccharomyces cerevisiae Proteins
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  • 60
    Publication Date: 1994-05-13
    Description: Many tumors express tumor-specific antigens capable of being presented to CD8+ T cells by major histocompatibility complex (MHC) class I molecules. Antigen presentation models predict that the tumor cell itself should present these antigens to T cells. However, when conditions for the priming of tumor-specific responses were examined in mice, no detectable presentation of MHC class I-restricted tumor antigens by the tumor itself was found. Rather, tumor antigens were exclusively presented by host bone marrow-derived cells. Thus, MHC class I-restricted antigens are efficiently transferred in vivo to bone marrow-derived antigen-presenting cells, which suggests that human leukocyte antigen matching may be less critical in the application of tumor vaccines than previously thought.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, A Y -- Golumbek, P -- Ahmadzadeh, M -- Jaffee, E -- Pardoll, D -- Levitsky, H -- New York, N.Y. -- Science. 1994 May 13;264(5161):961-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7513904" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/*immunology ; Antigens, Neoplasm/*immunology ; Bone Marrow/immunology ; Bone Marrow Cells ; Colonic Neoplasms/immunology ; Epitopes ; Female ; Granulocyte-Macrophage Colony-Stimulating Factor/genetics/immunology ; H-2 Antigens/immunology ; Histocompatibility Antigens Class I/*immunology ; Melanoma, Experimental/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nucleocapsid Proteins ; *Nucleoproteins ; T-Lymphocytes, Cytotoxic/*immunology ; Tumor Cells, Cultured ; Viral Core Proteins/immunology
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  • 61
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawler, A -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1315.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973716" target="_blank"〉PubMed〈/a〉
    Keywords: Copyright/*legislation & jurisprudence ; United States
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  • 62
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-02-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):600-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303261" target="_blank"〉PubMed〈/a〉
    Keywords: Clinical Trials as Topic ; Control Groups ; Double-Blind Method ; Federal Government ; *Fetal Research ; *Fetal Tissue Transplantation ; Financing, Government ; Humans ; National Institutes of Health (U.S.) ; Parkinson Disease/*surgery ; Peer Review, Research ; Research Subjects ; Research Support as Topic ; Risk Assessment ; United States
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  • 63
    Publication Date: 1994-09-23
    Description: The proposal that nitric oxide (NO) or its reactant products mediate toxicity in brain remains controversial in part because of the use of nonselective agents that block NO formation in neuronal, glial, and vascular compartments. In mutant mice deficient in neuronal NO synthase (NOS) activity, infarct volumes decreased significantly 24 and 72 hours after middle cerebral artery occlusion, and the neurological deficits were less than those in normal mice. This result could not be accounted for by differences in blood flow or vascular anatomy. However, infarct size in the mutant became larger after endothelial NOS inhibition by nitro-L-arginine administration. Hence, neuronal NO production appears to exacerbate acute ischemic injury, whereas vascular NO protects after middle cerebral artery occlusion. The data emphasize the importance of developing selective inhibitors of the neuronal isoform.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Z -- Huang, P L -- Panahian, N -- Dalkara, T -- Fishman, M C -- Moskowitz, M A -- NS10828/NS/NINDS NIH HHS/ -- NS2636/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1883-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stroke Research Laboratory, Massachusetts General Hospital, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7522345" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/antagonists & inhibitors/deficiency/*metabolism ; Animals ; Arginine/analogs & derivatives/pharmacology ; Brain/enzymology/*metabolism ; Brain Ischemia/complications/*metabolism ; Cerebral Infarction/*etiology ; Cerebrovascular Circulation ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutation ; Neurons/*enzymology ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase ; Nitroarginine
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  • 64
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-22
    Description: Many recent studies have implicated dietary factors in the cause and prevention of important diseases, including cancer, coronary heart disease, birth defects, and cataracts. There is strong evidence that vegetables and fruits protect against these diseases; however, the active constituents are incompletely identified. Whether fat per se is a major cause of disease is a question still under debate, although saturated and partially hydrogenated fats probably increase the risk of coronary heart disease. One clear conclusion from existing epidemiologic evidence is that many individuals in the United States have suboptimal diets and that the potential for disease prevention by improved nutrition is substantial.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willett, W C -- New York, N.Y. -- Science. 1994 Apr 22;264(5158):532-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Nutrition, Harvard School of Public Health, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8160011" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Coronary Disease/etiology/prevention & control ; Dairy Products ; *Diet ; Dietary Carbohydrates/administration & dosage ; Dietary Fats/administration & dosage ; Dietary Proteins/administration & dosage ; Female ; Fruit ; Humans ; Male ; Neoplasms/etiology/prevention & control ; *Nutritional Physiological Phenomena ; *Preventive Medicine ; United States ; Vegetables
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  • 65
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-03-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Mar 4;263(5151):1225-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8122104" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Science Disciplines ; Data Collection ; Educational Status ; *Health Knowledge, Attitudes, Practice ; Humans ; United States
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  • 66
    Publication Date: 1994-08-19
    Description: A small molecule called PD 153035 inhibited the epidermal growth factor (EGF) receptor tyrosine kinase with a 5-pM inhibition constant. The inhibitor was specific for the EGF receptor tyrosine kinase and inhibited other purified tyrosine kinases only at micromolar or higher concentrations. PD 153035 rapidly suppressed autophosphorylation of the EGF receptor at low nanomolar concentrations in fibroblasts or in human epidermoid carcinoma cells and selectively blocked EGF-mediated cellular processes including mitogenesis, early gene expression, and oncogenic transformation. PD 153035 demonstrates an increase in potency over that of other tyrosine kinase inhibitors of four to five orders of magnitude for inhibition of isolated EGF receptor tyrosine kinase and three to four orders of magnitude for inhibition of cellular phosphorylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fry, D W -- Kraker, A J -- McMichael, A -- Ambroso, L A -- Nelson, J M -- Leopold, W R -- Connors, R W -- Bridges, A J -- New York, N.Y. -- Science. 1994 Aug 19;265(5175):1093-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Parke-Davis Pharmaceutical Research, Division of Warner-Lambert Company, Ann Arbor, MI 48105.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066447" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Cell Transformation, Neoplastic/drug effects ; Epidermal Growth Factor/pharmacology ; Fibroblast Growth Factor 2/pharmacology ; Gene Expression/drug effects ; Humans ; Kinetics ; Mice ; Mitosis/drug effects ; Phosphorylation/drug effects ; Platelet-Derived Growth Factor/pharmacology ; Protein-Tyrosine Kinases/antagonists & inhibitors ; Quinazolines/*antagonists & inhibitors ; Receptor, Epidermal Growth Factor/*antagonists & inhibitors ; Tumor Cells, Cultured ; Tyrosine/metabolism
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  • 67
    Publication Date: 1994-06-03
    Description: The low density lipoprotein receptor-related protein (LRP) has been proposed to mediate in concert with the LDL receptor (LDLR) the uptake of dietary lipoproteins into the hepatocytes. This hypothesis was tested by transient inactivation of LRP in vivo. Receptor-associated protein (RAP), a dominant negative regulator of LRP function, was transferred by an adenoviral vector to the livers of mice lacking LDLR (LDLR-/-). The inactivation of LRP by RAP was associated with a marked accumulation of chylomicron remnants in LDLR-/- mice and to a lesser degree in normal mice, suggesting that both LDLR and LRP are involved in remnant clearance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willnow, T E -- Sheng, Z -- Ishibashi, S -- Herz, J -- HL20948/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1471-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7515194" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Animals ; Apolipoprotein B-48 ; Apolipoproteins B/*metabolism ; Carrier Proteins/genetics/*physiology ; Cholesterol/blood ; Chylomicrons/blood/*metabolism ; Gene Transfer Techniques ; Genetic Vectors ; Glycoproteins/genetics/*physiology ; LDL-Receptor Related Protein-Associated Protein ; Liver/*metabolism ; Low Density Lipoprotein Receptor-Related Protein-1 ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Immunologic/antagonists & inhibitors/*metabolism ; Receptors, LDL/metabolism ; Triglycerides/blood ; alpha-Macroglobulins/metabolism
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  • 68
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):754-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303290" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caenorhabditis elegans/genetics ; Caspase 1 ; Cells, Cultured ; Free Radicals/metabolism ; Metalloendopeptidases/*genetics/metabolism ; Mice ; Mice, Knockout ; Neurons/cytology ; Oxygen/metabolism ; Proto-Oncogene Proteins/genetics/physiology ; Proto-Oncogene Proteins c-bcl-2 ; Rats ; bcl-2-Associated X Protein ; bcl-X Protein
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  • 69
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stevens, J E -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):24-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8140414" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/epidemiology/*prevention & control ; Female ; Government Agencies ; Health Education ; Health Knowledge, Attitudes, Practice ; *Health Promotion ; Humans ; Indonesia/epidemiology ; Male ; United States ; World Health Organization
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  • 70
    Publication Date: 1994-10-07
    Description: In this study, a protein that interacts with sequences encoded by the first exon of the protein kinase Bcr was cloned. The Bcr-associated protein 1 (Bap-1) is a member of the 14-3-3 family of proteins. Bap-1 interacts with full-length c-Bcr and with the chimeric Bcr-Abl tyrosine kinase of Philadelphia chromosome (Ph1)-positive human leukemias. Bap-1 is a substrate for the Bcr serine-threonine kinase and is also phosphorylated on tyrosine by Bcr-Abl but not by c-Abl. Bap-1 may function in the regulation of c-Bcr and may contribute to the transforming activity of Bcr-Abl in vivo. 14-3-3 proteins are essential for cell proliferation and have a role in determining the timing of mitosis in yeast. Through direct binding to sequences present in Bcr and in other proteins implicated in signaling, the mammalian 14-3-3 proteins may link specific signaling protein components to mitogenic and cell-cycle control pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reuther, G W -- Fu, H -- Cripe, L D -- Collier, R J -- Pendergast, A M -- CA61033/CA/NCI NIH HHS/ -- DK01965/DK/NIDDK NIH HHS/ -- GM07184/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Oct 7;266(5182):129-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939633" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Animals ; Cell Division ; Cell Line ; Cell Transformation, Neoplastic ; Fusion Proteins, bcr-abl/*metabolism ; Humans ; Mice ; Phosphorylation ; Poly(ADP-ribose) Polymerases/metabolism ; Protein-Tyrosine Kinases/*metabolism ; Proteins/isolation & purification/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-bcr ; Rats ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; *Tyrosine 3-Monooxygenase
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  • 71
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-10-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolff, M S -- Landrigan, P J -- New York, N.Y. -- Science. 1994 Oct 28;266(5185):526-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7818673" target="_blank"〉PubMed〈/a〉
    Keywords: Body Burden ; Breast Neoplasms/*chemically induced/epidemiology ; DDT/*adverse effects ; Dichlorodiphenyl Dichloroethylene/analysis ; Environmental Exposure/adverse effects ; Environmental Pollutants/*adverse effects ; Female ; Humans ; Pesticide Residues/analysis ; United States
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  • 72
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-01-07
    Description: Heterotrimeric guanosine triphosphate (GTP)-binding proteins (G proteins) may participate in membrane traffic events. A complementary DNA (cDNA) was isolated from a mouse pituitary cDNA library that corresponded to an alternatively spliced form of the gene encoding the G protein alpha subunit G alpha i2. The cDNA was identical to that encoding G alpha i2 except that the region encoding for the carboxyl-terminal 24 amino acids was replaced by a longer region encoding 35 amino acids that have no sequence similarity with G alpha i2 or other members of the G protein family. This alternative spliced product and the corresponding protein (sGi2) were present in several tissues. Specific antibodies revealed that sGi2 was localized in the Golgi apparatus, suggesting a role in membrane transport. Thus, alternative splicing may generate from a single gene two G protein alpha subunits with differential cellular localization and function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montmayeur, J P -- Borrelli, E -- New York, N.Y. -- Science. 1994 Jan 7;263(5143):95-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes, CNRS, INSERM U184, Faculte de Medecine, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8272874" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cell Membrane/metabolism ; Coatomer Protein ; DNA, Complementary/genetics ; GTP-Binding Protein alpha Subunit, Gi2 ; *GTP-Binding Protein alpha Subunits, Gi-Go ; GTP-Binding Proteins/analysis/chemistry/genetics/*metabolism ; Golgi Apparatus/chemistry/*metabolism ; Mice ; Microtubule-Associated Proteins/analysis ; Molecular Sequence Data ; Oncogene Proteins/analysis/chemistry/genetics/*metabolism ; *Proto-Oncogene Proteins
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  • 73
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-01-14
    Description: Comparative studies suggest that sex chromosomes begin as ordinary autosomes that happen to carry a major sex determining locus. Over evolutionary time the Y chromosome is selected to stop recombining with the X chromosome, perhaps in response to accumulation of alleles beneficial to the heterogametic but harmful to the homogametic sex. Population genetic theory predicts that a nonrecombining Y chromosome should degenerate. Here this prediction is tested by application of specific selection pressures to Drosophila melanogaster populations. Results demonstrate the decay of a nonrecombining, nascent Y chromosome and the capacity for recombination to ameliorate such decay.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rice, W R -- New York, N.Y. -- Science. 1994 Jan 14;263(5144):230-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, Santa Cruz 95064.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8284674" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crosses, Genetic ; Drosophila melanogaster/*genetics/physiology ; Female ; Haplotypes ; Male ; Mutation ; *Recombination, Genetic ; *Y Chromosome
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  • 74
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monro, A M -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1141.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973684" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests/*statistics & numerical data ; Carcinogens/*administration & dosage/toxicity ; Dose-Response Relationship, Drug ; Female ; Humans ; Male ; Mice ; Mutagenicity Tests ; Neoplasms/*chemically induced ; Rats ; Risk Assessment
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  • 75
    Publication Date: 1994-02-25
    Description: Adult liver has the unusual ability to fully regenerate after injury. Although regeneration is accomplished by the division of mature hepatocytes, the replicative potential of these cells is unknown. Here, the replicative capacity of adult liver cells and their medical usefulness as donor cells for transplantation were investigated by transfer of adult mouse liver cells into transgenic mice that display an endogenous defect in hepatic growth potential and function. The transplanted liver cell populations replaced up to 80 percent of the diseased recipient liver. These findings demonstrate the enormous growth potential of adult hepatocytes, indicating the feasibility of liver cell transplantation as a method to replace lost or diseased hepatic parenchyma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rhim, J A -- Sandgren, E P -- Degen, J L -- Palmiter, R D -- Brinster, R L -- HD-23657/HD/NICHD NIH HHS/ -- HD09172/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1149-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8108734" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Genetic Markers ; Hepatectomy ; Liver/*cytology/physiology ; Liver Diseases/*surgery ; Liver Regeneration ; *Liver Transplantation ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mitotic Index ; Stem Cells/cytology/physiology
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  • 76
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lehrer, S -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):954.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973671" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; National Institutes of Health (U.S.)/*economics ; *Research Support as Topic ; United States
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  • 77
    Publication Date: 1994-03-25
    Description: The Drosophila decapentaplegic (dpp) gene encodes a transforming growth factor-beta (TGF-beta)-like protein that plays a key role in several aspects of development. Transduction of the DPP signal was investigated by cloning of serine-threonine kinase transmembrane receptors from Drosophila because this type of receptor is specific for the TGF-beta-like ligands. Here evidence is provided demonstrating that the Drosophila saxophone (sax) gene, a previously identified female sterile locus, encodes a TGF-beta-like type I receptor. Embryos from sax mothers and dpp embryos exhibit similar mutant phenotypes during early gastrulation, and these two loci exhibit genetic interactions, which suggest that they are utilized in the same pathway. These data suggest that sax encodes a receptor for dpp.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xie, T -- Finelli, A L -- Padgett, R W -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1756-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Waksman Institute, Rutgers University, Piscataway, NJ 08855-0759.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8134837" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; Drosophila/embryology/*genetics/metabolism ; *Drosophila Proteins ; Embryo, Nonmammalian/metabolism ; Female ; *Genes, Insect ; Insect Hormones/genetics/*metabolism ; Male ; Molecular Sequence Data ; Mutation ; Protein-Serine-Threonine Kinases/chemistry/*genetics/metabolism ; Receptors, Transforming Growth Factor beta/chemistry/*genetics/metabolism ; Signal Transduction ; Transforming Growth Factor beta/genetics/*metabolism
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  • 78
    Publication Date: 1994-06-03
    Description: The Arabidopsis ABI1 locus is essential for a wide spectrum of abscisic acid (ABA) responses throughout plant development. Here, ABI1 was shown to regulate stomatal aperture in leaves and mitotic activity in root meristems. The ABI1 gene was cloned and predicted to encode a signaling protein. Although its carboxyl-terminal domain is related to serine-threonine phosphatase 2C, the ABI1 protein has a unique amino-terminal extension containing an EF hand calcium-binding site. These results suggest that the ABI1 protein is a Ca(2+)-modulated phosphatase and functions to integrate ABA and Ca2+ signals with phosphorylation-dependent response pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leung, J -- Bouvier-Durand, M -- Morris, P C -- Guerrier, D -- Chefdor, F -- Giraudat, J -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1448-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut des Sciences Vegetales, Centre National de la Recherche Scientifique UPR 40, Gif-sur-Yvette, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7910981" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid/*pharmacology ; Amino Acid Sequence ; Arabidopsis/chemistry/cytology/*genetics/physiology ; *Arabidopsis Proteins ; Calcium/*metabolism ; Cloning, Molecular ; *Genes, Plant ; Mitosis ; Molecular Sequence Data ; Mutation ; Phenotype ; Phosphoprotein Phosphatases/chemistry/*genetics/*metabolism ; Phosphorylation ; Plants, Genetically Modified ; Polymorphism, Restriction Fragment Length ; Signal Transduction ; Transformation, Genetic
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  • 79
    Publication Date: 1994-02-25
    Description: The T cell antigen receptor (TCR) initiates signals by interacting with cytoplasmic protein tyrosine kinases (PTKs) through a 17-residue sequence motif [called the antigen recognition activation motif (ARAM)] that is contained in the TCR zeta and CD3 chains. TCR stimulation induces the tyrosine phosphorylation of several cellular substrates, including the ARAMs. Lck kinase activity is required for phosphorylation of two conserved tyrosine residues in an ARAM. This phosphorylation leads to the recruitment of a second cytoplasmic PTK, ZAP-70, through both of the ZAP-70 Src homology 2 domains and its phosphorylation. Thus, TCR signal transduction is initiated by the sequential interaction of two PTKs with TCR ARAMs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iwashima, M -- Irving, B A -- van Oers, N S -- Chan, A C -- Weiss, A -- AR-20684/AR/NIAMS NIH HHS/ -- GM39553/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1136-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7509083" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD8/metabolism ; Cell Line ; Cytoplasm/enzymology ; Haplorhini ; Humans ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Membrane Proteins/*metabolism ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Phosphotyrosine ; Protein-Tyrosine Kinases/*metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Signal Transduction ; Tumor Cells, Cultured ; Tyrosine/analogs & derivatives/metabolism ; ZAP-70 Protein-Tyrosine Kinase
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  • 80
    Publication Date: 1994-10-14
    Description: An engineered variant of subtilisin BPN', termed subtiligase, which efficiently ligates esterified peptides in aqueous solution, was used for the complete synthesis of ribonuclease (RNase) A that contains unnatural catalytic residues. Fully active RNase A (124 residues long) was produced in milligram quantities by stepwise ligation of six esterified peptide fragments (each 12 to 30 residues long) at yields averaging 70 percent per ligation. Variants of RNase A were produced in which the catalytic histidines at positions 12 and 119 were substituted with the unnatural amino acid 4-fluorohistidine, which has a pKa of 3.5 compared to 6.8 for histidine. Large changes in the profile of the pH as it affects rate occurred for the single and double mutants with surprisingly little change in the kcat for either the RNA cleavage or hydrolysis steps. The data indicate that these imidazoles function as general acids and bases, but that the proton transfer steps are not rate-limiting when the imidazoles are present in their correct protonation states. These studies indicate the potential of subtiligase for the blockwise synthesis of large proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jackson, D Y -- Burnier, J -- Quan, C -- Stanley, M -- Tom, J -- Wells, J A -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):243-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Protein Engineering, Genentech, Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939659" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Esterification ; Histidine/analogs & derivatives/analysis ; Hydrogen-Ion Concentration ; Molecular Sequence Data ; Mutation ; Nucleotides, Cyclic/metabolism ; Protein Engineering/*methods ; Ribonuclease, Pancreatic/*chemical synthesis/chemistry/isolation & purification ; Subtilisins/chemistry/genetics/*metabolism ; Uridine Monophosphate/metabolism
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  • 81
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-10-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crabbe, J C -- Belknap, J K -- Buck, K J -- New York, N.Y. -- Science. 1994 Oct 21;266(5184):352-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939673" target="_blank"〉PubMed〈/a〉
    Keywords: Alcoholism/genetics ; Animals ; Chromosome Mapping ; Mice ; Receptors, Dopamine D2/*genetics/physiology
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  • 82
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-01-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1994 Jan 28;263(5146):459.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8290947" target="_blank"〉PubMed〈/a〉
    Keywords: HIV/*isolation & purification ; History, 20th Century ; *Scientific Misconduct ; United States
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  • 83
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-23
    Description: The functional consequences of single proton transfers occurring in the pore of a cyclic nucleotide-gated channel were observed with patch recording techniques. These results led to three conclusions about the chemical nature of ion binding sites in the conduction pathway: The channel contains two identical titratable sites, even though there are more than two (probably four) identical subunits; the sites are formed by glutamate residues that have a pKa (where K(a) is the acid constant) of 7.6; and protonation of one site does not perturb the pKa of the other. These properties point to an unusual arrangement of carboxyl side-chain residues in the pore of a cation channel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Root, M J -- MacKinnon, R -- 5 T32 GM083113/GM/NIGMS NIH HHS/ -- GM47400/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1852-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7522344" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Calcium Channels/metabolism ; Catfishes ; Electric Conductivity ; Hydrogen-Ion Concentration ; Ion Channel Gating ; Ion Channels/chemistry/genetics/*metabolism ; Kinetics ; Molecular Sequence Data ; Mutation ; *Protons ; Sodium/metabolism ; Xenopus
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  • 84
    Publication Date: 1994-06-24
    Description: Mice lacking the known subunit of the type I interferon (IFN) receptor were completely unresponsive to type I IFNs, suggesting that this receptor chain is essential for type I IFN-mediated signal transduction. These mice showed no overt anomalies but were unable to cope with viral infections, despite otherwise normal immune responses. Comparison of mice lacking either type I or type II IFN receptors showed that, at least in response to some viruses, both IFN systems are essential for antiviral defense and are functionally nonredundant.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, U -- Steinhoff, U -- Reis, L F -- Hemmi, S -- Pavlovic, J -- Zinkernagel, R M -- Aguet, M -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1918-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biology I, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009221" target="_blank"〉PubMed〈/a〉
    Keywords: Alphavirus Infections/immunology ; Animals ; Antibodies, Viral/biosynthesis ; Disease Susceptibility ; Immunity, Innate ; Interferon Type I/*physiology ; Interferon-gamma/*physiology ; Lymphocytic Choriomeningitis/immunology ; Membrane Proteins ; Mice ; Mutation ; Receptor, Interferon alpha-beta ; Receptors, Interferon/genetics/*physiology ; Rhabdoviridae Infections/immunology ; Semliki forest virus ; Signal Transduction ; T-Lymphocytes/immunology ; Vesicular stomatitis Indiana virus ; Virus Diseases/*immunology
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  • 85
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, A -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1376-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073274" target="_blank"〉PubMed〈/a〉
    Keywords: Child ; *Child Welfare ; Child, Preschool ; *Developing Countries ; *Global Health ; Humans ; *Immunization Programs ; Infant ; Research ; United Nations ; United States ; *Vaccines, Combined
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  • 86
    Publication Date: 1994-12-09
    Description: Cystic fibrosis (CF) is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). A potential animal model of CF, the CFTR-/- mouse, has had limited utility because most mice die from intestinal obstruction during the first month of life. Human CFTR (hCFTR) was expressed in CFTR-/- mice under the control of the rat intestinal fatty acid-binding protein gene promoter. The mice survived and showed functional correction of ileal goblet cell and crypt cell hyperplasia and cyclic adenosine monophosphate-stimulated chloride secretion. These results support the concept that transfer of the hCFTR gene may be a useful strategy for correcting physiologic defects in patients with CF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, L -- Dey, C R -- Wert, S E -- DuVall, M D -- Frizzell, R A -- Whitsett, J A -- DK38518/DK/NIDDK NIH HHS/ -- HL49004/HL/NHLBI NIH HHS/ -- HL51832/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1705-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Hospital Medical Center, Division of Pulmonary Biology, Cincinnati, OH 45229-3039.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7527588" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Carrier Proteins/genetics ; Chlorides/metabolism ; Colforsin/pharmacology ; Colon/chemistry/pathology ; Cystic Fibrosis/genetics/metabolism/pathology/*therapy ; Cystic Fibrosis Transmembrane Conductance Regulator ; Disease Models, Animal ; Fatty Acid-Binding Proteins ; Gene Expression ; *Genetic Therapy ; Humans ; Intestinal Mucosa/chemistry/*pathology/secretion ; Intestine, Small/chemistry/pathology ; Membrane Proteins/analysis/*genetics/physiology ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; *Neoplasm Proteins ; *Nerve Tissue Proteins ; Promoter Regions, Genetic ; RNA, Messenger/analysis/genetics ; Rats ; Recombinant Proteins/biosynthesis ; *Tumor Suppressor Proteins
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  • 87
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-07-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1994 Jul 1;265(5168):19.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8016649" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome ; Humans ; National Institutes of Health (U.S.)/*organization & administration ; *Research ; United States
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  • 88
    Publication Date: 1994-11-11
    Description: Interleukin-2 (IL-2) signaling requires the dimerization of the IL-2 receptor beta.(IL-2R beta) and common gamma (gamma c) chains. Mutations of gamma c can result in X-linked severe combined immunodeficiency (XSCID). IL-2, IL-4, IL-7 (whose receptors are known to contain gamma c), and IL-9 (whose receptor is shown here to contain gamma c) induced the tyrosine phosphorylation and activation of the Janus family tyrosine kinases Jak1 and Jak3. Jak1 and Jak3 associated with IL-2R beta and gamma c, respectively; IL-2 induced Jak3-IL-2R beta and increased Jak3-gamma c associations. Truncations of gamma c, and a gamma c, point mutation causing moderate X-linked combined immunodeficiency (XCID), decreased gamma c-Jak3 association. Thus, gamma c mutations in at least some XSCID and XCID patients prevent normal Jak3 activation, suggesting that mutations of Jak3 may result in an XSCID-like phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Russell, S M -- Johnston, J A -- Noguchi, M -- Kawamura, M -- Bacon, C M -- Friedmann, M -- Berg, M -- McVicar, D W -- Witthuhn, B A -- Silvennoinen, O -- P30 CA21765/CA/NCI NIH HHS/ -- R01 DK42932/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1042-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973658" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Enzyme Activation ; Humans ; Interleukin-2/pharmacology ; Janus Kinase 1 ; Janus Kinase 3 ; Mutation ; Phosphorylation ; Point Mutation ; Protein-Tyrosine Kinases/genetics/*metabolism ; Receptors, Interleukin-2/genetics/*metabolism ; Severe Combined Immunodeficiency/genetics/*immunology/metabolism ; Transfection ; Tyrosine/metabolism
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  • 89
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-12-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zoon, K C -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1626.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7992037" target="_blank"〉PubMed〈/a〉
    Keywords: Drug Industry ; Government Agencies ; Humans ; Military Personnel ; Plague/*prevention & control ; Plague Vaccine/*standards ; United States ; United States Food and Drug Administration
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  • 90
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-02-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bivens, L W -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):593.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303258" target="_blank"〉PubMed〈/a〉
    Keywords: *Biomedical Research ; Federal Government ; *Government Regulation ; *Scientific Misconduct ; United States ; *United States Office of Research Integrity
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  • 91
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Danks, D M -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):13-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8140413" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosomes, Human, Pair 2 ; Colorectal Neoplasms, Hereditary Nonpolyposis/*diagnosis/genetics ; *Genetic Testing ; Humans ; Mutation
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  • 92
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-17
    Description: Modern molecular genetic and genomic approaches are revolutionizing the study of behavior in the mouse. "Reverse genetics" (from gene to phenotype) with targeted gene transfer provides a powerful tool to dissect behavior and has been used successfully to study the effects of null mutations in genes implicated in the regulation of long-term potentiation and spatial learning in mice. In addition, "forward genetics" (from phenotype to gene) with high-efficiency mutagenesis in the mouse can uncover unknown genes and has been used to isolate a behavioral mutant of the circadian system. With the recent availability of high-density genetic maps and physical mapping resources, positional cloning of virtually any mutation is now feasible in the mouse. Together, these approaches permit a molecular analysis of both known and previously unknown genes regulating behavior.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3830945/" 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/PMC3830945/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahashi, J S -- Pinto, L H -- Vitaterna, M H -- EY08467/EY/NEI NIH HHS/ -- MH39592/MH/NIMH NIH HHS/ -- MH49241/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- etc. -- New York, N.Y. -- Science. 1994 Jun 17;264(5166):1724-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8209253" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Animal ; Circadian Rhythm/genetics ; Female ; *Genetic Techniques ; Genetics, Behavioral/*methods ; Learning ; Long-Term Potentiation ; Male ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Mutagenesis
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  • 93
    Publication Date: 1994-04-15
    Description: The first step in oral absorption of many medically important peptide-based drugs is mediated by an intestinal proton-dependent peptide transporter. This transporter facilitates the oral absorption of beta-lactam antibiotics and angiotensin-converting enzyme inhibitors from the intestine into enterocytes lining the luminal wall. A monoclonal antibody that blocked uptake of cephalexin was used to identify and clone a gene that encodes an approximately 92-kilodalton membrane protein that was associated with the acquisition of peptide transport activity by transport-deficient cells. The amino acid sequence deduced from the complementary DNA sequence of the cloned gene indicated that this transport-associated protein shares several conserved structural elements with the cadherin superfamily of calcium-dependent, cell-cell adhesion proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dantzig, A H -- Hoskins, J A -- Tabas, L B -- Bright, S -- Shepard, R L -- Jenkins, I L -- Duckworth, D C -- Sportsman, J R -- Mackensen, D -- Rosteck, P R Jr -- New York, N.Y. -- Science. 1994 Apr 15;264(5157):430-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN 46285.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8153632" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Transport ; CHO Cells ; Cadherins/*chemistry ; Carrier Proteins/*chemistry/genetics/isolation & purification/metabolism ; Cephalexin/*metabolism ; Cloning, Molecular ; Cricetinae ; Glycosylation ; Humans ; Hydrogen-Ion Concentration ; Intestinal Mucosa/*metabolism ; Leucine/analogs & derivatives/metabolism ; *Membrane Transport Proteins ; Mice ; Mice, Inbred A ; Molecular Sequence Data ; Open Reading Frames ; Sequence Homology, Amino Acid ; Transfection ; Tumor Cells, Cultured
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  • 94
    Publication Date: 1994-07-22
    Description: Two molecular mechanisms of T cell-mediated cytotoxicity, one perforin-based, the other Fas-based, have been demonstrated. To determine the extent of their contribution to T cell-mediated cytotoxicity, a range of effector cells from normal control or perforin-deficient mice were tested against a panel of target cells with various levels of Fas expression. All cytotoxicity observed was due to either of these mechanisms, and no third mechanism was detected. Thus, the perforin- and Fas-based mechanisms may account for all T cell-mediated cytotoxicity in short-term in vitro assays.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kagi, D -- Vignaux, F -- Ledermann, B -- Burki, K -- Depraetere, V -- Nagata, S -- Hengartner, H -- Golstein, P -- New York, N.Y. -- Science. 1994 Jul 22;265(5171):528-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7518614" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD95 ; Antigens, Surface/*immunology ; Cells, Cultured ; Concanavalin A/pharmacology ; *Cytotoxicity, Immunologic ; Ionomycin/pharmacology ; Leukemia L1210 ; Lymphocyte Culture Test, Mixed ; Lymphocytic choriomeningitis virus/immunology ; Membrane Glycoproteins/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Molecular Sequence Data ; Perforin ; Pore Forming Cytotoxic Proteins ; T-Lymphocytes, Cytotoxic/*immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Tumor Cells, Cultured
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 95
    Publication Date: 1994-10-21
    Description: Assembly of antigen receptor V (variable), D (diversity), and J (joining) gene segments requires lymphocyte-specific genes and ubiquitous DNA repair activities. Severe combined immunodeficient (SCID) mice are defective in general double-strand (ds) DNA break repair and V(D)J coding joint formation, resulting in arrested lymphocyte development. A single treatment of newborn SCID mice with DNA-damaging agents restored functional, diverse, T cell receptor beta chain coding joints, as well as development and expansion of thymocytes expressing both CD4 and CD8 coreceptors, but did not promote B cell development. Thymic lymphoma developed in all mice treated with DNA-damaging agents, suggesting an interrelation between V(D)J recombination, dsDNA break repair, and lymphomagenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Danska, J S -- Pflumio, F -- Williams, C J -- Huner, O -- Dick, J E -- Guidos, C J -- New York, N.Y. -- Science. 1994 Oct 21;266(5184):450-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Surgical Research, Hospital for Sick Children Research Institute, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7524150" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; B-Lymphocytes/cytology/immunology ; Base Sequence ; Bleomycin/pharmacology ; Cell Transformation, Neoplastic ; *DNA Damage ; DNA Repair ; Gamma Rays ; *Gene Rearrangement ; Hematopoietic Stem Cells/cytology/immunology ; Lymphoma/etiology/pathology ; Mice ; Mice, SCID ; Molecular Sequence Data ; Receptors, Antigen, T-Cell, alpha-beta/*genetics ; T-Lymphocyte Subsets/cytology/immunology ; T-Lymphocytes/cytology/*immunology ; Thymus Neoplasms/etiology/pathology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
    Publication Date: 1994-09-23
    Description: The neuromodulator serotonin (5-hydroxytryptamine, 5-HT) has been associated with mood disorders such as depression, anxiety, and impulsive violence. To define the contribution of 5-HT receptor subtypes to behavior, mutant mice lacking the 5-HT1B receptor were generated by homologous recombination. These mice did not exhibit any obvious developmental or behavioral defects. However, the hyperlocomotor effect of the 5-HT1A/1B agonist RU24969 was absent in mutant mice, indicating that this effect is mediated by 5-HT1B receptors. Moreover, when confronted with an intruder, mutant mice attacked the intruder faster and more intensely than did wild-type mice, suggesting the participation of 5-HT1B receptors in aggressive behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saudou, F -- Amara, D A -- Dierich, A -- LeMeur, M -- Ramboz, S -- Segu, L -- Buhot, M C -- Hen, R -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1875-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes du CNRS, U184 de l'INSERM, Faculte de Medecine, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091214" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression/*physiology ; Animals ; Brain Chemistry ; Chimera ; Female ; Indoles/pharmacology ; Male ; Mice ; Motor Activity/drug effects ; Mutation ; Pindolol/analogs & derivatives/metabolism ; Receptor, Serotonin, 5-HT1B ; Receptors, Serotonin/analysis/genetics/*physiology ; Recombination, Genetic ; Serotonin Receptor Agonists/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abelson, P H -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1303.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973710" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests ; Diet ; Female ; *Fruit ; *Fungicides, Industrial/toxicity ; Humans ; Male ; Mice ; United States ; United States Environmental Protection Agency ; *Vegetables
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 98
    Publication Date: 1994-11-04
    Description: The therapeutic responsiveness of genetically defined tumors expressing or devoid of the p53 tumor suppressor gene was compared in immunocompromised mice. Tumors expressing the p53 gene contained a high proportion of apoptotic cells and typically regressed after treatment with gamma radiation or adriamycin. In contrast, p53-deficient tumors treated with the same regimens continued to enlarge and contained few apoptotic cells. Acquired mutations in p53 were associated with both treatment resistance and relapse in p53-expressing tumors. These results establish that defects in apoptosis, here caused by the inactivation of p53, can produce treatment-resistant tumors and suggest that p53 status may be an important determinant of tumor response to therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lowe, S W -- Bodis, S -- McClatchey, A -- Remington, L -- Ruley, H E -- Fisher, D E -- Housman, D E -- Jacks, T -- 5R27CA17575/CA/NCI NIH HHS/ -- CA14051/CA/NCI NIH HHS/ -- R01CA40602/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):807-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973635" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Doxorubicin/*therapeutic use ; Drug Resistance ; Fibrosarcoma/drug therapy/*genetics/radiotherapy/*therapy ; *Gamma Rays ; *Genes, p53/genetics ; Immunocompromised Host ; Mice ; Mice, Nude ; Mutation ; Neoplasm Recurrence, Local ; Neoplasm Transplantation ; Radiation Tolerance
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
    Publication Date: 1994-03-04
    Description: The invariant chain (Ii) binds nascent major histocompatibility complex (MHC) class II molecules, blocking peptide binding until the complex dissociates in the endosomes. This may serve to differentiate the MHC class I and II antigen presentation pathways and enable class II molecules to efficiently bind peptides in the endosomes. This hypothesis was addressed by probing spleen cells from a combination of knock-out and transgenic mice with a large panel of T cell hybridomas. The Ii molecule blocked the presentation of a range of endogenously synthesized epitopes, but some epitopes actually required Ii. Thus, the influence of Ii on presentation does not follow simple rules. In addition, mice expressing Ii were not tolerant to epitopes unmasked in its absence, a finding with possible implications for autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bodmer, H -- Viville, S -- Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1994 Mar 4;263(5151):1284-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes du CNRS, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7510069" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigen-Presenting Cells/*immunology ; *Antigens, Differentiation, B-Lymphocyte ; Epitopes/*immunology ; Histocompatibility Antigens Class II/genetics/*immunology ; Hybridomas ; Mice ; Mice, Knockout ; Mice, Transgenic ; Molecular Sequence Data ; Myelin Basic Protein/immunology ; Recombinant Fusion Proteins/immunology ; T-Lymphocytes/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saundry, P D -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):185.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146642" target="_blank"〉PubMed〈/a〉
    Keywords: *Environment ; *Government Agencies ; National Institutes of Health (U.S.) ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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