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  • Articles  (151)
  • Latest Papers from Table of Contents or Articles in Press  (151)
  • Mice  (97)
  • Rats  (61)
  • 1990-1994  (151)
  • 1935-1939
  • 1991  (151)
  • Natural Sciences in General  (151)
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  • Articles  (151)
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  • Latest Papers from Table of Contents or Articles in Press  (151)
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  • 1990-1994  (151)
  • 1935-1939
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  • 1
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    Subtle cerebellar phenotype in mice homozygous for a targeted deletion of the En-2 homeobox (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-08
    Description: The two mouse genes, En-1 and En-2, that are homologs of the Drosophila segmentation gene engrailed, show overlapping spatially restricted patterns of expression in the neural tube during embryogenesis, suggestive of a role in regional specification. Mice homozygous for a targeted mutation that deletes the homeobox were viable and showed no obvious defects in embryonic development. This may be due to functional redundancy of En-2 and the related En-1 gene product during embryogenesis. Consistent with this hypothesis, the mutant mice showed abnormal foliation in the adult cerebellum, where En-2, and not En-1, is normally expressed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joyner, A L -- Herrup, K -- Auerbach, B A -- Davis, C A -- Rossant, J -- HD25334/HD/NICHD NIH HHS/ -- NS18381/NS/NINDS NIH HHS/ -- NS20591/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1239-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1672471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst ; Cell Line ; Cerebellum/*anatomy & histology/embryology/pathology ; Chimera ; *Chromosome Deletion ; Female ; *Genes, Homeobox ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nervous System/embryology ; Phenotype
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Identification of the DNA binding site for NGFI-B by genetic selection in yeast (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-31
    Description: An in vivo selection system for isolating targets of DNA binding proteins in yeast was developed and used to identify the DNA binding site for the NGFI-B protein, a member of the steroid-thyroid hormone receptor superfamily. The feasibility of the technique was verified by selecting DNA fragments that contained binding sites for GCN4, a well-characterized yeast transcriptional activator. The DNA binding domain of NGFI-B, expressed as part of a LexA-NGFI-B-GAL4 chimeric activator, was then used to isolate a rat genomic DNA fragment that contained an NGFI-B binding site. The NGFI-B response element (NBRE) is similar to but functionally distinct from elements recognized by the estrogen and thyroid hormone receptors and the hormone receptor-like proteins COUP-TF, CF1, and H-2RIIBP. Cotransfection experiments in mammalian cells demonstrated that NGFI-B can activate transcription from the NBRE with or without its putative ligand binding domain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, T E -- Fahrner, T J -- Johnston, M -- Milbrandt, J -- NS01018/NS/NINDS NIH HHS/ -- P01 CA49712/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 May 31;252(5010):1296-300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, 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/1925541" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/metabolism ; Base Sequence ; Binding Sites ; Cloning, Molecular ; DNA, Fungal/*metabolism ; DNA-Binding Proteins/genetics/*metabolism/pharmacology ; Fungal Proteins/metabolism ; Molecular Sequence Data ; Nuclear Receptor Subfamily 4, Group A, Member 1 ; Plasmids ; *Protein Kinases ; Rats ; Receptors, Cytoplasmic and Nuclear ; Receptors, Steroid ; Repressor Proteins ; Saccharomyces cerevisiae/*genetics ; *Saccharomyces cerevisiae Proteins ; *Serine Endopeptidases ; Transcription Factors/genetics/*metabolism/pharmacology ; Transcription, Genetic ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Negative regulation of CD45 protein tyrosine phosphatase activity by ionomycin in T cells (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-09-20
    Description: CD45 is a leukocyte-specific, transmembrane protein tyrosine phosphatase (PTPase) required for T cell responsiveness. How the activity of PTPases is regulated in vivo is unclear. Treatment of murine thymocytes and a variety of murine T cell lines with the calcium ionophore ionomycin decreased CD45 PTPase activity. Ionomycin treatment also led to a decreased phosphorylation of serine residues in CD45. These results indicate that increased intracellular calcium modulates CD45 PTPase activity, demonstrating regulation of CD45 PTPase activity in vivo, and also implicate serine dephosphorylation as a possible mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ostergaard, H L -- Trowbridge, I S -- CA-17733/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Sep 20;253(5026):1423-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Salk Institute, San Diego, CA 92186.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1654595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*metabolism ; Antigens, CD45 ; Cell Line ; Histocompatibility Antigens/*metabolism ; Ionomycin/*pharmacology ; Kinetics ; Mice ; Mice, Inbred BALB C ; Phosphoprotein Phosphatases/*metabolism ; Protein Tyrosine Phosphatases ; Spleen/drug effects/enzymology/immunology ; T-Lymphocytes/drug effects/*enzymology/immunology ; Thymus Gland/immunology
    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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    Differentiation of 3T3-L1 fibroblasts to adipocytes induced by transfection of ras oncogenes (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-02
    Description: Mammalian 3T3-L1 cells differentiate into adipocytes after continuous exposure to pharmacological doses of insulin or physiological doses of insulin-like growth factor I (IGF-1). Expression of transfected ras oncogenes led to differentiation of these cells into adipocytes in the absence of externally added insulin or IGF-I. Cells transfected with normal ras genes or the tyrosine kinase trk oncogene did not differentiate. Transfection with a dominant inhibitory ras mutant resulted in inhibition of differentiation. Exposure of untransfected 3T3-L1 cells to insulin stimulated formation of the active Ras.GTP complex. These observations indicate that Ras proteins participate in signal transduction pathways initiated by insulin and IGF-I in these cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benito, M -- Porras, A -- Nebreda, A R -- Santos, E -- New York, N.Y. -- Science. 1991 Aug 2;253(5019):565-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institute of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1857988" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*cytology ; Animals ; Blotting, Northern ; *Cell Differentiation ; Cell Line ; *Cell Transformation, Neoplastic ; Fibroblasts/cytology ; *Genes, ras ; Mice ; RNA, Messenger/analysis/genetics ; *Transfection
    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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  • 5
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    An unexpectedly efficient catalytic antibody operating by ping-pong and induced fit mechanisms (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-03
    Description: A transition state analogue was used to produce a mouse antibody that catalyzes transesterification in water. The antibody behaves as a highly efficient catalyst with a covalent intermediate and the characteristic of induced fit. While some features of the catalytic pathway were programmed when the hapten was designed and reflect favorable substrate-antibody interactions, other features are a manifestation of the chemical potential of antibody diversity. The fact that antibodies recapitulate mechanisms and pathways previously thought to be a characteristic of highly evolved enzymes suggests that once an appropriate binding cavity is achieved, reaction pathways commensurate with the intrinsic chemical potential of proteins ensue.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wirsching, P -- Ashley, J A -- Benkovic, S J -- Janda, K D -- Lerner, R A -- GM43858-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 May 3;252(5006):680-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2024120" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Alcohols/metabolism ; Animals ; Antibodies, Monoclonal/immunology/*metabolism ; Antibody Specificity ; Binding Sites, Antibody ; *Catalysis ; Enzymes/metabolism ; Esterification ; Haptens ; Kinetics ; Mice ; Water
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Lateral movements of membrane glycoproteins restricted by dynamic cytoplasmic barriers (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-29
    Description: Cell membranes often are patchy, composed of lateral domains. These domains may be formed by barriers within or on either side of the membrane bilayer. Major histocompatibility complex (MHC) class 1 molecules that were either transmembrane- (H-2Db) or glycosylphosphatidylinositol (GPI)-anchored (Qa2) were labeled with antibody-coated gold particles and moved across the cell surface with a laser optical tweezers until they encountered a barrier, the barrier-free path length (BFP). At room temperature, the BFPs of Qa2 and H-2Db were 1.7 +/- 0.2 and 0.6 +/- 0.1 (micrometers +/- SEM), respectively. Barriers persisted at 34 degrees C, although the BFP for both MHC molecules was fivefold greater at 34 degrees C than at 23 degrees C. This indicates that barriers to lateral movement are primarily on the cytoplasmic half of the membrane and are dynamic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edidin, M -- Kuo, S C -- Sheetz, M P -- AL14584/PHS HHS/ -- GM 36277/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 29;254(5036):1379-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Johns Hopkins University, Baltimore, MD 21218.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1835798" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Cell Line ; Glycolipids/physiology ; Glycosylphosphatidylinositols ; Gold ; H-2 Antigens/*physiology ; Histocompatibility Antigens Class I/*physiology ; *Lipid Bilayers ; Membrane Glycoproteins/*physiology ; Mice ; Phosphatidylinositols/physiology ; Thermodynamics ; Transfection
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  • 7
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    Space may be bad for your health (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-09-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1991 Sep 27;253(5027):1491.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1896859" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Models, Biological ; Monitoring, Physiologic ; Motion Sickness/*etiology ; Rats ; Scyphozoa ; *Space Flight ; *Weightlessness
    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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  • 8
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    Split anergy in a CD8+ T cell: receptor-dependent cytolysis in the absence of interleukin-2 production (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-08
    Description: Engagement of the antigen-specific receptor (TCR) of CD4+ T lymphocytes without a second (costimulatory) signal prevents the subsequent production of interleukin-2 (IL-2) by these cells. Because IL-2 is a key immunoregulatory lymphokine and is also produced by a subset of CD8+ T cells that are able to kill target cells, the effect of engaging the TCR of one such clone in the absence of costimulatory signals was examined. The capacity for TCR-dependent IL-2 production was lost, indicating comparable costimulator-dependent signaling requirements for IL-2 production in CD4+ and CD8+ T cells. However, TCR-mediated cytotoxicity was not impaired, implying that costimulation is required for only certain TCR-dependent effector functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Otten, G R -- Germain, R N -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1228-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Biology Section, National Institute of Allergy and Infectious 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/1900952" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antigen-Presenting Cells/immunology ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Female ; Interleukin-2/biosynthesis/*physiology ; Kinetics ; Lymphocyte Activation ; Mice ; Mice, Inbred Strains ; Ovalbumin/immunology ; Rats ; Receptors, Antigen, T-Cell/*immunology ; Spleen/immunology/radiation effects ; T-Lymphocytes/*immunology
    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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  • 9
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    Lysyl oxidase and rrg messenger RNA (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kenyon, K -- Contente, S -- Trackman, P C -- Tang, J -- Kagan, H M -- Friedman, R M -- P01 HL13262/HL/NHLBI NIH HHS/ -- R01 CA37351-04A1/CA/NCI NIH HHS/ -- R37 AR18880/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Aug 16;253(5021):802.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1678898" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blotting, Northern ; Cell Line ; *Cell Transformation, Neoplastic ; Gene Expression ; *Genes, Tumor Suppressor ; In Vitro Techniques ; Mice ; Protein-Lysine 6-Oxidase/*physiology ; RNA, Messenger/genetics
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  • 10
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    Direct molecular identification of the mouse pink-eyed unstable mutation by genome scanning (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-26
    Description: DNA sequences associated with the mouse pink-eyed unstable mutation were identified in the absence of closely linked molecular markers and without prior knowledge of the encoded gene product. This was accomplished by "genome scanning," a technique in which high-resolution Southern blots of genomic DNAs were hybridized to a dispersed and moderately repetitive DNA sequence. In this assay, pink-eyed unstable DNA was distinguished from the DNA of wild-type and revertant mice by enhanced hybridization to one of several hundred resolved fragments. The fragment showing enhanced hybridization in pink-eyed unstable DNA was cloned and found to lie within a DNA duplication that is located close to, or within, the pink-eyed dilution locus. The duplication associated with the mouse pink-eyed unstable mutation may mediate the high reversion frequency characteristic of this mutation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brilliant, M H -- Gondo, Y -- Eicher, E M -- CA06927/CA/NCI NIH HHS/ -- GM43840/GM/NIGMS NIH HHS/ -- RR05529/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Apr 26;252(5005):566-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cancer Research, Fox Chase Cancer Center, Philadelphia, PA 19111.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1673574" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Blotting, Southern/methods ; DNA/genetics/isolation & purification ; Eye Color/*genetics ; *Genes ; Homozygote ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; *Mutation ; Restriction Mapping ; Tyrosine 3-Monooxygenase/genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Linkage of faulty major histocompatibility complex class I to autoimmune diabetes (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-20
    Description: Pancreatic islet cells are the targets of an autoimmune response in type I diabetes. In the nonobese diabetic (NOD) mouse model of autoimmune diabetes, expression of major histocompatibility complex (MHC) class I proteins was inversely correlated with diabetes; in this mouse a mutation in the MHC class II-linked gene for the putative MHC class I peptide transporter was also present. Mice deficient in MHC class I expression because they do not produce beta 2-microglobulin also developed late onset autoimmune diabetes. In cells from humans with type I diabetes expression of MHC class I was decreased; subsets of prediabetics categorized as most likely to become hyperglycemic also had low MHC class I. T cell responses to self antigens are faulty in diabetics. In sets of genetically identical twins that are discordant for diabetes, the defect appeared to reside with the antigen presenting cell. Thus, a lack of surface MHC class I protein is associated with autoimmune diabetes; the concomitant defect in antigen presentation may impair the development of self tolerance, which could result in autoimmune disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faustman, D -- Li, X P -- Lin, H Y -- Fu, Y E -- Eisenbarth, G -- Avruch, J -- Guo, J -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1756-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Harvard Medical School, Massachusetts General Hospital, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1763324" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/*genetics ; Cytotoxicity, Immunologic ; Diabetes Mellitus, Type 1/genetics/*immunology ; Diseases in Twins ; Flow Cytometry ; Gene Expression ; *Genes, MHC Class I ; Humans ; *Lymphocyte Activation ; Lymphocytes/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Prediabetic State/genetics/immunology ; Spleen/immunology ; T-Lymphocytes/immunology
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  • 12
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    How peptide hormones get ready for work (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1991 May 10;252(5007):779-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1674172" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Gene Expression Regulation, Enzymologic ; Hormones/*metabolism ; Mice ; Neurotransmitter Agents/metabolism ; Pro-Opiomelanocortin/metabolism ; Proprotein Convertase 2 ; Proprotein Convertases ; Protein Precursors/metabolism ; *Protein-Tyrosine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-fes ; Serine Endopeptidases/*physiology
    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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  • 13
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    Function of the homeodomain protein GHF1 in pituitary cell proliferation (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-12
    Description: Mutations that cause pituitary dwarfism in the mouse reside in the gene encoding the transcription factor growth hormone factor 1 (GHF1 or pit1). These dwarf mice (dw and dwJ) are deficient in growth hormone (GH) and prolactin (PRL) synthesis and exhibit pituitary hypoplasia, suggesting a stem cell defect. With antisense oligonucleotide technology, a cell culture model of this genetic defect was developed. Specific inhibition of GHF1 synthesis by complementary oligonucleotides led to a marked decrease in GH and PRL expression and to a marked decrease in proliferation of somatotrophic cell lines. These results provide direct evidence that the homeodomain protein GHF1 is required not only for the establishment and maintenance of the differentiated phenotype but for cell proliferation as well.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Castrillo, J L -- Theill, L E -- Karin, M -- DK38527/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 12;253(5016):197-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1677216" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antisense Elements (Genetics) ; Base Sequence ; *Cell Division ; Cells, Cultured ; DNA/biosynthesis ; DNA-Binding Proteins/*physiology ; Dwarfism/genetics ; Gene Expression Regulation ; *Genes, Homeobox ; Growth Hormone/genetics ; In Vitro Techniques ; Mice ; Molecular Sequence Data ; Pituitary Gland/*cytology/physiology ; Prolactin/genetics ; Transcription Factor Pit-1 ; Transcription Factors/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Modulation of cardiac sodium channels by cAMP receptors on the myocyte surface (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-09-13
    Description: The phosphorylation of the cardiac sodium channel by adenosine 3',5'-monophosphate (cAMP)-dependent protein kinase A leads to its inactivation. It was shown that extracellular cAMP can also modulate the sodium channel of rat, guinea pig, and frog ventricular myocytes in a rapid (less than 50 milliseconds), reversible, and dose-dependent manner. The decrease in the sodium current was accompanied by a 10- to 15-millivolt shift in the steady-state availability of the sodium channel toward more negative potentials and was inhibited by guanosine-5'-O-(2-thiodiphosphate) or pertussis toxin, suggesting that the extracellular modulation of the sodium channel by cAMP is mediated by a membrane-delimited mechanism that includes a pertussis toxin-sensitive G protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sorbera, L A -- Morad, M -- HL16152/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1991 Sep 13;253(5025):1286-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Pennsylvania, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1653970" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclic AMP/*pharmacology ; Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology ; Guanosine Diphosphate/analogs & derivatives/pharmacology ; Guinea Pigs ; Heart/drug effects/*physiology ; Isoproterenol/pharmacology ; Kinetics ; Membrane Potentials/drug effects ; Pertussis Toxin ; Rana pipiens ; Rats ; Receptors, Cyclic AMP/drug effects/*physiology ; Sodium Channels/drug effects/*physiology ; Thionucleotides/pharmacology ; Virulence Factors, Bordetella/pharmacology
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  • 15
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    ACh receptor-rich membrane domains organized in fibroblasts by recombinant 43-kildalton protein (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-01
    Description: Neurotransmitter receptors are generally clustered in the postsynaptic membrane. The mechanism of clustering was analyzed with fibroblast cell lines that were stably transfected with the four subunits for fetal (alpha, beta, gamma, delta) or adult (alpha, beta, epsilon, delta) type mouse muscle nicotinic acetylcholine receptors (AChRs). Immunofluorescent staining indicated that AChRs were dispersed on the surface of these cells. When transiently transfected with an expression construct encoding a 43-kilodalton protein that is normally concentrated under the postsynaptic membrane, AChRs expressed in these cells became aggregated in large cell-surface clusters, colocalized with the 43-kilodalton protein. This suggests that 43-kilodalton protein can induce AChR clustering and that cluster induction involves direct contact between AChR and 43-kilodalton protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Phillips, W D -- Kopta, C -- Blount, P -- Gardner, P D -- Steinbach, J H -- Merlie, J P -- R01 NS022356/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Feb 1;251(4993):568-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, 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/1703661" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/pharmacology ; Animals ; Cell Membrane/physiology ; Fetus ; Fibroblasts/cytology/physiology ; Fluorescent Antibody Technique ; Ion Channels/drug effects/physiology ; Macromolecular Substances ; Mice ; Molecular Weight ; Muscles/physiology ; Receptors, Nicotinic/analysis/genetics/*physiology ; Recombinant Proteins/analysis/metabolism ; Transfection
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  • 16
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    Cloning and expression of a cocaine-sensitive rat dopamine transporter (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-25
    Description: The action of dopamine and other monoamine neurotransmitters at synapses is terminated predominantly by high-affinity reuptake into presynaptic terminals by specific sodium-dependent neurotransmitter transport proteins. A complementary DNA encoding a rat dopamine transporter has been isolated that exhibits high sequence similarity with the previously cloned norepinephrine and gamma-aminobutyric acid transporters. Transient expression of the complementary DNA in HeLa cells confirms the cocaine sensitivity of this transporter.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kilty, J E -- Lorang, D -- Amara, S G -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):578-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Yale University, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948035" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Carrier Proteins/drug effects/*genetics/metabolism ; Cloning, Molecular ; Cocaine/*pharmacology ; Dopamine/*metabolism ; Dopamine Plasma Membrane Transport Proteins ; Gene Expression ; HeLa Cells ; Humans ; Kinetics ; *Membrane Glycoproteins ; *Membrane Transport Proteins ; Molecular Sequence Data ; *Nerve Tissue Proteins ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction/methods ; Rats ; Sequence Homology, Nucleic Acid ; Transfection
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  • 17
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    Protection against malaria by vaccination with sporozoite surface protein 2 plus CS protein (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-03
    Description: The circumsporozoite (CS) protein has been the target for development of malaria sporozoite vaccines for a decade. However, immunization with subunit vaccines based on the CS protein has never given the complete protection found after immunization with irradiated sporozoites. BALB/c mice immunized with irradiated Plasmodium yoelii sporozoites produced antibodies and cytotoxic T cells against a 140-kilodalton protein, sporozoite surface protein 2 (SSP2). Mice immunized with P815 cells that had been transfected with either SSP2 or CS genes were partially protected, and those immunized with a mixture of SSP2 and CS transfectants were completely protected against malaria. These studies emphasize the importance of vaccine delivery systems in achieving protection and define a multi-antigen sporozoite vaccine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Khusmith, S -- Charoenvit, Y -- Kumar, S -- Sedegah, M -- Beaudoin, R L -- Hoffman, S L -- New York, N.Y. -- Science. 1991 May 3;252(5006):715-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Malaria Program, Naval Medical Research Institute, Bethesda, MD 20889.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1827210" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antibodies, Protozoan/immunology ; Antigens, Protozoan/genetics/*immunology ; Immunization ; Malaria/*prevention & control ; Mice ; Mice, Inbred BALB C ; Molecular Weight ; Plasmodium yoelii/*immunology ; Protozoan Proteins/genetics/*immunology ; *Protozoan Vaccines ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Regulatory/immunology ; Transfection ; *Vaccination
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    In vitro and in vivo consequences of VLA-2 expression on rhabdomyosarcoma cells (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-03-29
    Description: Cloned integrin alpha 2 subunit complementary DNA was expressed on human rhabdomyosarcoma (RD) cells to give a functional VLA-2 (alpha 2 beta 1) adhesion receptor. The VLA-2-positive RDA2 cells not only showed increased adhesion to collagen and laminin in vitro, but also formed substantially more metastatic tumor colonies in nude mice after either intravenous or subcutaneous injection. These results show that a specific adhesion receptor (VLA-2) can markedly enhance both experimental and spontaneous metastasis. In contrast to the metastasis results, there was no difference in either the in vitro growth rate or apparent in vivo tumorigenicity of RD and RDA2 cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, B M -- Matsuura, N -- Takada, Y -- Zetter, B R -- Hemler, M E -- CA 37393/CA/NCI NIH HHS/ -- GM 38903/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Mar 29;251(5001):1600-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2011740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Adhesion ; Cell Line ; Collagen ; Fibronectins ; Humans ; Kinetics ; Laminin ; Lung Neoplasms/pathology/secondary ; Mice ; Mice, Nude ; Neoplasm Metastasis ; Neoplasm Transplantation ; Receptors, Very Late Antigen/genetics/*physiology ; Rhabdomyosarcoma/*pathology ; Transplantation, Heterologous
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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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    Exchange of conduction pathways between two related K+ channels (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-02-22
    Description: The structure of the ion conduction pathway or pore of voltage-gated ion channels is unknown, although the linker between the membrane spanning segments S5 and S6 has been suggested to form part of the pore in potassium channels. To test whether this region controls potassium channel conduction, a 21-amino acid segment of the S5-S6 linker was transplanted from the voltage-activated potassium channel NGK2 to another potassium channel DRK1, which has very different pore properties. In the resulting chimeric channel, the single channel conductance and blockade by external and internal tetraethylammonium (TEA) ion were characteristic of the donor NGK2 channel. Thus, this 21-amino acid segment controls the essential biophysical properties of the pore and may form the conduction pathway of these potassium channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hartmann, H A -- Kirsch, G E -- Drewe, J A -- Taglialatela, M -- Joho, R H -- Brown, A M -- NS08805/NS/NINDS NIH HHS/ -- NS23877/NS/NINDS NIH HHS/ -- NS28407/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Feb 22;251(4996):942-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2000495" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/physiology ; Chimera ; Cloning, Molecular ; Female ; Ion Channel Gating ; Membrane Potentials ; Molecular Sequence Data ; Oligonucleotide Probes ; Oocytes/physiology ; Polymerase Chain Reaction ; Potassium Channels/drug effects/genetics/*physiology ; Rats ; Restriction Mapping ; Sequence Homology, Nucleic Acid ; Tetraethylammonium ; Tetraethylammonium Compounds/pharmacology ; Xenopus
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Engineers open a dialogue with neurons (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-07-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amato, I -- New York, N.Y. -- Science. 1991 Jul 5;253(5015):34.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2063204" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biomedical Engineering ; Electric Stimulation ; Electrodes, Implanted ; *Neurons ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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    Deregulation of a homeobox gene, HOX11, by the t(10;14) in T cell leukemia (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-07-05
    Description: Molecular cloning of the t(10;14)(q24;q11) recurrent breakpoint of T cell acute lymphoblastic leukemia has demonstrated a transcript for the candidate gene TCL3. Characterization of this gene from chromosome segment 10q24 revealed it to be a new homeobox, HOX11. The HOX11 homeodomain is most similar to that of the murine gene Hlx and possesses a markedly glycine-rich variable region and an acidic carboxyl terminus. HOX11, while expressed in liver, was not detected in normal thymus or T cells. This lineage-restricted homeobox gene is deregulated upon translocation into the T cell receptor locus where it may act as an oncogene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hatano, M -- Roberts, C W -- Minden, M -- Crist, W M -- Korsmeyer, S J -- 1 PO1 CA49712/CA/NCI NIH HHS/ -- CA 21765/CA/NCI NIH HHS/ -- CA 30969/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 5;253(5015):79-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1676542" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Northern ; Chromosomes, Human, Pair 10 ; Chromosomes, Human, Pair 14 ; Cloning, Molecular ; *Gene Expression Regulation, Neoplastic ; *Genes, Homeobox ; Humans ; Leukemia-Lymphoma, Adult T-Cell/*genetics ; Mice ; Molecular Sequence Data ; Receptors, Antigen, T-Cell/genetics ; Restriction Mapping ; Sequence Homology, Nucleic Acid ; *Translocation, Genetic
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  • 22
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    Recognition of self antigens by skin-derived T cells with invariant gamma delta antigen receptors (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-06-07
    Description: Thy-1+ dendritic epidermal T cells (dECs) express invariant gamma delta antigen receptors and are found in intimate contact with keratinocytes in murine epidermis--thus raising the possibility that keratinocytes express a ligand for the antigen receptor of these T cells. Thy-1+ dECs were stimulated to produce lymphokines by interaction with keratinocytes in vitro. This stimulation was mediated through the dEC antigen receptor and did not appear to be restricted by the major histocompatibility complex. Thus, dECs can recognize self antigens and may participate in immune surveillance for cellular damage rather than for foreign antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Havran, W L -- Chien, Y H -- Allison, J P -- AI26942/AI/NIAID NIH HHS/ -- CA40041/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Jun 7;252(5011):1430-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1828619" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantigens/*immunology ; Cell Line ; Dendrites/immunology ; Epidermis ; *Immunity, Cellular ; In Vitro Techniques ; Interleukin-2/secretion ; Keratinocytes/physiology ; Mice ; Mice, Inbred BALB C ; Receptors, Antigen, T-Cell/*physiology ; Receptors, Antigen, T-Cell, gamma-delta ; T-Lymphocytes/*immunology
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  • 23
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    Protein kinase activity closely associated with a reconstituted calcium-activated potassium channel (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-08-02
    Description: Modulation of the activity of potassium and other ion channels is an essential feature of nervous system function. The open probability of a large conductance Ca(2+)-activated K+ channel from rat brain, incorporated into planar lipid bilayers, is increased by the addition of adenosine triphosphate (ATP) to the cytoplasmic side of the channel. This modulation takes place without the addition of protein kinase, requires Mg2+, and is mimicked by an ATP analog that serves as a substrate for protein kinases but not by a nonhydrolyzable ATP analog. Addition of protein phosphatase 1 reverses the modulation by MgATP. Thus, there may be an endogenous protein kinase activity firmly associated with this K+ channel. Some ion channels may exist in a complex that contains regulatory protein kinases and phosphatases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chung, S K -- Reinhart, P H -- Martin, B L -- Brautigan, D -- Levitan, I B -- DK31374/DK/NIDDK NIH HHS/ -- NS17910/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Aug 2;253(5019):560-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Department of Biochemistry, Brandeis University, Waltham, MA 02254.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1857986" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/pharmacology ; Animals ; Brain/*physiology ; Calcium/*pharmacology ; Kinetics ; Lipid Bilayers ; Potassium Channels/drug effects/metabolism/*physiology ; Protein Kinases/*metabolism ; Rats
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  • 24
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    Expression cDNA cloning of the KGF receptor by creation of a transforming autocrine loop (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-01-04
    Description: An expression cloning strategy was devised to isolate the keratinocyte growth factor (KGF) receptor complementary DNA. NIH/3T3 fibroblasts, which secrete this epithelial cell-specific mitogen, were transfected with a keratinocyte expression complementary DNA library. Among several transformed foci identified, one demonstrated the acquisition of specific high-affinity KGF binding sites. The pattern of binding competition by related fibroblast growth factors (FGFs) indicated that this receptor had high affinity for acidic FGF as well as KGF. The rescued 4.2-kilobase complementary DNA was shown to encode a predicted membrane-spanning tyrosine kinase related to but distinct from the basic FGF receptor. This expression cloning approach may be generally applicable to the isolation of genes that constitute limiting steps in mitogenic signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miki, T -- Fleming, T P -- Bottaro, D P -- Rubin, J S -- Ron, D -- Aaronson, S A -- New York, N.Y. -- Science. 1991 Jan 4;251(4989):72-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1846048" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding, Competitive ; Cell Line ; *Cloning, Molecular ; DNA/*genetics ; Fibroblast Growth Factor 10 ; Fibroblast Growth Factor 7 ; Fibroblast Growth Factors/metabolism ; Fibroblasts/metabolism ; *Gene Expression ; Growth Substances/metabolism ; Mice ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Plasmids ; Receptor, Fibroblast Growth Factor, Type 2 ; Receptors, Cell Surface/*genetics/metabolism ; *Receptors, Fibroblast Growth Factor ; Recombinant Proteins/metabolism ; Transfection ; Transformation, Genetic
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  • 25
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    Crystal structure of defensin HNP-3, an amphiphilic dimer: mechanisms of membrane permeabilization (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-03-22
    Description: Defensins (molecular weight 3500 to 4000) act in the mammalian immune response by permeabilizing the plasma membranes of a broad spectrum of target organisms, including bacteria, fungi, and enveloped viruses. The high-resolution crystal structure of defensin HNP-3 (1.9 angstrom resolution, R factor 0.19) reveals a dimeric beta sheet that has an architecture very different from other lytic peptides. The dimeric assembly suggests mechanisms by which defensins might bind to and permeabilize the lipid bilayer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hill, C P -- Yee, J -- Selsted, M E -- Eisenberg, D -- New York, N.Y. -- Science. 1991 Mar 22;251(5000):1481-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Eisenberg, Molecular Biology Institute, Los Angeles, CA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2006422" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blood Proteins/chemistry/*ultrastructure ; Cell Membrane Permeability ; Crystallography ; Defensins ; Guinea Pigs ; Humans ; Macromolecular Substances ; Membrane Proteins/chemistry/ultrastructure ; Models, Molecular ; Molecular Sequence Data ; Molecular Structure ; Protein Conformation ; Rabbits ; Rats ; Structure-Activity Relationship ; X-Ray Diffraction ; *alpha-Defensins
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  • 26
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    Requirement of heparan sulfate for bFGF-mediated fibroblast growth and myoblast differentiation (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-06-21
    Description: Basic fibroblast growth factor (bFGF) binds to heparan sulfate proteoglycans at the cell surface and to receptors with tyrosine kinase activity. Prevention of binding between cell surface heparan sulfate and bFGF (i) substantially reduces binding of fibroblast growth factor to its cell-surface receptors, (ii) blocks the ability of bFGF to support the growth of Swiss 3T3 fibroblasts, and (iii) induces terminal differentiation of MM14 skeletal muscle cells, which is normally repressed by fibroblast growth factor. These results indicate that cell surface heparan sulfate is directly involved in bFGF cell signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rapraeger, A C -- Krufka, A -- Olwin, B B -- 5T32H007118/PHS HHS/ -- AR39467/AR/NIAMS NIH HHS/ -- HD21881/HD/NICHD NIH HHS/ -- R01 AR039467/AR/NIAMS NIH HHS/ -- R01 HD021881/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1991 Jun 21;252(5013):1705-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Wisconsin, Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1646484" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Line ; Chlorates/pharmacology ; Fibroblast Growth Factor 2/*metabolism ; Fibroblasts/*cytology ; Heparitin Sulfate/*physiology ; In Vitro Techniques ; Mice ; Muscles/*cytology ; Polysaccharide-Lyases/pharmacology ; Protein Binding ; Receptors, Cell Surface/metabolism ; Structure-Activity Relationship
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  • 27
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    Modulation of the time course of fast EPSCs and glutamate channel kinetics by aniracetam (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-11
    Description: It is generally accepted that glutamate serves as the neurotransmitter at most excitatory synapses in the mammalian central nervous system (CNS). Synaptic release of glutamate may trigger a fast and a slow excitatory postsynaptic current (EPSC). The slow EPSC is mediated by N-methyl-D-aspartate (NMDA) receptor channels, whereas the fast EPSC is mediated by non-NMDA receptor channels. The nootropic agent aniracetam selectively and reversibly slows the desensitization kinetics of non-NMDA channels and lengthens their single-channel open times. Antiracetam also modulates the kinetics of the fast EPSC in a manner that mirrors its action on the kinetics of the non-NMDA channels. These results support the hypothesis that the properties of the non-NMDA glutamate channels rather than the rate of neurotransmitter clearance are the primary determinants of the kinetics of the fast EPSC in the mammalian CNS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, C M -- Shi, Q Y -- Katchman, A -- Lynch, G -- NS28158/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 11;254(5029):288-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of Pennsylvania, Philadelphia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1681589" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/*drug effects ; Animals ; Glutamates/*physiology ; Glutamic Acid ; Kinetics ; Pyrrolidinones/*pharmacology ; Rats ; Receptors, Glutamate ; Receptors, N-Methyl-D-Aspartate/drug effects ; Receptors, Neurotransmitter/drug effects ; Synapses/*drug effects
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    Requirement of nuclear prolactin for interleukin-2--stimulated proliferation of T lymphocytes (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-05
    Description: Prolactin (PRL) is necessary for the proliferation of cloned T lymphocytes in response to interleukin-2 (IL-2). Translocation of PRL into the nucleus occurs during IL-2--stimulated mitogenesis. Therefore, the function of intranuclear PRL in T cell proliferation was tested. Eukaryotic expression vectors were prepared to express wild-type PRL [PRL(WT)], PRL that lacks the signal sequence for translocation into the endoplasmic reticulum [PRL(ER-)], and chimeric PRL in which the signal peptide was replaced with the sequence that directs the nuclear translocation of the SV40 large T antigen [PRL(NT+)]. Expression of these constructs in a T cell line (Nb2) responsive to PRL and IL-2 resulted in localization of PRL in the extracellular milieu, cytoplasm, or nucleus, respectively. Stimulation with IL-2 alone resulted in a five- to tenfold increase in the incorporation of [3H]thymidine by cells expressing PRL(NT+) or PRL(WT) as compared to PRL(ER-) or the parental Nb2 cells. Only the PRL(NT+) clone proliferated continuously with IL-2 stimulation in the presence of antiserum to PRL. These results demonstrate that nuclear PRL is necessary for IL-2--stimulated proliferation and suggest that a peptide hormone can function in the nucleus without binding to its cell surface receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clevenger, C V -- Altmann, S W -- Prystowsky, M B -- GM-13901/GM/NIGMS NIH HHS/ -- GM-36962/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 5;253(5015):77-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2063207" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Transport, Active ; Cell Cycle/drug effects ; Cell Nucleus/metabolism ; Drug Synergism ; Genetic Vectors ; In Vitro Techniques ; Interleukin-2/pharmacology ; Lymphocyte Activation/*drug effects ; Molecular Sequence Data ; Prolactin/pharmacokinetics/*pharmacology ; Rats ; Transfection
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    Generation of cAMP-activated chloride currents by expression of CFTR (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-08
    Description: Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) cause cystic fibrosis. In order to evaluate its function, CFTR was expressed in HeLa, Chinese hamster ovary (CHO), and NIH 3T3 fibroblast cells, and anion permeability was assessed with a fluorescence microscopic assay and the whole-cell patch-clamp technique. Adenosine 3',5'-monophosphate (cAMP) increased anion permeability and chloride currents in cells expressing CFTR, but not in cells expressing a mutant CFTR (delta F508) or in nontransfected cells. The simplest interpretation of these observations is that CFTR is itself a cAMP-activated chloride channel. The alternative interpretation, that CFTR directly or indirectly regulates chloride channels, requires that these cells have endogenous cryptic, chloride channels that are stimulated by cAMP only in the presence of CFTR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, M P -- Rich, D P -- Gregory, R J -- Smith, A E -- Welsh, M J -- New York, N.Y. -- Science. 1991 Feb 8;251(4994):679-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1704151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chloride Channels ; Chlorides/*metabolism ; Cricetinae ; Cyclic AMP/*physiology ; Cystic Fibrosis Transmembrane Conductance Regulator ; Humans ; Membrane Proteins/*metabolism/*physiology ; Mice ; Mutation ; Recombinant Proteins ; Structure-Activity Relationship
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    Control of alternative splicing by the differential binding of U1 small nuclear ribonucleoprotein particle (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-01
    Description: Cellular factors controlling alternative splicing of precursor messenger RNA are largely unknown, even though this process plays a central role in specifying the diversity of proteins in the eukaryotic cell. For the identification of such factors, a segment of the rat preprotachykinin gene was used in which differential expression of neuropeptides gamma and K is dependent on alternative splicing of the fourth exon (E4). Sequence variants of the three-exon segment, (E3-E4-E5) were created, resulting in a sensitive assay for factors mediating the splicing switch between E4-skipping and E4-inclusion. A dinucleotide mutation in the 5' splice site of E4 that increase base-pairing of this site to U1 small nuclear RNA resulted in uniform selection of E4, whereas a control mutation that destroyed base-pairing resulted in uniform E4-skipping. Affinity selection of spliceosomes formed on these functionally distinct substrates revealed that the extreme difference in splicing was mediated by differential binding of the U1 small nuclear ribonucleoprotein particle (snRNP) to the 5' splice site of E4. These data show that, apart from its established role in selecting 5' splice sites, U1 snRNP plays a fundamental role in 3' exon selection and provides insight into possible mechanisms of alternative splicing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuo, H C -- Nasim, F H -- Grabowski, P J -- GM-39695/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Mar 1;251(4997):1045-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Biochemistry, Brown University, Providence, RI 02912.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1825520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA Mutational Analysis ; Exons ; Hydrogen Bonding ; Macromolecular Substances ; Molecular Sequence Data ; Protein Precursors/*genetics ; *RNA Splicing ; RNA, Messenger/*metabolism ; RNA, Small Nuclear/*physiology ; Rats ; Ribonucleoproteins/chemistry/*physiology ; Ribonucleoproteins, Small Nuclear ; Structure-Activity Relationship ; Tachykinins/*genetics
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    Putting new muscle into gene therapy (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, M -- New York, N.Y. -- Science. 1991 Dec 6;254(5037):1455-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1962203" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Genetic Therapy/*methods ; Growth Hormone/administration & dosage ; Mice ; Muscles/*cytology/secretion ; Recombinant Proteins/administration & dosage
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    A layer by layer look at the skin blister disease (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, M -- New York, N.Y. -- Science. 1991 Nov 22;254(5035):1111-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1720260" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Collagen/physiology ; Epidermis/*physiology ; Epidermolysis Bullosa/*physiopathology ; Humans ; Keratins/*physiology ; Mice ; Mice, Transgenic
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    Maintenance of normoglycemia in diabetic mice by subcutaneous xenografts of encapsulated islets (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-20
    Description: The goal of islet transplantation in human diabetes is to maintain the islet grafts in the recipients without the use of immunosuppression. One approach is to encapsulate the donor islets in permselective membranes. Hollow fibers fabricated from an acrylic copolymer were used to encapsulate small numbers of rat islets that were immobilized in an alginate hydrogel for transplantation in diabetic mice. The fibers were biocompatible, prevented rejection, and maintained normoglycemia when transplanted intraperitoneally; hyperglycemia returned when the fibers were removed at 60 days. Normoglycemia was also maintained by subcutaneous implants that had an appropriately constructed outer surface on the fibers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lacy, P E -- Hegre, O D -- Gerasimidi-Vazeou, A -- Gentile, F T -- Dionne, K E -- DK01226/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1782-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, 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/1763328" target="_blank"〉PubMed〈/a〉
    Keywords: *Acrylic Resins ; Animals ; Animals, Newborn ; Blood Glucose/*metabolism ; Diabetes Mellitus, Experimental/blood/*surgery ; In Vitro Techniques ; Insulin/secretion ; Islets of Langerhans/*secretion ; Islets of Langerhans Transplantation/*physiology ; Male ; Membranes, Artificial ; Mice ; Mice, Inbred C57BL ; *Polyvinyl Chloride ; Rats ; Rats, Inbred WF ; Time Factors ; Transplantation, Heterologous
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    Phosphorylation of c-Src on tyrosine 527 by another protein tyrosine kinase (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-10-25
    Description: The protein tyrosine kinase activity of the cellular Src protein is negatively regulated by phosphorylation at tyrosine residue 527 (Tyr527). It has not been established whether this regulatory modification of Src is mediated by autophosphorylation or by another cellular protein kinase. The phosphorylation of a modified form of c-Src that lacks kinase activity was examined in mouse cells that do not express endogenous Src (because of the targeted disruption of both src alleles). Phosphorylation of the inactive form of Src on Tyr527 occurred to a similar extent in cells lacking endogenous Src as it did in cells expressing Src. Therefore, Tyr527 phosphorylation, and thus negative control of Src kinase activity, is mediated by another cellular protein tyrosine kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomas, J E -- Soriano, P -- Brugge, J S -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):568-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Microbiology, University of Pennsylvania, School of Medicine, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1719633" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Cyanogen Bromide ; Embryo, Mammalian ; Mice ; Peptide Mapping ; Phosphopeptides/isolation & purification ; Phosphorylation ; Protein-Tyrosine Kinases ; Proto-Oncogene Proteins pp60(c-src)/*metabolism ; *Tyrosine
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    Identification of Ets- and notch-related subunits in GA binding protein (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-16
    Description: Recombinant cDNA clones that encode two distinct subunits of the transcription factor GA binding protein (GABP) have been isolated. The predicted amino acid sequence of one subunit, GABP alpha, exhibits similarity to the sequence of the product of the ets-1 protooncogene in a region known to encompass the Ets DNA binding domain. The sequence of the second subunit, GABP beta, contains four 33-amino acid repeats located close to the NH2-terminus of the subunit. The sequences of these repeats are similar to repeats in several transmembrane proteins, including Notch from Drosophila melanogaster and Glp-1 and Lin-12 from Caenorhabditis elegans. Avid, sequence-specific binding to DNA required the presence of both polypeptides, revealing a conceptual convergence of nuclear transforming proteins and membrane-anchored proteins implicated in developmentally regulated signal transduction processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LaMarco, K -- Thompson, C C -- Byers, B P -- Walton, E M -- McKnight, S L -- New York, N.Y. -- Science. 1991 Aug 16;253(5021):789-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Research Laboratories, Carnegie Institution of Washington, Department of Embryology, Baltimore, MD 21210.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1876836" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Cloning, Molecular ; DNA-Binding Proteins/*chemistry/genetics ; GA-Binding Protein Transcription Factor ; Gene Expression ; Molecular Sequence Data ; Nuclear Proteins/chemistry/genetics ; Peptides/chemistry ; Proto-Oncogene Protein c-ets-1 ; Proto-Oncogene Proteins/chemistry ; Proto-Oncogene Proteins c-ets ; RNA, Messenger/genetics ; Rats ; Recombinant Proteins ; Transcription Factors/*chemistry/genetics
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    More pieces in the dioxin puzzle (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, L -- New York, N.Y. -- Science. 1991 Oct 18;254(5030):377.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1656528" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogens/*toxicity ; Dioxins/*toxicity ; Dose-Response Relationship, Drug ; Models, Theoretical ; Rats ; Receptors, Aryl Hydrocarbon ; Receptors, Drug/metabolism ; Risk
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  • 37
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    Convergence of Ets- and notch-related structural motifs in a heteromeric DNA binding complex (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-16
    Description: Analysis of the heteromeric DNA binding protein GABP has revealed the interaction of two distinct peptide sequence motifs normally associated with proteins located in different cellular compartments. The alpha subunit of GABP contains an 85-amino acid segment related to the Ets family of DNA binding proteins. The ETS domain of GABP alpha facilitates weak binding to DNA and, together with an adjacent segment of 37 amino acids, mediates stable interaction with GABP beta. The beta subunit of GABP contains four imperfect repeats of a sequence present in several transmembrane proteins including the product of the Notch gene of Drosophila melanogaster. These amino-terminal repeats of GABP beta mediate stable interaction with GABP alpha and, when complexed with GABP alpha, directly contact DNA. These observations provide evidence for a distinct biochemical role for the 33-amino acid repeats, and suggest that they may serve as a module for the generation of specific dimerization interfaces.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, C C -- Brown, T A -- McKnight, S L -- New York, N.Y. -- Science. 1991 Aug 16;253(5021):762-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Research Laboratories, Carnegie Institution of Washington, Department of Embryology, Baltimore, MD 21210.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1876833" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Cross-Linking Reagents ; DNA/metabolism ; DNA-Binding Proteins/*chemistry/metabolism ; GA-Binding Protein Transcription Factor ; Macromolecular Substances ; Molecular Sequence Data ; Molecular Weight ; Multigene Family ; Nuclear Proteins/*chemistry/metabolism ; Oligonucleotides/chemistry ; Proto-Oncogene Proteins/chemistry ; Proto-Oncogene Proteins c-ets ; Rats ; Recombinant Proteins ; Structure-Activity Relationship ; Transcription Factors/*chemistry/metabolism
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    Gene trees and the origins of inbred strains of mice (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-10-25
    Description: Extensive data on genetic divergence among 24 inbred strains of mice provide an opportunity to examine the concordance of gene trees and species trees, especially whether structured subsamples of loci give congruent estimates of phylogenetic relationships. Phylogenetic analyses of 144 separate loci reproduce almost exactly the known genealogical relationships among these 24 strains. Partitioning these loci into structured subsets representing loci coding for proteins, the immune system and endogenous viruses give incongruent phylogenetic results. The gene tree based on protein loci provides an accurate picture of the genealogical relationships among strains; however, gene trees based upon immune and viral data show significant deviations from known genealogical affinities.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atchley, W R -- Fitch, W M -- GM-45344/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):554-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, North Carolina State University, Raleigh 27695.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948030" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Alleles ; Analysis of Variance ; Animals ; Genes, Immunoglobulin ; Genotype ; Mice ; Mice, Inbred Strains/*genetics ; *Phylogeny ; Probability ; Proteins/genetics
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  • 39
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    Stimulation of protein tyrosine phosphorylation by NMDA receptor activation (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-23
    Description: The N-methyl-D-aspartate (NMDA) receptor, a subtype of glutamate receptors, plays a key role in synaptic plasticity in the nervous system. After NMDA receptor activation, calcium entry into the postsynaptic neuron is a critical initial event. However, the subsequent mechanisms by which the NMDA receptor signal is processed are incompletely understood. Stimulation of cultured rat hippocampal cells with glutamate resulted in the rapid and transient tyrosine phosphorylation of a 39-kilodalton protein (p39). Tyrosine phosphorylation of p39 was triggered by the NMDA receptor and required an influx of Ca2+ from the extracellular medium. Because p39 was found to be highly related or identical to the microtubule-associated protein 2 kinase, the NMDA receptor signal may be processed by a sequential activation of protein kinases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bading, H -- Greenberg, M E -- CA 43855/CA/NCI NIH HHS/ -- NS 28829/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Aug 23;253(5022):912-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1715095" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinases ; Cells, Cultured ; Glutamates/pharmacology ; Glutamic Acid ; Hippocampus/drug effects/metabolism ; Immunoblotting ; Kinetics ; Phosphoproteins/*metabolism ; Phosphorylation ; Phosphotyrosine ; Protein Kinases/metabolism ; Rats ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Tyrosine/*analogs & derivatives/metabolism
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    New vector delivers genes to lung cells (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, M -- New York, N.Y. -- Science. 1991 Apr 19;252(5004):374.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2017677" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/*genetics ; Animals ; Emphysema/therapy ; Genetic Therapy ; *Genetic Vectors ; Humans ; *Lung ; Rats ; *Transfection ; alpha 1-Antitrypsin/genetics
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    EPA moves to reassess the risk of dioxin (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, L -- New York, N.Y. -- Science. 1991 May 17;252(5008):911.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2035022" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests ; *Carcinogens ; Dioxins/*toxicity ; Humans ; National Institute for Occupational Safety and Health (U.S.) ; Neoplasms, Experimental/chemically induced ; Rats ; Risk Factors ; United States ; *United States Environmental Protection Agency
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    Human immunodeficiency virus infection of human-PBL-SCID mice (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-15
    Description: Severe combined immunodeficient (SCID) mice reconstituted with human peripheral blood leukocytes (hu-PBL-SCID mice) have inducible human immune function and may be useful as a small animal model for acquired immunodeficiency syndrome (AIDS) research. Hu-PBL-SCID mice infected with human immunodeficiency virus-1 (HIV-1) contained virus that was recoverable by culture from the peritoneal cavity, spleen, peripheral blood, and lymph nodes for up to 16 weeks after infection; viral sequences were also detected by in situ hybridization and by amplification with the polymerase chain reaction (PCR). Mice could be infected with multiple strains of HIV-1, including LAV-1/Bru, IIIB, MN, SF2, and SF13. HIV-1 infection affected the concentration of human immunoglobulin and the number of CD4+ T cells in the mice. These results support the use of the hu-PBL-SCID mouse for studies of the pathogenesis and treatment of AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mosier, D E -- Gulizia, R J -- Baird, S M -- Wilson, D B -- Spector, D H -- Spector, S A -- AI-27703/AI/NIAID NIH HHS/ -- AI-29182/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1991 Feb 15;251(4995):791-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, Medical Biology Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1990441" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Transfusion ; Chimera/*immunology ; *Disease Models, Animal ; *HIV Infections/immunology ; *HIV-1/isolation & purification ; Humans ; Immunologic Deficiency Syndromes/genetics/*immunology ; Lymphocyte Transfusion ; Mice ; Mice, Mutant Strains/*immunology ; Spleen/microbiology
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    Inhibition of morphine tolerance and dependence by the NMDA receptor antagonist MK-801 (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-01-04
    Description: The N-methyl-D-aspartate (NMDA) subtype of the glutamate receptor is an important mediator of several forms of neural and behavioral plasticity. The present studies examined whether NMDA receptors might be involved in the development of opiate tolerance and dependence, two examples of behavioral plasticity. The noncompetitive NMDA receptor antagonist MK-801 attenuated the development of tolerance to the analgesic effect of morphine without affecting acute morphine analgesia. In addition, MK-801 attenuated the development of morphine dependence as assessed by naloxone-precipitated withdrawal. These results suggest that NMDA receptors may be important in the development of opiate tolerance and dependence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trujillo, K A -- Akil, H -- DA02265/DA/NIDA NIH HHS/ -- DA05336/DA/NIDA NIH HHS/ -- MH422251/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1991 Jan 4;251(4989):85-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mental Health Research Institute, University of Michigan, Ann Arbor 48109-0720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1824728" target="_blank"〉PubMed〈/a〉
    Keywords: *Analgesia ; Animals ; Behavior, Animal/drug effects ; Dizocilpine Maleate/*pharmacology ; Drug Tolerance ; Male ; *Morphine ; Naloxone/pharmacology ; Pain Measurement ; Rats ; Rats, Inbred Strains ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/*physiology ; *Substance-Related Disorders
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    The brain as "sexual organ" (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, A -- New York, N.Y. -- Science. 1991 Aug 30;253(5023):957-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1887226" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*anatomy & histology/physiology ; Corpus Callosum/anatomy & histology/physiology ; Female ; Humans ; Hypothalamus/*anatomy & histology/physiology ; Male ; Rats ; *Sex Characteristics
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  • 45
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    Antibody-mediated clearance of alphavirus infection from neurons (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-08
    Description: Humoral immunity is important for protection against viral infection and neutralization of extracellular virus, but clearance of virus from infected tissues is thought to be mediated solely by cellular immunity. However, in a SCID mouse model of persistent alphavirus encephalomyelitis, adoptive transfer of hyperimmune serum resulted in clearance of infectious virus and viral RNA from the nervous system, whereas adoptive transfer of sensitized T lymphocytes had no effect on viral replication. Three monoclonal antibodies to two different epitopes on the E2 envelope glycoprotein mediated viral clearance. Treatment of alphavirus-infected primary cultured rat neurons with these monoclonal antibodies to E2 resulted in decreased viral protein synthesis, followed by gradual termination of mature infectious virion production. Thus, antibody can mediate clearance of alphavirus infection from neurons by restricting viral gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levine, B -- Hardwick, J M -- Trapp, B D -- Crawford, T O -- Bollinger, R C -- Griffin, D E -- NS29234/NS/NINDS NIH HHS/ -- T32-NS-07000/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 8;254(5033):856-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, 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/1658936" target="_blank"〉PubMed〈/a〉
    Keywords: Alphavirus/immunology/isolation & purification/*physiology ; Animals ; Antibodies, Monoclonal/*therapeutic use ; Central Nervous System/immunology/*microbiology ; Encephalomyelitis/*immunology/microbiology/therapy ; *Immunotherapy, Adoptive ; Mice ; Mice, Inbred Strains ; Mice, SCID ; Neurons/immunology/*microbiology ; RNA, Viral/isolation & purification ; T-Lymphocytes/*immunology ; Togaviridae Infections/*immunology/therapy ; Virus Replication
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    CCAAT-enhancer binding protein: a component of a differentiation switch (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-01-18
    Description: The CCAAT-enhancer binding protein (C/EBP) has now been found to promote the terminal differentiation of adipocytes. During the normal course of adipogenesis, C/EBP expression is restricted to a terminal phase wherein proliferative growth is arrested, and specialized cell phenotype is first manifested. A conditional form of C/EBP was developed, making it feasible to test its capacity to regulate the differentiation of cultured adipocytes. Premature expression of C/EBP in adipoblasts caused a direct cessation of mitotic growth. Moreover, when abetted by the effects of three adipogenic hormones, C/EBP promoted terminal cell differentiation. Since C/EBP is expressed in a variety of tissues, it may have a fundamental role in regulating the balance between cell growth and differentiation in higher animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Umek, R M -- Friedman, A D -- McKnight, S L -- New York, N.Y. -- Science. 1991 Jan 18;251(4991):288-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Research Laboratories, Department of Embryology, Carnegic Institution of Washington, Baltimore, MD 21210.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1987644" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*cytology ; Animals ; CCAAT-Enhancer-Binding Proteins ; *Cell Differentiation ; Cell Division ; DNA-Binding Proteins/*physiology ; Gene Expression Regulation ; L Cells (Cell Line) ; Mice ; Nuclear Proteins/*physiology ; Receptors, Steroid/physiology ; Regulatory Sequences, Nucleic Acid ; Structure-Activity Relationship
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  • 47
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    Clusters of coupled neuroblasts in embryonic neocortex (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-26
    Description: The neocortex of the brain develops from a simple germinal layer into a complex multilayer structure. To investigate cellular interactions during early neocortical development, whole-cell patch clamp recordings were made from neuroblasts in the ventricular zone of fetal rats. During early corticogenesis, neuroblasts are physiologically coupled by gap junctions into clusters of 15 to 90 cells. The coupled cells form columns within the ventricular zone and, by virtue of their membership in clusters, have low apparent membrane resistances and generate large responses to the inhibitory neurotransmitter gamma-aminobutyric acid. As neuronal migration out of the ventricular zone progresses, the number of cells within the clusters decreases. These clusters allow direct cell to cell interaction at the earliest stages of corticogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lo Turco, J J -- Kriegstein, A R -- NS07280/NS/NINDS NIH HHS/ -- NS12151/NS/NINDS NIH HHS/ -- NS21223/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Apr 26;252(5005):563-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1850552" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebral Cortex/cytology/embryology/*physiology ; Electric Conductivity ; Electrophysiology/methods ; Embryo, Mammalian ; Evoked Potentials/drug effects ; In Vitro Techniques ; Membrane Potentials/drug effects ; Neurons/cytology/drug effects/*physiology ; Rats ; Receptors, GABA-A/physiology ; gamma-Aminobutyric Acid/pharmacology
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    Transmission between pairs of hippocampal slice neurons: quantal levels, oscillations, and LTP (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-05-03
    Description: Long-term potentiation (LTP) of synaptic transmission after coincident pre- and postsynaptic activity is considered a cellular model of changes underlying learning and memory. In intact tissue, LTP has been observed only between populations of neurons, making analysis of mechanisms difficult. Transmission between individual pre- and postsynaptic hippocampal cells was studied, suggesting quantal amplitude distributions with little variability in quantal size. LTP between such pairs is manifested by large, persistent, and synapse-specific potentiation with a shift in amplitude distribution that suggests presynaptic changes. Oscillations in amplitude of transmission, apparently of presynaptic origin, are common and can be triggered by LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malinow, R -- New York, N.Y. -- Science. 1991 May 3;252(5006):722-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1850871" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Conductivity ; Electrophysiology ; Hippocampus/*cytology ; Kinetics ; Membrane Potentials ; Neurons/*physiology ; Rats ; Statistics as Topic ; Synapses/*physiology ; Synaptic Transmission/*physiology
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    Atomic structure of adenosine deaminase complexed with a transition-state analog: understanding catalysis and immunodeficiency mutations (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-05-31
    Description: The crystal structure of a murine adenosine deaminase complexed with 6-hydroxyl-1,6-dihydropurine ribonucleoside, a nearly ideal transition-state analog, has been determined and refined at 2.4 angstrom resolution. The structure is folded as an eight-stranded parallel alpha/beta barrel with a deep pocket at the beta-barrel COOH-terminal end wherein the inhibitor and a zinc are bound and completely sequestered. The presence of the zinc cofactor and the precise structure of the bound analog were not previously known. The 6R isomer of the analog is very tightly held in place by the coordination of the 6-hydroxyl to the zinc and the formation of nine hydrogen bonds. On the basis of the structure of the complex a stereoselective addition-elimination or SN2 mechanism of the enzyme is proposed with the zinc atom and the Glu and Asp residues playing key roles. A molecular explanation of a hereditary disease caused by several point mutations of an enzyme is also presented.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, D K -- Rudolph, F B -- Quiocho, F A -- CA14030/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 May 31;252(5010):1278-84.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1925539" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/*chemistry/deficiency/metabolism ; Amino Acid Sequence ; Animals ; Binding Sites ; Catalysis ; Crystallization ; Immunologic Deficiency Syndromes/*enzymology/genetics ; Mice ; Models, Molecular ; Molecular Structure ; Mutation ; Protein Conformation ; Purine Nucleosides/chemistry/*metabolism ; Ribonucleosides/chemistry/*metabolism ; Zinc/metabolism
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    Primary structure and functional expression of the 5HT3 receptor, a serotonin-gated ion channel (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-18
    Description: The neurotransmitter serotonin (5HT) activates a variety of second messenger signaling systems and through them indirectly regulates the function of ion channels. Serotonin also activates ion channels directly, suggesting that it may also mediate rapid, excitatory responses. A complementary DNA clone containing the coding sequence of one of these rapidly responding channels, a 5HT3 subtype of the serotonin receptor, has been isolated by screening a neuroblastoma expression library for functional expression of serotonin-gated currents in Xenopus oocytes. The predicted protein product has many of the features shared by other members of the ligand-gated ion channel family. The pharmacological and electrophysiological characteristics of the cloned receptor are largely consistent with the properties of native 5HT3 receptors. Messenger RNA encoding this receptor is found in the brain, spinal cord, and heart. This receptor defines a new class of excitatory ligand-gated channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maricq, A V -- Peterson, A S -- Brake, A J -- Myers, R M -- Julius, D -- GM44298/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 18;254(5030):432-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Francisco 94143-0450.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1718042" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding, Competitive ; Cell Line ; Ion Channels/*chemistry/drug effects/physiology ; Mice ; Molecular Sequence Data ; Oocytes/metabolism ; Poly A ; RNA, Messenger ; Radioligand Assay ; Receptors, Serotonin/*chemistry/drug effects/physiology ; Xenopus
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    The trk proto-oncogene product: a signal transducing receptor for nerve growth factor (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-26
    Description: The trk proto-oncogene encodes a 140-kilodalton, membrane-spanning protein tyrosine kinase (p140prototrk) that is expressed only in neural tissues. Nerve growth factor (NGF) stimulates phosphorylation of p140prototrk in neural cell lines and in embryonic dorsal root ganglia. Affinity cross-linking and equilibrium binding experiments with 125I-labeled NGF indicate that p140prototrk binds NGF specifically in cultured cells with a dissociation constant of 10(-9) molar. The identification of p140prototrk as an NGF receptor indicates that this protein participates in the primary signal transduction mechanism of NGF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaplan, D R -- Hempstead, B L -- Martin-Zanca, D -- Chao, M V -- Parada, L F -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Apr 26;252(5005):554-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Eukaryotic Signal Transduction Group, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1850549" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/physiology ; Cross-Linking Reagents ; Embryo, Mammalian ; Ganglia, Spinal/*metabolism ; Humans ; Kinetics ; Mice ; Nerve Growth Factors/metabolism/*physiology ; Neuroblastoma ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; *Proto-Oncogenes ; Receptor, trkA ; Receptors, Cell Surface/metabolism/*physiology ; Receptors, Nerve Growth Factor ; *Signal Transduction
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    Oscillations of cytosolic sodium during calcium oscillations in exocrine acinar cells (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-11-15
    Description: In acinar cells from rat salivary glands, cholinergic agonists cause oscillations in cytoplasmic free calcium concentration, which then drive oscillations of cell volume that reflect oscillating cell solute content and fluid secretion. By quantitative fluorescence ratio microscopy of an intracellular indicator dye for sodium, it has now been shown that large amplitude oscillations of sodium concentration were associated with the calcium and cell volume oscillations. Both calcium and sodium oscillations were dependent on the continued presence of calcium in the extracellular medium and were abolished by the specific sodium-potassium adenosine triphosphatase inhibitor ouabain. Thus, calcium oscillations in salivary acinar cells, by modulating the activities of ion transport pathways in the plasma membrane, can cause significant oscillations of monovalent ions that may in turn feed back to regulate calcium oscillations and fluid secretion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, M M -- Foskett, J K -- New York, N.Y. -- Science. 1991 Nov 15;254(5034):1014-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology, Research Institute, Hospital for Sick Children, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*physiology ; Chlorides/physiology ; Cytosol/physiology ; In Vitro Techniques ; Male ; Ouabain/pharmacology ; Parotid Gland/*physiology ; Periodicity ; Potassium/physiology ; Rats ; Rats, Inbred Strains ; Sodium/*physiology ; Water-Electrolyte Balance
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    Effect of light chain V region duplication on IgG oligomerization and in vivo efficacy (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-05-03
    Description: A human immunoglobulin G1 (IgG1) antibody oligomer was isolated from a transfected myeloma cell line that produced a monoclonal antibody to group B streptococci. Compared to the IgG1 monomer, the oligomer was significantly more effective at protecting neonatal rats from infection in vivo. The oligomer was also shown to cross the placenta and to be stable in neonatal rats. Immunochemical analysis and complementary DNA sequencing showed that the transfected cell line produced two distinct kappa light chains: a normal light chain (Ln) with a molecular mass of 25 kilodaltons and a 37-kilodalton species (L37), the domain composition of which was variable-variable-constant (V-V-C). Cotransfection of vectors encoding the heavy chain and L37 resulted in production of oligomeric IgG.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shuford, W -- Raff, H V -- Finley, J W -- Esselstyn, J -- Harris, L J -- New York, N.Y. -- Science. 1991 May 3;252(5006):724-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immune Sciences, Bristol-Myers Squibb Pharmaceutical Research Institute-Seattle, WA 98121.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1902593" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antibodies, Bacterial/biosynthesis/immunology/pharmacokinetics ; Antibodies, Monoclonal/biosynthesis/immunology/pharmacokinetics ; Cell Line ; Female ; Humans ; Immunization, Passive ; Immunoglobulin G/*biosynthesis/genetics/immunology ; Immunoglobulin M/genetics ; Immunoglobulin Variable Region/*biosynthesis/genetics/immunology ; Immunoglobulin kappa-Chains/*biosynthesis/genetics/immunology ; Macromolecular Substances ; Maternal-Fetal Exchange ; Multiple Myeloma ; Pregnancy ; Rats ; Streptococcal Infections/prevention & control ; Streptococcus agalactiae/immunology ; Transfection
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    Carcinogenesis models (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-01-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1991 Jan 11;251(4990):142-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1987635" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carcinogenicity Tests ; Cell Division ; Mathematics ; Mice ; Mitosis
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    OPC-21268, an orally effective, nonpeptide vasopressin V1 receptor antagonist (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-04-26
    Description: An orally effective, nonpeptide, vasopressin V1 receptor antagonist, OPC-21268, has been identified. This compound selectively antagonized binding to the V1 subtype of the vasopressin receptor in a competitive manner. In vivo, the compound acted as a specific antagonist of arginine vasopressin (AVP)-induced vasoconstriction. After oral administration in conscious rats, the compound also antagonized pressor responses to AVP. OPC-21268 can be used to study the physiological role of AVP and may be therapeutically useful in the treatment of hypertension and congestive heart failure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamamura, Y -- Ogawa, H -- Chihara, T -- Kondo, K -- Onogawa, T -- Nakamura, S -- Mori, T -- Tominaga, M -- Yabuuchi, Y -- New York, N.Y. -- Science. 1991 Apr 26;252(5005):572-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Second Tokushima Institute of New Drug Research, Otsuka Pharmaceutical Co., Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1850553" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Angiotensin II/pharmacology ; Animals ; Arginine Vasopressin/antagonists & inhibitors/metabolism/*pharmacology ; Binding, Competitive ; Blood Pressure/*drug effects ; Cell Membrane/metabolism ; Kidney/metabolism ; Kinetics ; Liver/metabolism ; Norepinephrine/pharmacology ; Piperidines/administration & dosage/*pharmacology ; Quinolones/administration & dosage/*pharmacology ; Rats ; Receptors, Angiotensin/*drug effects/metabolism ; Receptors, Vasopressin ; Time Factors
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  • 56
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    The anion paradox in sodium taste reception: resolution by voltage-clamp studies (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-01
    Description: Sodium salts are potent taste stimuli, but their effectiveness is markedly dependent on the anion, with chloride yielding the greatest response. The cellular mechanisms that mediate this phenomenon are not known. This "anion paradox" has been resolved by considering the field potential that is generated by restricted electrodiffusion of the anion through paracellular shunts between taste-bud cells. Neural responses to sodium chloride, sodium acetate, and sodium gluconate were studied while the field potential was voltage-clamped. Clamping at electronegative values eliminated the anion effect, whereas clamping at electropositive potentials exaggerated it. Thus, field potentials across the lingual epithelium modulate taste reception, indicating that the functional unit of taste reception includes the taste cell and its paracellular microenvironment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ye, Q -- Heck, G L -- DeSimone, J A -- DC00122/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 1;254(5032):724-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Virginia Commonwealth University, Richmond 23298-0551.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948054" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anions ; Chemoreceptor Cells/physiology ; Epithelium/physiology ; Evoked Potentials ; Female ; Models, Biological ; Mouth Mucosa/innervation/*physiology ; Neurons/physiology ; Rats ; Rats, Inbred Strains ; *Sodium ; *Sodium Chloride ; Taste/*physiology ; Tongue/*innervation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The effect of anti-neoplastic drugs on murine acquired immunodeficiency syndrome (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-01-18
    Description: The murine acquired immunodeficiency syndrome (MAIDS) is associated with proliferation of target cells that have been infected by a defective retrovirus. To control the growth of this primary neoplasia, virus-inoculated mice were treated with anti-neoplastic drugs. Paradoxically, cyclophosphamide, which is also immunosuppressive, was very effective in preventing the appearance and progression of the disease, in restoring a normal T cell function, and in depleting the number of infected target cells. This result suggests that the proliferating infected target cells were responsible for the immunodeficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simard, C -- Jolicoeur, P -- New York, N.Y. -- Science. 1991 Jan 18;251(4991):305-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Biology, Clinical Research Institute of Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1987646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*therapeutic use ; Blotting, Northern ; Blotting, Southern ; Cell Division ; Cyclophosphamide/therapeutic use ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Murine Acquired Immunodeficiency Syndrome/*drug therapy/pathology ; RNA, Viral/analysis ; Spleen/pathology ; Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Prevention of xenograft rejection by masking donor HLA class I antigens (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-06-21
    Description: Destruction of target cells by cytotoxic T lymphocytes requires the presence of HLA (human lymphocyte antigen) class I antigens on the target cells for adhesion as well as for triggering of the antigen-specific T cell receptor. Rejection of xenogeneic human pancreatic islets and liver was circumvented by masking, before transplantation, donor antigens with F(ab')2 antibody fragments to HLA class I or tissue-specific epitopes. This strategy eliminated the need for recipient immunosuppression and allowed islet xenograft survival beyond 200 days, as demonstrated functionally by C peptide secretion as well as by histology. These in vivo observations are consistent with the importance of donor HLA class I in eliciting graft rejection and have potential applicability to the successful transplantation of other HLA class I-bearing donor tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faustman, D -- Coe, C -- New York, N.Y. -- Science. 1991 Jun 21;252(5013):1700-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Diabetes Unit, Massachusetts General Hospital, Harvard Medical School, Boston 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1710828" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antigen-Antibody Complex ; Antigens, CD/immunology ; Antigens, CD29 ; C-Peptide/blood ; *Graft Rejection ; Histocompatibility Antigens Class I/*immunology ; Humans ; Immunoglobulin Fab Fragments/immunology ; Islets of Langerhans/*immunology ; Islets of Langerhans Transplantation/*immunology ; Mice ; Mice, Inbred BALB C ; T-Lymphocytes/*immunology ; Transplantation, Heterologous
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  • 59
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    Dynamic organization of developing Purkinje cells revealed by transgene expression (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-01
    Description: The cerebellum has many properties that make it a useful model for investigating neural development. Purkinje cells, the major output neurons of the cerebellar cortex, have drawn special attention because of the availability of biochemical markers and mutants that affect their development. The spatial expression of L7, a protein specific for Purkinje cells, and L7 beta Gal, a gene expressed in transgenic mice that was constructed from the L7 promoter and the marker beta-galactosidase, delineated bands of Purkinje cells that increased in number during early postnatal development. Expression of the transgene in adult reeler mutant mice, which show inverted cortical lamination, and in primary culture showed that the initial expression of L7 is intrinsic to Purkinje cells and does not depend on extracellular signals. This may reflect an underlying developmental map in cerebellum.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smeyne, R J -- Oberdick, J -- Schilling, K -- Berrebi, A S -- Mugnaini, E -- Morgan, J I -- NRSA 08-08601/NR/NINR NIH HHS/ -- NS-09904/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 1;254(5032):719-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosciences, Roche Institute of Molecular Biology, Roche Research Center, Nutley, NJ 07110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948052" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Cerebellum/cytology/embryology/*growth & development ; Embryonic and Fetal Development ; Mice ; Mice, Neurologic Mutants ; Mice, Transgenic ; Purkinje Cells/cytology/*physiology ; Recombinant Proteins/metabolism ; beta-Galactosidase/*genetics/metabolism
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    Zinc finger-DNA recognition: crystal structure of a Zif268-DNA complex at 2.1 A (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-10
    Description: The zinc finger DNA-binding motif occurs in many proteins that regulate eukaryotic gene expression. The crystal structure of a complex containing the three zinc fingers from Zif268 (a mouse immediate early protein) and a consensus DNA-binding site has been determined at 2.1 angstroms resolution and refined to a crystallographic R factor of 18.2 percent. In this complex, the zinc fingers bind in the major groove of B-DNA and wrap part way around the double helix. Each finger has a similar relation to the DNA and makes its primary contacts in a three-base pair subsite. Residues from the amino-terminal portion of an alpha helix contact the bases, and most of the contracts are made with the guanine-rich strand of the DNA. This structure provides a framework for understanding how zinc fingers recognize DNA and suggests that this motif may provide a useful basis for the design of novel DNA-binding proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pavletich, N P -- Pabo, C O -- GM-31471/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 May 10;252(5007):809-17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, 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/2028256" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Crystallography ; DNA/*metabolism ; DNA-Binding Proteins/*chemistry/isolation & purification/physiology ; Early Growth Response Protein 1 ; *Immediate-Early Proteins ; Mice ; Models, Molecular ; Molecular Sequence Data ; Molecular Structure ; Transcription Factors/*chemistry/isolation & purification/physiology ; Zinc Fingers/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Identification of a gene located at chromosome 5q21 that is mutated in colorectal cancers (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-15
    Description: Recent studies have suggested the existence of a tumor suppressor gene located at chromosome region 5q21. DNA probes from this region were used to study a panel of sporadic colorectal carcinomas. One of these probes, cosmid 5.71, detected a somatically rearranged restriction fragment in the DNA from a single tumor. Further analysis of the 5.71 cosmid revealed two regions that were highly conserved in rodent DNA. These sequences were used to identify a gene, MCC (mutated in colorectal cancer), which encodes an 829-amino acid protein with a short region of similarity to the G protein-coupled m3 muscarinic acetylcholine receptor. The rearrangement in the tumor disrupted the coding region of the MCC gene. Moreover, two colorectal tumors were found with somatically acquired point mutations in MCC that resulted in amino acid substitutions. MCC is thus a candidate for the putative colorectal tumor suppressor gene located at 5q21. Further studies will be required to determine whether the gene is mutated in other sporadic tumors or in the germ line of patients with an inherited predisposition to colonic tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kinzler, K W -- Nilbert, M C -- Vogelstein, B -- Bryan, T M -- Levy, D B -- Smith, K J -- Preisinger, A C -- Hamilton, S R -- Hedge, P -- Markham, A -- 6M 07184/PHS HHS/ -- CA 06973/CA/NCI NIH HHS/ -- CA 09243/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Mar 15;251(4999):1366-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics Laboratory, Johns Hopkins Oncology Center, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1848370" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli/*genetics ; Amino Acid Sequence ; Animals ; Base Sequence ; *Chromosomes, Human, Pair 5 ; Colorectal Neoplasms/*genetics ; Exons ; GTP-Binding Proteins/metabolism ; Gene Expression ; *Genes, Tumor Suppressor ; Humans ; Molecular Sequence Data ; Mutation ; Oligonucleotides/chemistry ; Polymerase Chain Reaction ; Proteins/*genetics/metabolism ; Rats ; Sequence Homology, Nucleic Acid ; *Tumor Suppressor Proteins
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    Anti-HIV and anti-anti-MHC antibodies in alloimmune and autoimmune mice (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-09-06
    Description: Alloimmune mice (mice that have been exposed to cells from another murine strain) were shown to make antibodies against gp120 and p24 of human immunodeficiency virus (HIV), and mice of the autoimmune strains MRL-lpr/lpr and MRL-(+)/+ made antibodies against gp120. This is surprising because the mice were not exposed to HIV. Furthermore, anti-anti-MHC antibodies (molecules that have shapes similar to those of major histocompatibility complex molecules) were detected in both alloimmune sera and MRL mice. These results are discussed in the context of a possible role for allogeneic stimuli in the pathogenesis of acquired immunodeficiency syndrome, as suggested by an idiotypic network model.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kion, T A -- Hoffmann, G W -- New York, N.Y. -- Science. 1991 Sep 6;253(5024):1138-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of British Columbia, Vancouver, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1909456" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; *Antibody Formation ; Autoimmune Diseases/genetics/*immunology/microbiology ; Enzyme-Linked Immunosorbent Assay ; Gene Products, gag/*immunology ; HIV Antibodies/*biosynthesis ; HIV Antigens/*immunology ; HIV Core Protein p24 ; HIV Envelope Protein gp120/*immunology ; Histocompatibility Antigens Class II/*immunology ; Isoantibodies/*biosynthesis ; *Major Histocompatibility Complex ; Mice ; Mice, Inbred BALB C ; Mice, Inbred CBA ; Mice, Mutant Strains ; T-Lymphocytes/immunology ; Viral Core Proteins/*immunology
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    Human hemoglobin switching (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stamatoyannopoulos, G -- New York, N.Y. -- Science. 1991 Apr 19;252(5004):383.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2017679" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/genetics ; Animals ; Fetus/metabolism ; *Gene Expression Regulation ; Globins/*genetics ; Humans ; Mice ; Mice, Transgenic ; Regulatory Sequences, Nucleic Acid ; Thalassemia/genetics
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    GPI-anchored cell-surface molecules complexed to protein tyrosine kinases (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-15
    Description: Binding of ligand or antibody to certain cell-surface proteins that are anchored to the membrane by glycophosphatidylinositol (GPI) can cause activation of leukocytes. However, it is not known how these molecules, which lack intracellular domains, can transduce signals. The GPI-linked human molecules CD59, CD55, CD48, CD24, and CD14 as well as the mouse molecules Thy-1 and Ly-6 were found to associate with protein tyrosine kinases, key regulators of cell activation and signal transduction. A protein tyrosine kinase associated with the GPI-linked proteins CD59, CD55, and CD48 in human T cells, and with Thy-1 in mouse T cells was identified as p56lck, a protein tyrosine kinase related to Src. This interaction of GPI-linked molecules with protein tyrosine kinases suggests a potential mechanism of signal transduction in cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stefanova, I -- Horejsi, V -- Ansotegui, I J -- Knapp, W -- Stockinger, H -- New York, N.Y. -- Science. 1991 Nov 15;254(5034):1016-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Immunology-Vienna International Research Cooperation Center, University of Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1719635" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*physiology ; Antigens, Differentiation/physiology ; Cell Adhesion Molecules/physiology ; Glycolipids/physiology ; Glycosylphosphatidylinositols ; Humans ; Membrane Glycoproteins/physiology ; Membrane Proteins/*physiology ; Mice ; Phosphatidylinositols/physiology ; Phosphorylation ; Phosphotyrosine ; Protein-Tyrosine Kinases/*physiology ; Receptor Aggregation ; Receptors, Cell Surface/*physiology ; Signal Transduction ; Tyrosine/analogs & derivatives/metabolism
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    Suppression of the immune response by a soluble complement receptor of B lymphocytes (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-10-04
    Description: The CD19-CR2 complex of B lymphocytes contains proteins that participate in two host-defense systems, the immune and complement systems. The ligand for the subunit of the immune system, CD19, is not known, but the complement receptor subunit, CR2 (CD21), binds activation fragments of the C3 component of the complement system and may mediate immunopotentiating effects of complement. A recombinant, soluble CR2 was prepared by fusing the C3-binding region of the receptor to immunoglobulin G1 (IgG1). The (CR2)2-IgG1 chimera competed with cellular CR2 for C3 binding and suppressed the antibody response to a T cell-dependent antigen when administered to mice at the time of immunization. This inhibitory effect of (CR2)2-IgG1 demonstrates the B cell-activating function of the CD19-CR2 complex and suggests a new method for humoral immunosuppression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hebell, T -- Ahearn, J M -- Fearon, D T -- AI-22833/AI/NIAID NIH HHS/ -- AI-28191/AI/NIAID NIH HHS/ -- GM-43803/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 4;254(5028):102-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, 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/1718035" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Antibody Formation ; Antigens, CD/*physiology ; Antigens, CD19 ; Antigens, Differentiation, B-Lymphocyte/chemistry/*physiology ; B-Lymphocytes/*physiology ; Base Sequence ; Binding, Competitive ; Cloning, Molecular ; Immunosuppression ; In Vitro Techniques ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Molecular Sequence Data ; Receptors, Complement/chemistry/*physiology ; Receptors, Complement 3d ; Recombinant Fusion Proteins ; Signal Transduction ; Solubility
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    Characterization of a cofactor that regulates dimerization of a mammalian homeodomain protein (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-20
    Description: Dimerization among transcription factors has become a recurrent theme in the regulation of eukaryotic gene expression. Hepatocyte nuclear factor-1 alpha (HNF-1 alpha) is a homeodomain-containing protein that functions as a dimer. A dimerization cofactor of HNF-1 alpha (DCoH) was identified that displayed a restricted tissue distribution and did not bind to DNA, but, rather, selectively stabilized HNF-1 alpha dimers. The formation of a stable tetrameric DCoH-HNF-1 alpha complex, which required the dimerization domain of HNF-1 alpha, did not change the DNA binding characteristics of HNF-1 alpha, but enhanced its transcriptional activity. However, DCoH did not confer transcriptional activation to the GAL4 DNA binding domain. These results indicate that DCoH regulates formation of transcriptionally active tetrameric complexes and may contribute to the developmental specificity of the complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mendel, D B -- Khavari, P A -- Conley, P B -- Graves, M K -- Hansen, L P -- Admon, A -- Crabtree, G R -- CA 09302/CA/NCI NIH HHS/ -- HD 07201/HD/NICHD NIH HHS/ -- HL 33942/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1762-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1763325" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Nucleus/physiology ; Chromosome Deletion ; DNA-Binding Proteins/*metabolism ; Gene Library ; Hepatocyte Nuclear Factor 1 ; Hepatocyte Nuclear Factor 1-alpha ; Hepatocyte Nuclear Factor 1-beta ; Humans ; *Hydro-Lyases ; Liver/physiology ; Macromolecular Substances ; Mice ; Molecular Sequence Data ; *Nuclear Proteins ; Protein Biosynthesis ; RNA, Messenger/genetics ; Rabbits ; Rats ; Reticulocytes/metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic
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    Control of granulocytes and macrophages: molecular, cellular, and clinical aspects (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-25
    Description: The production and functional activity of two important white blood cells, the granulocytes and macrophages, are regulated mainly by a group of glycoprotein colony-stimulating factors. The colony-stimulating factors have been mass-produced with recombinant technology and are now proving of value in preventing or suppressing infections in a variety of individuals with subnormal or defective formation of blood cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Metcalf, D -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):529-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Post Office Royal Melbourne Hospital, Victoria, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948028" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/therapy ; Anemia, Aplastic/therapy ; Animals ; Colony-Stimulating Factors/genetics/*physiology/therapeutic use ; Granulocytes/cytology/*physiology ; Hematopoiesis ; Hematopoietic Stem Cells/cytology/*physiology ; Humans ; Macrophages/cytology/*physiology ; Mice ; Neoplasms/therapy ; Neutropenia/therapy ; Recombinant Proteins/therapeutic use
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    Of genes and genomes (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hillis, D M -- Bull, J J -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):528.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Texas, Austin 78712.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948027" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Genes ; *Genome ; Mice ; Mice, Inbred Strains/*genetics ; *Phylogeny ; Polymorphism, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Energy transfer between two peptides bound to one MHC class II molecule (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-04
    Description: The 17-amino acid peptide from chicken ovalbumin, Ova(323-339), was labeled at the amino terminus with fluorescein [FOva(323-339)] and near the carboxyl terminus with Texas Red [AcOva(323-338)KTR]. Fluorescence spectroscopy was carried out on resolved electrophoretic bands on nonreducing polyacrylamide gels derived from incubation mixtures containing major histocompatibility complex (MHC) class II molecules IAd and the FOva(323-339)- and AcOva(323-338)KTR-labeled peptides. Energy transfer between fluorescein and Texas Red was observed in the "floppy" alpha beta heterodimer band, but not in the "compact" alpha beta heterodimer band. Energy transfer was detected between the truncated peptides FOva(323-328)CONH2 and AcOva(331-338)KTR in both the compact alpha beta and floppy alpha beta gel bands. The energy-transfer data suggest that the two binding sites of floppy alpha beta arise from splitting apart a putative large, single binding site region in compact alpha beta.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tampe, R -- Clark, B R -- McConnell, H M -- 2R37 AI 13587-16/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 4;254(5028):87-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stauffer Laboratory for Physical Chemistry, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1656526" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Energy Transfer ; Histocompatibility Antigens Class II/chemistry/*metabolism ; In Vitro Techniques ; Mice ; Molecular Sequence Data ; Ovalbumin/chemistry ; Peptides/chemistry/*metabolism ; Spectrometry, Fluorescence ; Structure-Activity Relationship
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    Generation and analysis of interleukin-4 deficient mice (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-01
    Description: Interleukin-4 (IL-4) promotes the growth and differentiation of many hematopoietic cells in vitro; in particular, it directs the immunoglobulin (Ig) class switch to IgG1 and IgE. Mice homozygous for a mutation that inactivates the IL-4 gene were generated to test the requirement for IL-4 in vivo. In the mutant mice T and B cell development was normal, but the serum levels of IgG1 and IgE were strongly reduced. The IgG1 dominance in a T cell-dependent immune response was lost, and IgE was not detectable upon nematode infection. Thus, some but not all of the in vitro properties of IL-4 are critical for the physiology of the immune system in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuhn, R -- Rajewsky, K -- Muller, W -- New York, N.Y. -- Science. 1991 Nov 1;254(5032):707-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948049" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Alleles ; Animals ; B-Lymphocytes/immunology ; Blotting, Southern ; Chromosome Deletion ; Concanavalin A ; DNA/genetics/isolation & purification ; Female ; Interleukin-4/deficiency/*genetics ; Lymph Nodes/growth & development/immunology ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Restriction Mapping ; Spleen/growth & development/immunology ; T-Lymphocytes/immunology ; Thymus Gland/growth & development/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Cloning of a serotonin transporter affected by antidepressants (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-25
    Description: A complementary DNA clone for a serotonin (5HT) transporter has been isolated from rat basophilic leukemia cells. The complementary DNA sequence predicts a 653-amino acid protein with 12 to 13 putative transmembrane domains. The 5HT transporter has significant homology to the gamma-aminobutyric acid, dopamine, and norepinephrine transporters. Uptake by CV-1 cells expressing the transporter complementary DNA resembles 5HT uptake by platelets and brain synaptosomes; it is sensitive to antidepressants, amphetamine derivatives, and cocaine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, B J -- Mezey, E -- Brownstein, M J -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):579-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948036" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antidepressive Agents/*pharmacology ; Base Sequence ; Carrier Proteins/drug effects/*genetics/metabolism ; Cell Line ; Cloning, Molecular ; Kinetics ; Leukemia, Basophilic, Acute ; Molecular Sequence Data ; Oligonucleotide Probes ; Rats ; Serotonin/*metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Genes for epilepsy mapped in the mouse (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-09
    Description: The neurological mutant mouse strain E1 is a model for complex partial seizures in humans. The inheritance of epileptic seizures with seven conventional chromosomal markers and over 60 endogenous proviral markers was studied by means of back-crosses of E1 with two seizure-resistant strains, DBA/2J and ABP/LeJ. The major gene responsible for this epileptic phenotype (El-1) was localized to a region distal with respect to the centromere on chromosome 9. At least one other gene, El-2, linked to proviral markers on chromosome 2, also influences the seizure phenotype. In addition, a potential modifier of seizures was detected in the DBA/2J background. The location of El-1 on distal chromosome 9 may allow identification of an epilepsy candidate gene in humans on the basis of conserved synteny with human chromosome 3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rise, M L -- Frankel, W N -- Coffin, J M -- Seyfried, T N -- NS 23355/NS/NINDS NIH HHS/ -- R35CA44385/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Aug 9;253(5020):669-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Boston College, Chestnut Hill 02167.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1871601" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Crosses, Genetic ; Epilepsy/*genetics ; Female ; Genetic Predisposition to Disease ; Male ; Mice ; Mice, Inbred Strains ; Mice, Neurologic Mutants/*genetics ; Recombination, Genetic ; Seizures/genetics ; Software
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Peripheral selection of the T cell repertoire (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-08
    Description: T lymphocytes undergo selection events not only in the thymus, but also after they leave the thymus and reside in the periphery. Peripheral selection was found to be dependent on T cell receptor (TCR)-ligand interactions but to differ from thymic selection with regard to specificity and mechanism. Unlike thymic selection, peripheral selection required binding of antigen to the TCR, and it induced expansion of T cell clones. Tolerance to self antigens that are restricted to the periphery occurred through the elimination of self-reactive T cells and by the clonal anergy, which was associated with down-regulation of the alpha beta TCR and CD8.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rocha, B -- von Boehmer, H -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1225-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite INSERM U-25 CNRS UA-122, Hopital Necker, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1900951" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/immunology ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/immunology ; Cells, Cultured ; Down-Regulation ; Female ; Histocompatibility Antigens Class I/immunology ; Immunotherapy, Adoptive ; Male ; Mice ; Mice, Nude ; Receptors, Antigen, T-Cell/*physiology ; T-Lymphocytes/*immunology ; Thymectomy ; Thymus Gland/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A dominant negative form of transcription activator mTFE3 created by differential splicing (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-10-04
    Description: Transcription factor E3 (mTFE3) is a murine transcription activator that binds to the intronic enhancer of the immunoglobulin heavy chain gene. A naturally occurring splice product of mTFE3 messenger RNA (mRNA) lacked 105 nucleotides that encode an activation domain; both absolute and relative amounts of long and truncated mRNAs varied in different tissues. Cells were cotransfected with complementary DNAs that encoded the two mRNA forms in amounts that corresponded to the amounts of each mRNA found in different cells. Small changes in substoichiometric amounts of the truncated form of mRNA effected trans-dominant negative modulation of mTFE3 activity. These findings identify a function for differential splicing in the regulation of transcription factor activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roman, C -- Cohn, L -- Calame, K -- R01CA38571/CA/NCI NIH HHS/ -- R01GM28361/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 4;254(5028):94-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1840705" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; DNA-Binding Proteins/*genetics ; *Gene Expression Regulation ; Mice ; Molecular Sequence Data ; RNA Splicing ; RNA, Messenger/genetics ; Regulatory Sequences, Nucleic Acid ; Structure-Activity Relationship ; Transcription Factors/*genetics ; *Transcription, Genetic
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    Oct-3 and the beginning of mammalian development (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosner, M H -- Vigano, M A -- Rigby, P W -- Arnheiter, H -- Staudt, L M -- New York, N.Y. -- Science. 1991 Jul 12;253(5016):144-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1853199" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Replication ; DNA-Binding Proteins/*physiology ; Embryo, Mammalian/*physiology ; Gene Expression Regulation ; Mice ; Octamer Transcription Factor-3 ; Stem Cells/physiology ; Teratoma/genetics/pathology ; Transcription Factors/*physiology
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    Hypotensive activity of fibroblast growth factor (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-22
    Description: Acidic and basic fibroblast growth factors (FGFs) are members of a family of proteins that are broad-spectrum mitogens, have diverse hormone-like activities, and function in tumorigenesis. FGF's ability to raise the concentration of intracellular calcium ion suggests that FGF could induce the synthesis of endothelium-derived relaxing factor (EDRF) and consequently vasodilation. Systemic administration of FGF decreased arterial blood pressure. This effect was mediated by EDRF and by adenosine triphosphate-sensitive potassium ion channels. The hypotensive effect of FGF was segregated from its mitogenic activity by protein engineering. These results extend the range of FGF autocrine activities and potential therapeutic applications, emphasize the role of endothelium as an arterial blood pressure--regulating organ, and provide insight on the structural basis of FGF functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cuevas, P -- Carceller, F -- Ortega, S -- Zazo, M -- Nieto, I -- Gimenez-Gallego, G -- New York, N.Y. -- Science. 1991 Nov 22;254(5035):1208-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hospital Universitario Ramon y Cajal, Carretera de Colmenar, Madrid, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1957172" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Pressure/*drug effects ; Dose-Response Relationship, Drug ; Fibroblast Growth Factors/chemistry/*pharmacology ; Glyburide/pharmacology ; Nitric Oxide/physiology ; Potassium Channels/drug effects ; Rabbits ; Rats ; Structure-Activity Relationship ; Time Factors
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    MHC class I deficiency: susceptibility to natural killer (NK) cells and impaired NK activity (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-12
    Description: The role of major histocompatibility complex (MHC) class I expression in natural killer (NK) cell target recognition is controversial. Normal T cell blasts from MHC class I-deficient mutant mice were found to serve as target cells for NK cells in vitro, which suggests that MHC class I molecules are directly involved in NK cell recognition. Spleen cells from the mutant mice were deficient in their ability to lyse MHC class I-deficient target cells or NK-susceptible tumor targets, and mutant mice could not reject allogeneic bone marrow. Thus, class I molecules may participate in the positive selection or tolerance induction of NK cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liao, N S -- Bix, M -- Zijlstra, M -- Jaenisch, R -- Raulet, D -- R01 AI30171/AI/NIAID NIH HHS/ -- R35 CA44339/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 12;253(5016):199-202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1853205" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytotoxicity, Immunologic ; Histocompatibility Antigens Class I/*immunology ; *Immunity, Cellular ; *Immunity, Innate ; Killer Cells, Natural/*immunology ; Major Histocompatibility Complex ; Mice ; Mice, Inbred Strains ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Cytotoxic/immunology ; beta 2-Microglobulin/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Inhibition of PDGF beta receptor signal transduction by coexpression of a truncated receptor (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-10
    Description: A mutated form of the platelet-derived growth factor (PDGF) beta receptor lacking most of its cytoplasmic domain was tested for its ability to block wild-type PDGF receptor function. PDGF induced the formation of complexes consisting of wild-type and truncated receptors. Such complexes were defective in autophosphorylation. When truncated receptors were expressed in excess compared to wild-type receptors, stimulation by PDGF of receptor autophosphorylation, association of phosphatidylinositol-3 kinase with the receptor, and calcium mobilization were blocked. Thus, a truncated receptor can inactivate wild-type receptor function by forming ligand-dependent receptor complexes (probably heterodimers) that are incapable of mediating the early steps of signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ueno, H -- Colbert, H -- Escobedo, J A -- Williams, L T -- P01 HL-43821/HL/NHLBI NIH HHS/ -- R01 HL-32898/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1991 May 10;252(5007):844-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1851331" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Centrifugation, Density Gradient ; Cricetinae ; In Vitro Techniques ; Ligands ; Mice ; Mice, Inbred BALB C ; Phosphorylation ; Platelet-Derived Growth Factor ; Receptors, Cell Surface/*antagonists & inhibitors/physiology ; Receptors, Platelet-Derived Growth Factor ; Signal Transduction/*physiology
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    Enhanced motility in NIH 3T3 fibroblasts that overexpress gelsolin (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-03-08
    Description: Increasing the content of the actin-binding protein gelsolin in cultured mouse fibroblasts by up to 125 percent by gene transfection proportionally enhanced the rate at which the cells migrated through porous filters toward a gradient of serum and closed a wound made on a confluent monolayer of cells in a tissue culture dish. These results provide direct evidence that gelsolin, which promotes both actin assembly and disassembly in vitro, is an important element in fibroblast locomotion and demonstrate that the manipulation of intracellular machinery can increase cell motility.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cunningham, C C -- Stossel, T P -- Kwiatkowski, D J -- AI28465/AI/NIAID NIH HHS/ -- HL07680/HL/NHLBI NIH HHS/ -- HL19429/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1233-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hematology-Oncology Unit, Massachusetts General Hospital, Boston 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1848726" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Binding Proteins/genetics/*physiology ; Cell Line ; *Chemotaxis ; Fibroblasts/physiology ; Gelsolin ; Gene Expression ; Humans ; Kinetics ; Mice ; Microfilament Proteins/genetics/*physiology ; RNA Splicing ; RNA, Messenger/genetics ; Transfection
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    Functional modulation of brain sodium channels by protein kinase C phosphorylation (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-10-04
    Description: Voltage-gated sodium channels, which are responsible for the generation of action potentials in the brain, are phosphorylated by protein kinase C (PKC) in purified form. Activation of PKC decreases peak sodium current up to 80 percent and slows its inactivation for sodium channels in rat brain neurons and for rat brain type IIA sodium channel alpha subunits heterologously expressed in Chinese hamster ovary cells. These effects are specific for PKC because they can be blocked by specific peptide inhibitors of PKC and can be reproduced by direct application of PKC to the cytoplasmic surface of sodium channels in excised inside-out membrane patches. Modulation of brain sodium channels by PKC is likely to have important effects on signal transduction and synaptic transmission in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Numann, R -- Catterall, W A -- Scheuer, T -- NS15751/NS/NINDS NIH HHS/ -- NS25704/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 4;254(5028):115-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1656525" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/physiology ; CHO Cells ; Cloning, Molecular ; Cricetinae ; Diglycerides/pharmacology ; In Vitro Techniques ; Neurons/physiology ; Phosphoproteins/physiology ; Phosphorylation ; Protein Kinase C/*physiology ; Protein Kinases/physiology ; Rats ; Sodium/*physiology ; Sodium Channels/*physiology
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    NMDA antagonist neurotoxicity: mechanism and prevention (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-12-06
    Description: Antagonists of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor, including phencyclidine (PCP) and ketamine, protect against brain damage in neurological disorders such as stroke. However, these agents have psychotomimetic properties in humans and morphologically damage neurons in the cerebral cortex of rats. It is now shown that the morphological damage can be prevented by certain anticholinergic drugs or by diazepam and barbiturates, which act at the gamma-aminobutyric acid (GABA) receptor-channel complex and are known to suppress the psychotomimetic symptoms caused by ketamine. Thus, it may be possible to prevent the unwanted side effects of NMDA antagonists, thereby enhancing their utility as neuroprotective drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olney, J W -- Labruyere, J -- Wang, G -- Wozniak, D F -- Price, M T -- Sesma, M A -- AG 05681/AG/NIA NIH HHS/ -- DA 53568/DA/NIDA NIH HHS/ -- MH 38894/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1991 Dec 6;254(5037):1515-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, 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/1835799" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Barbiturates/pharmacology ; Chick Embryo ; Dizocilpine Maleate/*antagonists & inhibitors ; Neurotoxins/*antagonists & inhibitors ; Parasympatholytics/pharmacology ; Pilocarpine/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/*drug effects ; Scopolamine Hydrobromide/pharmacology ; Vacuoles/ultrastructure
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    Structure of the calcium-dependent lectin domain from a rat mannose-binding protein determined by MAD phasing (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-12-13
    Description: Calcium-dependent (C-type) animal lectins participate in many cell surface recognition events mediated by protein-carbohydrate interactions. The C-type lectin family includes cell adhesion molecules, endocytic receptors, and extracellular matrix proteins. Mammalian mannose-binding proteins are C-type lectins that function in antibody-independent host defense against pathogens. The crystal structure of the carbohydrate-recognition domain of a rat mannose-binding protein, determined as the holmium-substituted complex by multiwavelength anomalous dispersion (MAD) phasing, reveals an unusual fold consisting of two distinct regions, one of which contains extensive nonregular secondary structure stabilized by two holmium ions. The structure explains the conservation of 32 residues in all C-type carbohydrate-recognition domains, suggesting that the fold seen here is common to these domains. The strong anomalous scattering observed at the Ho LIII edge demonstrates that traditional heavy atom complexes will be generally amenable to the MAD phasing method.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weis, W I -- Kahn, R -- Fourme, R -- Drickamer, K -- Hendrickson, W A -- GM34102/GM/NIGMS NIH HHS/ -- GM42628/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Dec 13;254(5038):1608-15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1721241" target="_blank"〉PubMed〈/a〉
    Keywords: Acute-Phase Proteins/*chemistry ; Amino Acid Sequence ; Animals ; Calcium/metabolism ; Calcium-Binding Proteins/*chemistry ; Carrier Proteins/*chemistry ; Collagen/chemistry ; Crystallography ; Holmium ; Hydrogen Bonding ; Lanthanum ; Lectins/*chemistry ; Ligands ; Mannose-Binding Lectins ; Models, Molecular ; Molecular Sequence Data ; Molecular Structure ; Protein Conformation ; Rats ; Recombinant Proteins/chemistry ; Sequence Alignment ; X-Ray Diffraction/methods
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  • 83
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    Depletion of CD4+ T cells in major histocompatibility complex class II-deficient mice (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-09-20
    Description: The maturation of T cells in the thymus is dependent on the expression of major histocompatibility complex (MHC) molecules. By disruption of the MHC class II Ab beta gene in embryonic stem cells, mice were generated that lack cell surface expression of class II molecules. These MHC class II-deficient mice were depleted of mature CD4+ T cells and were deficient in cell-mediated immune responses. These results provide genetic evidence that class II molecules are required for the maturation and function of mature CD4+ T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grusby, M J -- Johnson, R S -- Papaioannou, V E -- Glimcher, L H -- AI21569/AI/NIAID NIH HHS/ -- HD27295/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1991 Sep 20;253(5026):1417-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Harvard School of Public Health, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1910207" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/*immunology ; Crosses, Genetic ; Embryo, Mammalian ; Enzyme-Linked Immunosorbent Assay ; Female ; *Genes, MHC Class II ; Immunity, Cellular/genetics ; Immunoglobulin G/analysis/classification ; Immunoglobulin M/analysis ; Immunologic Deficiency Syndromes/*genetics ; *Lymphocyte Depletion ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Stem Cells/immunology ; T-Lymphocyte Subsets/*immunology
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  • 84
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    Induction of inflammatory arthropathy resembling rheumatoid arthritis in mice transgenic for HTLV-I (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-30
    Description: Human T cell leukemia virus type-I (HTLV-I) is the etiologic agent of adult T cell leukemia and has also been suggested to be involved in other diseases such as chronic arthritis or myelopathy. To elucidate pathological roles of the virus in disease, transgenic mice were produced that carry the HTLV-I genome. At 2 to 3 months of age, many of the mice developed chronic arthritis resembling rheumatoid arthritis. Synovial and periarticular inflammation with articular erosion caused by invasion of granulation tissues were marked. These observations suggest a possibility that HTLV-I is one of the etiologic agents of chronic arthritis in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iwakura, Y -- Tosu, M -- Yoshida, E -- Takiguchi, M -- Sato, K -- Kitajima, I -- Nishioka, K -- Yamamoto, K -- Takeda, T -- Hatanaka, M -- New York, N.Y. -- Science. 1991 Aug 30;253(5023):1026-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Medical Science, University of Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1887217" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis, Rheumatoid/*genetics/pathology/physiopathology ; Genes, Viral ; Human T-lymphotropic virus 1/*genetics ; Inflammation ; Joints/pathology ; Mice ; Mice, Inbred Strains ; Mice, Transgenic ; RNA, Messenger/genetics ; Repetitive Sequences, Nucleic Acid ; Viral Envelope Proteins/genetics
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  • 85
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    Induction of type I diabetes by Kilham's rat virus in diabetes-resistant BB/Wor rats (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-15
    Description: Type I diabetes mellitus is an autoimmune disease resulting from the interaction of genetic and environmental factors. A virus that was identified serologically as Kilham's rat virus (KRV) was isolated from a spontaneously diabetic rat and reproducibly induced diabetes in naive diabetes-resistant (DR) BB/Wor rats. Viral antigen was not identified in pancreatic islet cells, and beta cell cytolysis was not observed until after the appearance of lymphocytic insulitis. KRV did not induce diabetes in major histocompatibility complex-concordant and discordant non-BB rats and did not accelerate diabetes in diabetes-prone BB/Wor rats unless the rats had been reconstituted with DR spleen cells. This model of diabetes may provide insight regarding the interaction of viruses and autoimmune disease [corrected]〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guberski, D L -- Thomas, V A -- Shek, W R -- Like, A A -- Handler, E S -- Rossini, A A -- Wallace, J E -- Welsh, R M -- DK07302/DK/NIDDK NIH HHS/ -- DK19155/DK/NIDDK NIH HHS/ -- DK7-2287/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Nov 15;254(5034):1010-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Massachusetts Medical Center, Worcester 01655.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1658938" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Laboratory ; Diabetes Mellitus, Type 1/genetics/*microbiology/pathology ; Disease Outbreaks/veterinary ; Genes, MHC Class I ; Haplotypes ; Islets of Langerhans/immunology/pathology ; Parvoviridae Infections/complications/pathology/*veterinary ; Rats ; Rats, Inbred BB
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  • 86
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    Suppression of tumorigenicity in Wilms tumor by the p15.5-p14 region of chromosome 11 (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-11
    Description: Wilms tumor has been associated with genomic alterations at both the 11p13 and 11p15 regions. To differentiate between the involvement of these two loci, a chromosome 11 was constructed that had one or the other region deleted, and this chromosome was introduced into the tumorigenic Wilms tumor cell line G401. When assayed for tumor-forming activity in nude mice, the 11p13-deleted, but not the 11p15.5-p14.1-deleted chromosome, retained its ability to suppress tumor formation. These results provide in vivo functional evidence for the existence of a second genetic locus (WT2) involved in suppressing the tumorigenic phenotype of Wilms tumor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dowdy, S F -- Fasching, C L -- Araujo, D -- Lai, K M -- Livanos, E -- Weissman, B E -- Stanbridge, E J -- CA19104/CA/NCI NIH HHS/ -- CA44470/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 11;254(5029):293-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, University of California, Irvine 92717.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1656527" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chromosome Mapping ; *Chromosomes, Human, Pair 11 ; Genes, Tumor Suppressor/*genetics ; *Genes, Wilms Tumor/genetics ; Humans ; Karyotyping ; Kidney Neoplasms/*genetics ; Mice ; Mice, Nude ; Wilms Tumor/*genetics
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  • 87
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    Membrane-bound phosphotyrosine phosphatases (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, A F -- New York, N.Y. -- Science. 1991 May 10;252(5007):764.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1851327" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD45 ; Antigens, Differentiation ; Cell Membrane/*enzymology ; Histocompatibility Antigens ; Mice ; *Phosphoprotein Phosphatases ; Protein Tyrosine Phosphatases ; Rats
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  • 88
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    Identification of a zinc finger protein that inhibits IL-2 gene expression (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-20
    Description: Transient activation of the interleukin-2 (IL-2) gene after antigen recognition by T lymphocytes is crucial for subsequent T cell proliferation and differentiation. Several IL-2 gene regulatory elements and binding factors necessary for activation of the IL-2 gene have been defined. However, little is known about negative regulation of IL-2 expression, which is likely to be important in the rapid shut-off of IL-2 transcription. A nucleotide sequence element (NRE-A) that negatively regulates IL-2 expression has been identified within the IL-2 gene. T cell nuclear extracts contained an NRE-A binding activity. A complementary DNA was isolated that encodes a zinc finger-containing protein that suppressed IL-2 gene expression. The observation of negative regulation of the immunoglobulin heavy chain gene enhancer by an element similar to NRE-A suggests that related proteins may regulate multiple immune response genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, T M -- Moolten, D -- Burlein, J -- Romano, J -- Bhaerman, R -- Godillot, A -- Mellon, M -- Rauscher, F J 3rd -- Kant, J A -- AI23879/AI/NIAID NIH HHS/ -- CA23413/CA/NCI NIH HHS/ -- CA54428/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1791-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, School of Medicine, University of New Mexico, Albuquerque 87131.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1840704" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA Probes ; *Enhancer Elements, Genetic ; *Gene Expression Regulation ; *Genes, Immunoglobulin ; Humans ; Immunoglobulin Heavy Chains/*genetics ; Interleukin-2/*genetics ; Mice ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Regulatory Sequences, Nucleic Acid ; Restriction Mapping ; T-Lymphocytes/*immunology ; *Transcription, Genetic ; Zinc Fingers/*genetics/physiology
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  • 89
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    Regulation of B cell antigen receptor signal transduction and phosphorylation by CD45 (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-06-28
    Description: CD45 is a member of a family of membrane proteins that possess phosphotyrosine phosphatase activity, and is the source of much of the tyrosine phosphatase activity in lymphocytes. In view of its enzymatic activity and high copy number, it seems likely that CD45 functions in transmembrane signal transduction by lymphocyte receptors that are coupled to activation of tyrosine kinases. The B cell antigen receptor was found to transduce a Ca(2+)-mobilizing signal only if cells expressed CD45. Also, both membrane immunoglobulin M (mIgM) and CD45 were lost from the surface of cells treated with antibody to CD45, suggesting a physical interaction between these proteins. Finally, CD45 dephosphorylated a complex of mIg-associated proteins that appears to function in signal transduction by the antigen receptor. These data indicate that CD45 occurs as a component of a complex of proteins associated with the antigen receptor, and that CD45 may regulate signal transduction by modulating the phosphorylation state of the antigen receptor subunits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Justement, L B -- Campbell, K S -- Chien, N C -- Cambier, J C -- AI20519/AI/NIAID NIH HHS/ -- AI21768/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1991 Jun 28;252(5014):1839-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1648262" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD45 ; Antigens, Differentiation/genetics/*physiology ; B-Lymphocytes/*immunology ; Calcium/physiology ; Cell Line ; Cell Membrane/physiology ; Cells, Cultured ; Clone Cells ; Histocompatibility Antigens/genetics/*physiology ; Immunoglobulin M/physiology ; Membrane Glycoproteins/*physiology ; Mice ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Plasmacytoma ; Protein Tyrosine Phosphatases ; RNA, Messenger/genetics ; Receptors, Antigen, B-Cell/*physiology ; *Signal Transduction ; Spleen/immunology ; Transfection
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  • 90
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    An analog of myristic acid with selective toxicity for African trypanosomes (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-06-28
    Description: Trypanosoma brucei, the protozoan parasite responsible for African sleeping sickness, evades the host immune response through the process of antigenic variation. The variant antigen, known as the variant surface glycoprotein (VSG), is anchored to the cell surface by a glycosyl phosphatidylinositol (GPI) structure that contains myristate (n-tetradecanoate) as its only fatty acid component. The utilization of heteroatom-containing analogs of myristate was studied both in a cell-free system and in vivo. Results indicated that the specificity of fatty acid incorporation depends on chain length rather than on hydrophobicity. One analog, 10-(propoxy)decanoic acid, was highly toxic to trypanosomes in culture although it is nontoxic to mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doering, T L -- Raper, J -- Buxbaum, L U -- Adams, S P -- Gordon, J I -- Hart, G W -- Englund, P T -- 5T32GM07309/GM/NIGMS NIH HHS/ -- AI21334/AI/NIAID NIH HHS/ -- AI27179/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1991 Jun 28;252(5014):1851-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, Johns Hopkins Medical School, Baltimore, MD 21210.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1829548" target="_blank"〉PubMed〈/a〉
    Keywords: Acyl Coenzyme A/metabolism ; Animals ; Cell-Free System ; Glycolipids/metabolism ; Glycosylphosphatidylinositols ; Kinetics ; Mice ; Myristic Acid ; Myristic Acids/*metabolism/*pharmacology ; Phosphatidylinositols/metabolism ; Structure-Activity Relationship ; Trypanosoma brucei brucei/*drug effects/metabolism/ultrastructure
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  • 91
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    CREB: a Ca(2+)-regulated transcription factor phosphorylated by calmodulin-dependent kinases (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-06-07
    Description: The mechanism by which Ca2+ mediates gene induction in response to membrane depolarization was investigated. The adenosine 3',5'-monophosphate (cAMP) response element-binding protein (CREB) was shown to function as a Ca(2+)-regulated transcription factor and as a substrate for depolarization-activated Ca(2+)-calmodulin-dependent protein kinases (CaM kinases) I and II. CREB residue Ser133 was the major site of phosphorylation by the CaM kinases in vitro and of phosphorylation after membrane depolarization in vivo. Mutation of Ser133 impaired the ability of CREB to respond to Ca2+. These results suggest that CaM kinases may transduce electrical signals to the nucleus and that CREB functions to integrate Ca2+ and cAMP signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheng, M -- Thompson, M A -- Greenberg, M E -- R01 CA 43855/CA/NCI NIH HHS/ -- R01 NS 28829/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Jun 7;252(5011):1427-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1646483" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*pharmacology ; Calcium-Calmodulin-Dependent Protein Kinases ; Chromosome Mapping ; Cloning, Molecular ; Cyclic AMP/physiology ; Cyclic AMP Response Element-Binding Protein ; DNA-Binding Proteins/*physiology ; Electrophoresis, Polyacrylamide Gel ; Fungal Proteins/pharmacology ; Gene Expression Regulation/*drug effects ; Genes, Regulator/physiology ; Humans ; In Vitro Techniques ; Phosphorylation ; Protein Kinases/pharmacology ; Rats ; Recombinant Fusion Proteins/pharmacology ; *Saccharomyces cerevisiae Proteins ; Serine/chemistry ; Signal Transduction ; TATA Box ; Transcription Factors/*physiology ; Transcription, Genetic/drug effects ; Transcriptional Activation
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  • 92
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    Induction of Plasmodium falciparum transmission-blocking antibodies by recombinant vaccinia virus (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-31
    Description: Many candidate antigens of malaria vaccines have limited immunological recognition. One exception is Pfs25, a cysteine-rich, 25-kilodalton sexual stage surface protein of Plasmodium falciparum. Pfs25 is a target of monoclonal antibodies that block transmission of malaria from vertebrate host to mosquito vector. The surface of mammalian cells infected with a recombinant vaccinia virus that expressed Pfs25 specifically bound transmission-blocking monoclonal antibodies. Furthermore, major histocompatibility complex-disparate congenic mouse strains immunized with recombinant Pfs25 elicited transmission-blocking antibodies, demonstrating that the capacity to develop transmission-blocking antibodies is not genetically restricted in mice. Live recombinant viruses may provide an inexpensive, easily administered alternative to subunit vaccines prepared from purified recombinant proteins to block transmission of malaria in developing countries.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaslow, D C -- Isaacs, S N -- Quakyi, I A -- Gwadz, R W -- Moss, B -- Keister, D B -- New York, N.Y. -- Science. 1991 May 31;252(5010):1310-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Malaria Section, National Institute of Allergy and Infectious 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/1925544" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/analysis/immunology ; Antibodies, Protozoan/*immunology ; Antigens, Protozoan ; Immunization ; Malaria, Falciparum/*prevention & control ; Mice ; Plasmodium falciparum/*immunology ; Protozoan Proteins/genetics/*immunology ; Recombinant Proteins/immunology ; Transfection ; Vaccinia virus/genetics/*immunology
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  • 93
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    Association of B cell antigen receptor with protein tyrosine kinase Lyn (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-01-11
    Description: Antigen is thought to cross-link membrane-bound immunoglobulins (Igs) of B cells, causing proliferation and differentiation or the inhibition of growth. Protein tyrosine kinases are probably involved in signal transduction for cell proliferation and differentiation. The Src-like protein tyrosine kinase Lyn is expressed preferentially in B cells. The Lyn protein and its kinase activity could be coimmunoprecipitated with IgM from detergent lysates. Cross-linking of membrane-bound IgM induced a rapid increase in tyrosine phosphorylation of at least ten distinct proteins of B cells. Thus, Lyn is physically associated with membrane-bound IgM, and is suggested to participate in antigen-mediated signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamanashi, Y -- Kakiuchi, T -- Mizuguchi, J -- Yamamoto, T -- Toyoshima, K -- New York, N.Y. -- Science. 1991 Jan 11;251(4990):192-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncology, University of Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1702903" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Cell Line ; Detergents ; Electrophoresis, Polyacrylamide Gel ; Immunoblotting ; Immunoglobulin M/metabolism ; Immunosorbent Techniques ; Mice ; Molecular Weight ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphotyrosine ; Protein-Tyrosine Kinases/genetics/*metabolism ; Receptors, Antigen, B-Cell/*metabolism ; Signal Transduction ; Tyrosine/analogs & derivatives/metabolism ; *src-Family Kinases
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  • 94
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    Chimeric NGF-EGF receptors define domains responsible for neuronal differentiation (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-04-26
    Description: To determine the domains of the low-affinity nerve growth factor (NGF) receptor required for appropriate signal transduction, a series of hybrid receptors were constructed that consisted of the extracellular ligand-binding domain of the human epidermal growth factor (EGF) receptor (EGFR) fused to the transmembrane and cytoplasmic domains of the human low-affinity NGF receptor (NGFR). Transfection of these chimeric receptors into rat pheochromocytoma PC12 cells resulted in appropriate cell surface expression. Biological activity mediated by the EGF-NGF chimeric receptor was assayed by the induction of neurite outgrowth in response to EGF in stably transfected cells. Furthermore, the chimeric receptor mediated nuclear signaling, as evidenced by the specific induction of transin messenger RNA, an NGF-responsive gene. Neurite outgrowth was not observed with chimeric receptors that contained the transmembrane domain from the EGFR, suggesting that the membrane-spanning region and cytoplasmic domain of the low-affinity NGFR are necessary for signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yan, H -- Schlessinger, J -- Chao, M V -- New York, N.Y. -- Science. 1991 Apr 26;252(5005):561-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Anatomy, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1850551" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Gland Neoplasms ; Animals ; Axons/drug effects/physiology/ultrastructure ; *Cell Differentiation ; Cell Line ; Chimera ; Epidermal Growth Factor/pharmacology ; Humans ; Nerve Growth Factors/pharmacology/*physiology ; Neurons/*cytology ; Pheochromocytoma ; Rats ; Receptor, Epidermal Growth Factor/genetics/*physiology ; Receptors, Cell Surface/genetics/*physiology ; Receptors, Nerve Growth Factor ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 95
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    Excessive fear of PCBs (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abelson, P H -- New York, N.Y. -- Science. 1991 Jul 26;253(5018):361.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1907400" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chlorine/toxicity ; Environmental Pollutants/*toxicity ; Environmental Pollution/*prevention & control ; Humans ; Neoplasms, Experimental/*chemically induced ; Polychlorinated Biphenyls/*toxicity ; Rats ; United States ; United States Environmental Protection Agency
    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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  • 96
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    Separation of IL-4 production from Th cell proliferation by an altered T cell receptor ligand (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-31
    Description: In the presence of antigen presenting cells, a murine T helper (Th) cell specific for murine hemoglobin (Hb) responded to its immunogenic peptide by both cytokine (interleukin-4) secretion and proliferation. An altered Hb peptide with a single amino acid substitution induced only cytokine secretion and did not induce proliferation. Interleukin-1 costimulated and restored the Th proliferative response to normal levels. The altered peptide also supported cognate T cell-B cell interactions indicative of T cell helper function. Thus, this result suggests that the T cell receptor has the capacity of differential signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Evavold, B D -- Allen, P M -- AI24157/AI/NIAID NIH HHS/ -- ESO7066/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1991 May 31;252(5010):1308-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, 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/1833816" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Division ; Clone Cells ; Hemoglobins/chemistry/*immunology ; Interleukin-4/*biosynthesis ; Lymphocyte Activation/*immunology ; Mice ; Molecular Sequence Data ; Peptide Fragments/chemistry/*immunology ; Receptors, Antigen, T-Cell/immunology/*metabolism ; Signal Transduction ; T-Lymphocytes, Helper-Inducer/cytology/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
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    Ability of the c-mos product to associate with and phosphorylate tubulin (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-08
    Description: The mos proto-oncogene product, pp39mos, is a protein kinase and has been equated with cytostatic factor (CSF), an activity in unfertilized eggs that is thought to be responsible for the arrest of meiosis at metaphase II. The biochemical properties and potential substrates of pp39mos were examined in unfertilized eggs and in transformed cells in order to study how the protein functions both as CSF and in transformation. The pp39mos protein associated with polymers under conditions that favor tubulin oligomerization and was present in an approximately 500-kilodalton "core" complex under conditions that favor depolymerization. beta-Tubulin was preferentially coprecipitated in pp39mos immunoprecipitates and was the major phosphorylated product in a pp39mos-dependent immune complex kinase assay. Immunofluorescence analysis of NIH 3T3 cells transformed with Xenopus c-mos showed that pp39mos colocalizes with tubulin in the spindle during metaphase and in the midbody and asters during telophase. Disruption of microtubules with nocodazole affected tubulin and pp39mos organization in the same way. It therefore appears that pp39mos is a tubulin-associated protein kinase and may thus participate in the modification of microtubules and contribute to the formation of the spindle. This activity expressed during interphase in somatic cells may be responsible for the transforming activity of pp39mos.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, R P -- Oskarsson, M -- Paules, R S -- Schulz, N -- Cleveland, D -- Vande Woude, G F -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Feb 8;251(4994):671-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1825142" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal ; Cell Line ; Cell Transformation, Neoplastic/metabolism ; Macromolecular Substances ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Phosphoproteins/metabolism ; Precipitin Tests ; Protein Binding ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-mos ; Tubulin/*metabolism
    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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  • 98
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    Pre-Botzinger complex: a brainstem region that may generate respiratory rhythm in mammals (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-01
    Description: The location of neurons generating the rhythm of breathing in mammals is unknown. By microsection of the neonatal rat brainstem in vitro, a limited region of the ventral medulla (the pre-Botzinger Complex) that contains neurons essential for rhythmogenesis was identified. Rhythm generation was eliminated by removal of only this region. Medullary slices containing the pre-Botzinger Complex generated respiratory-related oscillations similar to those generated by the whole brainstem in vitro, and neurons with voltage-dependent pacemaker-like properties were identified in this region. Thus, the respiratory rhythm in the mammalian neonatal nervous system may result from a population of conditional bursting pacemaker neurons in the pre-Botzinger Complex.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3209964/" 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/PMC3209964/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, J C -- Ellenberger, H H -- Ballanyi, K -- Richter, D W -- Feldman, J L -- HL02204/HL/NHLBI NIH HHS/ -- HL4095/HL/NHLBI NIH HHS/ -- NS24742/NS/NINDS NIH HHS/ -- R01 HL070029/HL/NHLBI NIH HHS/ -- R01 HL070029-01A1/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 1;254(5032):726-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Kinesiology, University of California, Los Angeles 90024-1527.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1683005" target="_blank"〉PubMed〈/a〉
    Keywords: 6-Cyano-7-nitroquinoxaline-2,3-dione ; Activity Cycles ; Animals ; Animals, Newborn ; Evoked Potentials/drug effects ; In Vitro Techniques ; Mammals/*physiology ; Medulla Oblongata/cytology/*physiology ; Neurons/cytology/drug effects/*physiology ; Quinoxalines/pharmacology ; Rats ; Respiration/*physiology
    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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  • 99
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    Inhibition of neointimal smooth muscle accumulation after angioplasty by an antibody to PDGF (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-09-06
    Description: Approximately 30 to 40 percent of atherosclerotic coronary arteries treated by angioplasty or by bypass surgery occlude as a result of restenosis. This restenosis is due principally to the accumulation of neointimal smooth muscle cells, which is also a prominent feature of the advanced lesions of atherosclerosis. The factors responsible for the accumulation of intimal smooth muscle cells have not been identified. Platelet-derived growth factor (PDGF) is a potent smooth muscle chemoattractant and mitogen. It is present in platelets and can be formed by endothelium, smooth muscle, and monocyte-derived macrophages. The development of an intimal lesion in the carotid artery of athymic nude rats induced by intraarterial balloon catheter deendothelialization was inhibited by a polyclonal antibody to PDGF. These data demonstrate that endogenous PDGF is involved in the accumulation of neointimal smooth muscle cells associated with balloon injury and may be involved in restenosis after angioplasty, and perhaps in atherogenesis as well.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferns, G A -- Raines, E W -- Sprugel, K H -- Motani, A S -- Reidy, M A -- Ross, R -- HL-03174/HL/NHLBI NIH HHS/ -- HL-18645/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1991 Sep 6;253(5024):1129-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉William Harvey Research Institute, St. Bartholomew's Hospital Medical College, London, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1653454" target="_blank"〉PubMed〈/a〉
    Keywords: Angioplasty, Balloon/*adverse effects ; Animals ; Antibodies/*therapeutic use ; Arteriosclerosis/etiology/*prevention & control ; Carotid Arteries/*pathology ; DNA Replication ; Goats/immunology ; Humans ; Immunoglobulin G/*therapeutic use ; Muscle, Smooth, Vascular/*pathology ; Platelet-Derived Growth Factor/*immunology/metabolism ; Rats ; Rats, Nude ; Receptors, Cell Surface/metabolism ; Receptors, Platelet-Derived Growth Factor
    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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  • 100
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    An in vivo model of somatic cell gene therapy for human severe combined immunodeficiency (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-15
    Description: Deficiency of adenosine deaminase (ADA) results in severe combined immunodeficiency (SCID), a candidate genetic disorder for somatic cell gene therapy. Peripheral blood lymphocytes from patients affected by ADA- SCID were transduced with a retroviral vector for human ADA and injected into immunodeficient mice. Long-term survival of vector-transduced human cells was demonstrated in recipient animals. Expression of vector-derived ADA restored immune functions, as indicated by the presence in reconstituted animals of human immunoglobulin and antigen-specific T cells. Retroviral vector gene transfer, therefore, is necessary and sufficient for development of specific immune functions in vivo and has therapeutic potential to correct this lethal immunodeficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferrari, G -- Rossini, S -- Giavazzi, R -- Maggioni, D -- Nobili, N -- Soldati, M -- Ungers, G -- Mavilio, F -- Gilboa, E -- Bordignon, C -- New York, N.Y. -- Science. 1991 Mar 15;251(4999):1363-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Hematology, Istituto Scientifico H.S. Raffaele, Milano, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1848369" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/*deficiency/genetics ; Animals ; Base Sequence ; Genetic Therapy ; Genetic Vectors ; Humans ; Immunologic Deficiency Syndromes/*genetics/therapy ; Kanamycin Kinase ; Lymphocyte Transfusion ; Lymphocytes/physiology ; Mice ; Mice, Mutant Strains ; Oligonucleotides/chemistry ; Phosphotransferases/genetics ; Polymerase Chain Reaction ; Retroviridae/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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