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  • Cells, Cultured  (113)
  • American Association for the Advancement of Science (AAAS)  (113)
  • Annual Reviews
  • Elsevier
  • 2015-2019
  • 2005-2009  (33)
  • 1995-1999  (33)
  • 1990-1994
  • 1980-1984  (47)
  • 2005  (33)
  • 1998  (33)
  • 1983  (47)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (113)
  • Annual Reviews
  • Elsevier
Years
  • 2015-2019
  • 2005-2009  (33)
  • 1995-1999  (33)
  • 1990-1994
  • 1980-1984  (47)
Year
  • 1
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    Induction of lens differentiation by activation of a bZIP transcription factor, L-Maf (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-29
    Description: After the vertebrate lens is induced from head ectoderm, lens-specific genes are expressed. Transcriptional regulation of the lens-specific alphaA-crystallin gene is controlled by an enhancer element, alphaCE2. A gene encoding an alphaCE2-binding protein, L-maf(lens-specific maf), was isolated. L-maf expression is initiated in the lens placode and is restricted to lens cells. The gene product L-Maf regulates the expression of multiple genes expressed in the lens, and ectopic expression of this transcription factor converts chick embryonic ectodermal cells and cultured cells into lens fibers. Thus, vertebrate lens induction and differentiation can be triggered by the activation of L-Maf.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogino, H -- Yasuda, K -- New York, N.Y. -- Science. 1998 Apr 3;280(5360):115-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma 630-0101, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9525857" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Basic-Leucine Zipper Transcription Factors ; Cell Differentiation ; Cells, Cultured ; Chick Embryo ; Crystallins/genetics ; DNA, Complementary ; DNA-Binding Proteins/chemistry/genetics ; Ectoderm ; Enhancer Elements, Genetic ; Eye Proteins/genetics ; G-Box Binding Factors ; *Gene Expression Regulation, Developmental ; Genes, Reporter ; Intermediate Filament Proteins/genetics ; Lens, Crystalline/*cytology/*embryology/metabolism ; Maf Transcription Factors ; Molecular Sequence Data ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/metabolism ; Transcription Factors/chemistry/genetics/*metabolism ; *Transcription, Genetic ; Transcriptional Activation ; Transfection
    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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    Molecular basis of T cell inactivation by CTLA-4 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-18
    Description: CTLA-4, a negative regulator of T cell function, was found to associate with the T cell receptor (TCR) complex zeta chain in primary T cells. The association of TCRzeta with CTLA-4, reconstituted in 293 transfectants, was enhanced by p56(lck)-induced tyrosine phosphorylation. Coexpression of the CTLA-4-associated tyrosine phosphatase, SHP-2, resulted in dephosphorylation of TCRzeta bound to CTLA-4 and abolished the p56(lck)-inducible TCRzeta-CTLA-4 interaction. Thus, CTLA-4 inhibits TCR signal transduction by binding to TCRzeta and inhibiting tyrosine phosphorylation after T cell activation. These findings have broad implications for the negative regulation of T cell function and T cell tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, K M -- Chuang, E -- Griffin, M -- Khattri, R -- Hong, D K -- Zhang, W -- Straus, D -- Samelson, L E -- Thompson, C B -- Bluestone, J A -- P01 AI35294-6/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2263-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ben May Institute for Cancer Research, and Committee on Immunology, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856951" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antigens, CD ; Antigens, Differentiation/*metabolism ; CTLA-4 Antigen ; Cell Line ; Cells, Cultured ; Humans ; *Immunoconjugates ; Intracellular Signaling Peptides and Proteins ; *Lymphocyte Activation ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/genetics/metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Inbred BALB C ; Models, Immunological ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 ; Protein Tyrosine Phosphatases/genetics/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Recombinant Fusion Proteins/metabolism ; SH2 Domain-Containing Protein Tyrosine Phosphatases ; *Signal Transduction ; T-Lymphocytes/*immunology ; Transfection ; src Homology Domains
    Print ISSN: 0036-8075
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  • 3
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    FADD: essential for embryo development and signaling from some, but not all, inducers of apoptosis (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-16
    Description: FADD (also known as Mort-1) is a signal transducer downstream of cell death receptor CD95 (also called Fas). CD95, tumor necrosis factor receptor type 1 (TNFR-1), and death receptor 3 (DR3) did not induce apoptosis in FADD-deficient embryonic fibroblasts, whereas DR4, oncogenes E1A and c-myc, and chemotherapeutic agent adriamycin did. Mice with a deletion in the FADD gene did not survive beyond day 11.5 of embryogenesis; these mice showed signs of cardiac failure and abdominal hemorrhage. Chimeric embryos showing a high contribution of FADD null mutant cells to the heart reproduce the phenotype of FADD-deficient mutants. Thus, not only death receptors, but also receptors that couple to developmental programs, may use FADD for signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeh, W C -- de la Pompa, J L -- McCurrach, M E -- Shu, H B -- Elia, A J -- Shahinian, A -- Ng, M -- Wakeham, A -- Khoo, W -- Mitchell, K -- El-Deiry, W S -- Lowe, S W -- Goeddel, D V -- Mak, T W -- CA13106/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Mar 20;279(5358):1954-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen Institute, University of Toronto, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9506948" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/genetics/physiology ; *Apoptosis ; Carrier Proteins/genetics/*physiology ; Cell Transformation, Neoplastic ; Cells, Cultured ; Doxorubicin/pharmacology ; *Embryonic and Fetal Development ; Endothelium, Vascular/embryology ; Fas-Associated Death Domain Protein ; Female ; Gene Expression ; Gene Targeting ; Heart/*embryology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Oncogenes ; Receptors, Tumor Necrosis Factor/genetics/physiology ; Signal Transduction ; Tumor Necrosis Factor-alpha/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Cloned transgenic calves produced from nonquiescent fetal fibroblasts (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: An efficient system for genetic modification and large-scale cloning of cattle is of importance for agriculture, biotechnology, and human medicine. Here, actively dividing fetal fibroblasts were genetically modified with a marker gene, a clonal line was selected, and the cells were fused to enucleated mature oocytes. Out of 28 embryos transferred to 11 recipient cows, three healthy, identical, transgenic calves were generated. Furthermore, the life-span of near senescent fibroblasts could be extended by nuclear transfer, as indicated by population doublings in fibroblast lines derived from a 40-day-old fetal clone. With the ability to extend the life-span of these primary cultured cells, this system would be useful for inducing complex genetic modifications in cattle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cibelli, J B -- Stice, S L -- Golueke, P J -- Kane, J J -- Jerry, J -- Blackwell, C -- Ponce de Leon, F A -- Robl, J M -- New York, N.Y. -- Science. 1998 May 22;280(5367):1256-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA 01003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9596577" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Genetically Modified ; Blastocyst ; Cattle/embryology/*genetics ; Cell Aging ; Cell Division ; Cell Nucleus/genetics ; Cells, Cultured ; Clone Cells ; *Cloning, Organism ; Embryo Transfer ; Female ; Fetus/cytology ; Fibroblasts/*cytology ; G1 Phase ; Male ; Nuclear Transfer Techniques ; Oocytes/cytology ; Transfection ; Transgenes
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    An essential role for ectodomain shedding in mammalian development (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-13
    Description: The ectodomains of numerous proteins are released from cells by proteolysis to yield soluble intercellular regulators. The responsible protease, tumor necrosis factor-alpha converting enzyme (TACE), has been identified only in the case when tumor necrosis factor-alpha (TNFalpha) is released. Analyses of cells lacking this metalloproteinase-disintegrin revealed an expanded role for TACE in the processing of other cell surface proteins, including a TNF receptor, the L-selectin adhesion molecule, and transforming growth factor-alpha (TGFalpha). The phenotype of mice lacking TACE suggests an essential role for soluble TGFalpha in normal development and emphasizes the importance of protein ectodomain shedding in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peschon, J J -- Slack, J L -- Reddy, P -- Stocking, K L -- Sunnarborg, S W -- Lee, D C -- Russell, W E -- Castner, B J -- Johnson, R S -- Fitzner, J N -- Boyce, R W -- Nelson, N -- Kozlosky, C J -- Wolfson, M F -- Rauch, C T -- Cerretti, D P -- Paxton, R J -- March, C J -- Black, R A -- CA43793/CA/NCI NIH HHS/ -- DK53804/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1281-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Corporation, Seattle, WA 98101, USA. peschon@immunex.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9812885" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins ; Amino Acid Sequence ; Animals ; Catalytic Domain ; Cell Membrane/*metabolism ; Cells, Cultured ; Crosses, Genetic ; *Embryonic and Fetal Development ; L-Selectin/metabolism ; Ligands ; Membrane Proteins/*metabolism ; Metalloendopeptidases/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Phenotype ; Protein Processing, Post-Translational ; Receptors, Tumor Necrosis Factor/metabolism ; Transforming Growth Factor alpha/metabolism ; Tumor Necrosis Factor-alpha/*metabolism
    Print ISSN: 0036-8075
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  • 6
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    Biological action of leptin as an angiogenic factor (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-11
    Description: Leptin is a hormone that regulates food intake, and its receptor (OB-Rb) is expressed primarily in the hypothalamus. Here, it is shown that OB-Rb is also expressed in human vasculature and in primary cultures of human endothelial cells. In vitro and in vivo assays revealed that leptin has angiogenic activity. In vivo, leptin induced neovascularization in corneas from normal rats but not in corneas from fa/fa Zucker rats, which lack functional leptin receptors. These observations indicate that the vascular endothelium is a target for leptin and suggest a physiological mechanism whereby leptin-induced angiogenesis may facilitate increased energy expenditure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sierra-Honigmann, M R -- Nath, A K -- Murakami, C -- Garcia-Cardena, G -- Papapetropoulos, A -- Sessa, W C -- Madge, L A -- Schechner, J S -- Schwabb, M B -- Polverini, P J -- Flores-Riveros, J R -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1683-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06536, USA. rocio_sierra-honigmann@qm.yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733517" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/metabolism ; Amino Acid Sequence ; Animals ; Carrier Proteins/analysis/*physiology ; Cells, Cultured ; Corneal Neovascularization ; DNA-Binding Proteins/metabolism ; Endothelial Growth Factors/pharmacology ; Endothelium, Vascular/chemistry/cytology/*physiology ; Energy Metabolism ; Humans ; Leptin ; Lipid Metabolism ; Lymphokines/pharmacology ; Molecular Sequence Data ; *Neovascularization, Physiologic ; Phosphorylation ; Proteins/pharmacology/*physiology ; Rats ; Rats, Zucker ; *Receptors, Cell Surface ; Receptors, Leptin ; STAT3 Transcription Factor ; Trans-Activators/metabolism ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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  • 7
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    Conversion of neuronal growth cone responses from repulsion to attraction by cyclic nucleotides (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-04
    Description: Nerve growth is regulated by attractive and repulsive factors in the nervous system. Microscopic gradients of Collapsin-1/Semaphorin III/D (Sema III) and myelin-associated glycoprotein trigger repulsive turning responses by growth cones of cultured Xenopus spinal neurons; the repulsion can be converted to attraction by pharmacological activation of the guanosine 3',5'-monophosphate (cGMP) and adenosine 3',5'-monophosphate signaling pathways, respectively. Sema III also causes the collapse of cultured rat sensory growth cones, which can be inhibited by activation of the cGMP pathway. Thus cyclic nucleotides can regulate growth cone behaviors and may be targets for designing treatments to alleviate the inhibition of nerve regeneration by repulsive factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, H -- Ming, G -- He, Z -- Lehmann, M -- McKerracher, L -- Tessier-Lavigne, M -- Poo, M -- NS22764/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1515-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California at San Diego, La Jolla, CA 92093-0357, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9727979" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Calcium/physiology ; Cells, Cultured ; Cyclic AMP/analogs & derivatives/pharmacology/*physiology ; Cyclic GMP/analogs & derivatives/pharmacology/*physiology ; Ganglia, Spinal/cytology ; Glycoproteins/*physiology ; Myelin-Associated Glycoprotein/physiology ; Nerve Growth Factors/*physiology ; Nerve Tissue Proteins/physiology ; Neurites/*physiology ; Neurons/cytology/*physiology ; Neuropilin-1 ; Rats ; Recombinant Proteins ; Semaphorin-3A ; Spinal Cord/cytology ; Thionucleotides/pharmacology ; Xenopus
    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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    Regulation of nerve growth mediated by inositol 1,4,5-trisphosphate receptors in growth cones (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-30
    Description: The inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) acts as a Ca2+ release channel on internal Ca2+ stores. Type 1 IP3R (IP3R1) is enriched in growth cones of neurons in chick dorsal root ganglia. Depletion of internal Ca2+ stores and inhibition of IP3 signaling with drugs inhibited neurite extension. Microinjection of heparin, a competitive IP3R blocker, induced neurite retraction. Acute localized loss of function of IP3R1 in the growth cone induced by chromophore-assisted laser inactivation resulted in growth arrest and neurite retraction. IP3-induced Ca2+ release in growth cones appears to have a crucial role in control of nerve growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takei, K -- Shin, R M -- Inoue, T -- Kato, K -- Mikoshiba, K -- New York, N.Y. -- Science. 1998 Nov 27;282(5394):1705-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Calciosignal Net Project, Exploratory Research for Advanced Technology (ERATO), Japan Science and Technology Corporation (JST), Bunkyo-Ku, Tokyo 113-0021, Japan. kohtaro@ims.u-tokyo.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9831561" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels/*metabolism ; Calcium Signaling ; Cells, Cultured ; Cerebellum/metabolism ; Chick Embryo ; Ganglia, Spinal/cytology ; Growth Cones/*metabolism ; Heparin/pharmacology ; Inositol 1,4,5-Trisphosphate/*metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; Lasers ; Lithium Chloride/pharmacology ; Mice ; Microscopy, Video ; Microsomes/metabolism ; Microtubules/metabolism ; Neurites/drug effects/*physiology ; Pseudopodia/drug effects/physiology ; Receptors, Cytoplasmic and Nuclear/*metabolism ; Signal Transduction ; Thapsigargin/pharmacology
    Print ISSN: 0036-8075
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  • 9
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    Homing viruses (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1998 Jun 19;280(5371):1956-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9669951" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Dependovirus/*genetics ; Drug Resistance/genetics ; *Gene Targeting ; *Genetic Vectors ; HeLa Cells ; Humans ; Hypoxanthine Phosphoribosyltransferase/genetics ; Neomycin/pharmacology ; *Recombination, Genetic ; *Transfection ; Virus Integration
    Print ISSN: 0036-8075
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  • 10
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    Entry of alphaherpesviruses mediated by poliovirus receptor-related protein 1 and poliovirus receptor (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-11
    Description: A human member of the immunoglobulin superfamily was shown to mediate entry of several alphaherpesviruses, including herpes simplex viruses (HSV) 1 and 2, porcine pseudorabies virus (PRV), and bovine herpesvirus 1 (BHV-1). This membrane glycoprotein is poliovirus receptor-related protein 1 (Prr1), designated here as HveC. Incubation of HSV-1 with a secreted form of HveC inhibited subsequent infection of a variety of cell lines, suggesting that HveC interacts directly with the virus. Poliovirus receptor (Pvr) itself mediated entry of PRV and BHV-1 but not of the HSV strains tested. HveC was expressed in human cells of epithelial and neuronal origin; it is the prime candidate for the coreceptor that allows both HSV-1 and HSV-2 to infect epithelial cells on mucosal surfaces and spread to cells of the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geraghty, R J -- Krummenacher, C -- Cohen, G H -- Eisenberg, R J -- Spear, P G -- NS-30606/NS/NINDS NIH HHS/ -- NS-36731/NS/NINDS NIH HHS/ -- R01 AI 36293/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1618-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology-Immunology, Northwestern University Medical School, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616127" target="_blank"〉PubMed〈/a〉
    Keywords: Alphaherpesvirinae/*physiology ; Animals ; Base Sequence ; CHO Cells ; Cell Adhesion Molecules/genetics/*physiology ; Cells, Cultured ; Cricetinae ; Epithelial Cells/virology ; Gene Expression ; Herpesvirus 1, Bovine/physiology ; Herpesvirus 1, Human/*physiology ; Herpesvirus 1, Suid/physiology ; Herpesvirus 2, Human/*physiology ; Humans ; *Membrane Proteins ; Molecular Sequence Data ; Neurons/virology ; Polymerase Chain Reaction ; *Receptors, Virus ; Transfection ; Tumor Cells, Cultured ; Viral Envelope Proteins/metabolism
    Print ISSN: 0036-8075
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  • 11
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    An antimicrobial activity of cytolytic T cells mediated by granulysin (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-02
    Description: Cytolytic T lymphocytes (CTLs) kill intracellular pathogens by a granule-dependent mechanism. Granulysin, a protein found in granules of CTLs, reduced the viability of a broad spectrum of pathogenic bacteria, fungi, and parasites in vitro. Granulysin directly killed extracellular Mycobacterium tuberculosis, altering the membrane integrity of the bacillus, and, in combination with perforin, decreased the viability of intracellular M. tuberculosis. The ability of CTLs to kill intracellular M. tuberculosis was dependent on the presence of granulysin in cytotoxic granules, defining a mechanism by which T cells directly contribute to immunity against intracellular pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stenger, S -- Hanson, D A -- Teitelbaum, R -- Dewan, P -- Niazi, K R -- Froelich, C J -- Ganz, T -- Thoma-Uszynski, S -- Melian, A -- Bogdan, C -- Porcelli, S A -- Bloom, B R -- Krensky, A M -- Modlin, R L -- New York, N.Y. -- Science. 1998 Oct 2;282(5386):121-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, UCLA School of Medicine, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9756476" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Differentiation, T-Lymphocyte/analysis/*immunology/pharmacology ; Cell Line ; Cell Membrane/ultrastructure ; Cells, Cultured ; Cytoplasmic Granules/immunology ; *Cytotoxicity, Immunologic ; Humans ; Macrophages/immunology/microbiology ; Membrane Glycoproteins/immunology/pharmacology ; Microscopy, Confocal ; Microscopy, Electron, Scanning ; Mycobacterium tuberculosis/*immunology/physiology/ultrastructure ; Perforin ; Pore Forming Cytotoxic Proteins ; Recombinant Proteins/pharmacology ; T-Lymphocytes, Cytotoxic/*immunology
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  • 12
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    Inhibitory function of p21Cip1/WAF1 in differentiation of primary mouse keratinocytes independent of cell cycle control (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-06
    Description: The cyclin-dependent kinase inhibitor p21(Cip1/WAF1) has been implicated as an inducer of differentiation. However, although expression of p21 is increased in postmitotic cells immediately adjacent to the proliferative compartment, its expression is decreased in cells further along the differentiation program. Expression of the p21 protein was decreased in terminally differentiated primary keratinocytes of mice, and this occurred by a proteasome-dependent pathway. Forced expression of p21 in these cells inhibited the expression of markers of terminal differentiation at both the protein and messenger RNA levels. These inhibitory effects on differentiation were not observed with a carboxyl-terminal truncation mutant or with the unrelated cyclin-dependent kinase inhibitor p16(INK4a), although all these molecules exerted similar inhibition of cell growth. These findings reveal an inhibitory role of p21 in the late stages of differentiation that does not result from the effects of p21 on the cell cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Cunto, F -- Topley, G -- Calautti, E -- Hsiao, J -- Ong, L -- Seth, P K -- Dotto, G P -- AR39190/AR/NIAMS NIH HHS/ -- CA16038/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 May 15;280(5366):1069-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, 13th Street, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9582119" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcysteine/analogs & derivatives/pharmacology ; Adenoviridae/genetics/physiology ; Animals ; Animals, Newborn ; *Cell Cycle ; *Cell Differentiation ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinases/antagonists & inhibitors/metabolism ; Cyclins/genetics/*metabolism ; Enzyme Inhibitors/metabolism ; Gene Expression Regulation ; Keratinocytes/*cytology/metabolism/virology ; Leupeptins/pharmacology ; Membrane Proteins/biosynthesis/genetics ; Mice ; Mutation ; Promoter Regions, Genetic ; Protein Precursors/biosynthesis/genetics ; RNA, Messenger/genetics/metabolism ; Succinates/pharmacology ; Transfection
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  • 13
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    Is apoptosis key in Alzheimer's disease? (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1998 Aug 28;281(5381):1303-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9735049" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism/*pathology ; Amyloid beta-Peptides/biosynthesis/physiology ; *Apoptosis ; Brain/metabolism/*pathology ; Cells, Cultured ; Cysteine Endopeptidases/metabolism ; DNA Fragmentation ; Humans ; Membrane Proteins/genetics/physiology ; Mutation ; Neurons/metabolism/*pathology ; Presenilin-1 ; Presenilin-2
    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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  • 14
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    Positive selection through a motif in the alphabeta T cell receptor (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-07
    Description: The two lineages of T cells, alphabeta and gammadelta, differ in their developmental requirements: only alphabeta T cells require major histocompatibility complex recognition, a process known as positive selection. The alphabeta T cell receptor (TCR), but not its gammadelta counterpart, contains a motif within the alpha-chain connecting peptide domain (alpha-CPM) that has been conserved over the last 500 million years. In transgenic mice expressing an alphabeta TCR lacking the alpha-CPM, thymocytes were blocked in positive selection but could undergo negative selection. Thus, the alpha-CPM seems to participate in the generation of signals required for positive selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Backstrom, B T -- Muller, U -- Hausmann, B -- Palmer, E -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):835-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, CH-4005 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694657" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigen-Presenting Cells/immunology ; Antigens, CD3/analysis ; CD4-Positive T-Lymphocytes/immunology ; Cell Lineage ; Cells, Cultured ; Histocompatibility Antigens Class II/immunology ; Ligands ; Lymphocyte Count ; Membrane Proteins/analysis ; Mice ; Mice, Inbred C57BL ; Mice, Nude ; Mice, Transgenic ; Molecular Sequence Data ; Mutation ; Receptor-CD3 Complex, Antigen, T-Cell/immunology/metabolism ; Receptors, Antigen, T-Cell/analysis ; Receptors, Antigen, T-Cell, alpha-beta/*chemistry/genetics/*immunology ; Signal Transduction ; T-Lymphocyte Subsets/*immunology ; Thymus Gland/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Cell surface trafficking of Fas: a rapid mechanism of p53-mediated apoptosis (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-09
    Description: p53 acts as a tumor suppressor by inducing both growth arrest and apoptosis. p53-induced apoptosis can occur without new RNA synthesis through an unknown mechanism. In human vascular smooth muscle cells, p53 activation transiently increased surface Fas (CD95) expression by transport from the Golgi complex. Golgi disruption blocked both p53-induced surface Fas expression and apoptosis. p53 also induced Fas-FADD binding and transiently sensitized cells to Fas-induced apoptosis. In contrast, lpr and gld fibroblasts were resistant to p53-induced apoptosis. Thus, p53 can mediate apoptosis through Fas transport from cytoplasmic stores.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bennett, M -- Macdonald, K -- Chan, S W -- Luzio, J P -- Simari, R -- Weissberg, P -- HL34073/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1998 Oct 9;282(5387):290-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 2QQ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9765154" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/genetics/*metabolism ; *Apoptosis/drug effects ; Brefeldin A/pharmacology ; Carrier Proteins/metabolism ; Cell Membrane/*metabolism ; Cells, Cultured ; Enzyme Inhibitors/pharmacology ; Etoposide/pharmacology ; Fas Ligand Protein ; Fas-Associated Death Domain Protein ; Golgi Apparatus/metabolism ; Humans ; Membrane Glycoproteins/genetics/metabolism ; Mice ; Muscle, Smooth, Vascular/cytology ; Mutation ; Protein Synthesis Inhibitors/pharmacology ; Rats ; Topoisomerase II Inhibitors ; Tumor Suppressor Protein p53/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Eight calves cloned from somatic cells of a single adult (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-16
    Description: Eight calves were derived from differentiated cells of a single adult cow, five from cumulus cells and three from oviductal cells out of 10 embryos transferred to surrogate cows (80 percent success). All calves were visibly normal, but four died at or soon after birth from environmental causes, and postmortem analysis revealed no abnormality. These results show that bovine cumulus and oviductal epithelial cells of the adult have the genetic content to direct the development of newborn calves.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kato, Y -- Tani, T -- Sotomaru, Y -- Kurokawa, K -- Kato, J -- Doguchi, H -- Yasue, H -- Tsunoda, Y -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):2095-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Animal Reproduction, College of Agriculture and Research Institute for Animal Developmental Biotechnology, Kinki University, 3327-204, Nakamachi, Nara, 631-8505, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9851933" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Husbandry ; Animals ; Blastocyst/cytology ; Cattle/embryology/*genetics ; Cell Fusion ; Cells, Cultured ; Cloning, Organism/*methods ; Cytoplasm/physiology ; Embryo Transfer/veterinary ; Epithelial Cells/cytology ; Fallopian Tubes/*cytology ; Female ; Microsatellite Repeats ; *Nuclear Transfer Techniques ; Oocytes/*cytology ; Ovarian Follicle/*cytology ; Pregnancy ; Pregnancy, Multiple
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  • 17
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    A viral mechanism for inhibition of the cellular phosphatase calcineurin (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-24
    Description: The transcription factor NFAT (nuclear factor of activated T cells) controls the expression of many immunomodulatory proteins. African swine fever virus inhibits proinflammatory cytokine expression in infected macrophages, and a viral protein A238L was found to display the activity of the immunosuppressive drug cyclosporin A by inhibiting NFAT-regulated gene transcription in vivo. This it does by binding the catalytic subunit of calcineurin and inhibiting calcineurin phosphatase activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miskin, J E -- Abrams, C C -- Goatley, L C -- Dixon, L K -- New York, N.Y. -- Science. 1998 Jul 24;281(5376):562-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Animal Health, Pirbright Laboratory, Pirbright, Surrey, GU24 0NF, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9677199" target="_blank"〉PubMed〈/a〉
    Keywords: African Swine Fever Virus/*physiology ; Amino Acid Sequence ; Animals ; Binding Sites ; Calcineurin/metabolism ; *Calcineurin Inhibitors ; Cell Nucleus/metabolism ; Cells, Cultured ; Cercopithecus aethiops ; Cyclosporine/pharmacology ; DNA-Binding Proteins/genetics/*metabolism ; Genes, Reporter ; Macrophages, Alveolar/*virology ; Molecular Sequence Data ; NF-kappa B/metabolism ; NFATC Transcription Factors ; *Nuclear Proteins ; Recombinant Proteins/metabolism ; Swine ; Transcription Factors/genetics/*metabolism ; *Transcription, Genetic ; Vero Cells ; Viral Proteins/genetics/*metabolism
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  • 18
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    RNA-splicing machinery revealed (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferber, D -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1581-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9767017" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cells, Cultured ; DNA, Complementary ; Databases, Factual ; Gene Expression ; Humans ; Mass Spectrometry ; Proteins/*chemistry/genetics/isolation & purification ; *RNA Splicing ; Spliceosomes/*chemistry
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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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    The importance of telomerase (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelner, K L -- New York, N.Y. -- Science. 1997 Oct 24;278(5338):600.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9381167" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Mice ; Mice, Transgenic ; Telomerase/genetics/*metabolism ; Telomere/*metabolism
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  • 20
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    Role of alpha-dystroglycan as a Schwann cell receptor for Mycobacterium leprae (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-16
    Description: alpha-Dystroglycan (alpha-DG) is a component of the dystroglycan complex, which is involved in early development and morphogenesis and in the pathogenesis of muscular dystrophies. Here, alpha-DG was shown to serve as a Schwann cell receptor for Mycobacterium leprae, the causative organism of leprosy. Mycobacterium leprae specifically bound to alpha-DG only in the presence of the G domain of the alpha2 chain of laminin-2. Native alpha-DG competitively inhibited the laminin-2-mediated M. leprae binding to primary Schwann cells. Thus, M. leprae may use linkage between the extracellular matrix and cytoskeleton through laminin-2 and alpha-DG for its interaction with Schwann cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rambukkana, A -- Yamada, H -- Zanazzi, G -- Mathus, T -- Salzer, J L -- Yurchenco, P D -- Campbell, K P -- Fischetti, V A -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):2076-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Bacterial Pathogenesis and Immunology, Rockefeller University, New York, NY 10021, USA. rambuka@rockvax.rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9851927" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bacterial Adhesion ; Binding Sites ; Calcium/physiology ; Cell Line, Transformed ; Cells, Cultured ; Cytoskeletal Proteins/*metabolism/pharmacology ; Dystroglycans ; Edetic Acid/pharmacology ; Glycosylation ; Humans ; Laminin/chemistry/*metabolism ; Membrane Glycoproteins/*metabolism/pharmacology ; Mycobacterium leprae/*metabolism ; Peripheral Nerves/chemistry ; Rats ; Receptors, Laminin/metabolism ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/chemistry/metabolism ; Schwann Cells/metabolism/*microbiology
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  • 21
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    Reaction to stem cells: a tale of the ticker (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malakoff, D -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1239.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9867624" target="_blank"〉PubMed〈/a〉
    Keywords: Biotechnology/*economics ; *Cell Culture Techniques ; Cells, Cultured ; Humans ; *Investments ; Stem Cells/*cytology ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 22
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    Differentiation of monocytes into dendritic cells in a model of transendothelial trafficking (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-17
    Description: Essential to the dendritic cell system of antigen-presenting cells are the veiled dendritic cells that traverse afferent lymph to enter lymph nodes, where they initiate immune responses. The origin of veiled cells, which were discovered 20 years ago, is unclear. Monocytes cultured with endothelium differentiated into dendritic cells within 2 days, particularly after phagocytosing particles in subendothelial collagen. These nascent dendritic cells migrated across the endothelium in the ablumenal-to-lumenal direction, as would occur during entry into lymphatics. Monocytes that remained in the subendothelial matrix became macrophages. Therefore, monocytes have two potential fates associated with distinct patterns of migration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Randolph, G J -- Beaulieu, S -- Lebecque, S -- Steinman, R M -- Muller, W A -- AI13013/AI/NIAID NIH HHS/ -- AI40045/AI/NIAID NIH HHS/ -- HL46849/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Oct 16;282(5388):480-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Cornell University Medical College, 1300 York Avenue, Room C-420, New York, NY 10021, USA. GJRandol@mail.med.cornell.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9774276" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD/analysis ; Carrier Proteins/analysis ; Cell Count ; Cell Differentiation ; Cell Movement ; Cells, Cultured ; Collagen ; Dendritic Cells/cytology/immunology/*physiology ; Endothelium, Vascular/cytology/*physiology ; HLA-DR Antigens/analysis ; Humans ; Lymphocyte Activation ; Lymphocyte Culture Test, Mixed ; Macrophages/cytology/immunology/physiology ; Microfilament Proteins/analysis ; Monocytes/cytology/immunology/*physiology ; Phagocytosis ; T-Lymphocytes/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 23
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    Signaling path may lead to better heart-failure therapies (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1998 Apr 17;280(5362):383.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9575084" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcineurin/metabolism ; *Calcineurin Inhibitors ; Calcium/metabolism ; Cardiomegaly/etiology/metabolism ; Cells, Cultured ; Cyclosporine/*pharmacology/therapeutic use ; DNA-Binding Proteins/metabolism ; Enzyme Inhibitors/pharmacology ; GATA4 Transcription Factor ; Heart Failure/*drug therapy/etiology/metabolism ; Humans ; Mice ; Myocardium/*metabolism ; NFATC Transcription Factors ; *Nuclear Proteins ; Signal Transduction ; Tacrolimus/pharmacology ; Transcription Factors/metabolism
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  • 24
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    Rapid identification of subtype-selective agonists of the somatostatin receptor through combinatorial chemistry (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-23
    Description: Nonpeptide agonists of each of the five somatostatin receptors were identified in combinatorial libraries constructed on the basis of molecular modeling of known peptide agonists. In vitro experiments using these selective compounds demonstrated the role of the somatostatin subtype-2 receptor in inhibition of glucagon release from mouse pancreatic alpha cells and the somatostatin subtype-5 receptor as a mediator of insulin secretion from pancreatic beta cells. Both receptors regulated growth hormone release from the rat anterior pituitary gland. The availability of high-affinity, subtype-selective agonists for each of the somatostatin receptors provides a direct approach to defining their physiological functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rohrer, S P -- Birzin, E T -- Mosley, R T -- Berk, S C -- Hutchins, S M -- Shen, D M -- Xiong, Y -- Hayes, E C -- Parmar, R M -- Foor, F -- Mitra, S W -- Degrado, S J -- Shu, M -- Klopp, J M -- Cai, S J -- Blake, A -- Chan, W W -- Pasternak, A -- Yang, L -- Patchett, A A -- Smith, R G -- Chapman, K T -- Schaeffer, J M -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):737-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biochemistry and Physiology, Merck Research Laboratories, Post Office Box 2000, Rahway, NJ 07065, USA. susanvrohrer@merck.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9784130" target="_blank"〉PubMed〈/a〉
    Keywords: Amides/metabolism/*pharmacology ; Amino Acid Sequence ; Animals ; Cell Line ; Cells, Cultured ; Cricetinae ; Drug Design ; Glucagon/secretion ; Growth Hormone/secretion ; Insulin/secretion ; Islets of Langerhans/drug effects/secretion ; Ligands ; Membrane Proteins ; Mice ; Models, Chemical ; Molecular Sequence Data ; Pituitary Gland, Anterior/drug effects/metabolism ; Rats ; Receptors, Somatostatin/*agonists/physiology
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  • 25
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    Molecular plumbing (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peters, R -- Sikorski, R -- New York, N.Y. -- Science. 1998 Feb 20;279(5354):1230-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9508694" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biomedical Engineering ; *Blood Vessel Prosthesis ; Blood Vessel Prosthesis Implantation ; Cells, Cultured ; Culture Techniques ; Dogs ; Endothelium, Vascular/cytology ; Fibroblasts/cytology ; Humans ; Muscle, Smooth, Vascular/cytology ; Transplantation, Heterologous
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  • 26
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    Role of PML in cell growth and the retinoic acid pathway (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: The PML gene is fused to the retinoic acid receptor alpha (RARalpha) gene in chromosomal translocations associated with acute promyelocytic leukemia (APL). Ablation of murine PML protein by homologous recombination revealed that PML regulates hemopoietic differentiation and controls cell growth and tumorigenesis. PML function was essential for the tumor-growth-suppressive activity of retinoic acid (RA) and for its ability to induce terminal myeloid differentiation of precursor cells. PML was needed for the RA-dependent transactivation of the p21WAF1/CIP1 gene, which regulates cell cycle progression and cellular differentiation. These results indicate that PML is a critical component of the RA pathway and that disruption of its activity by the PML-RARalpha fusion protein may be important in APL pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Z G -- Delva, L -- Gaboli, M -- Rivi, R -- Giorgio, M -- Cordon-Cardo, C -- Grosveld, F -- Pandolfi, P P -- CA 71692/CA/NCI NIH HHS/ -- CA-08748/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Mar 6;279(5356):1547-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics and Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, Sloan-Kettering Division, Graduate School of Medical Sciences, Cornell University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9488655" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Differentiation/drug effects ; *Cell Division ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/genetics ; Female ; Fibroblasts/cytology ; Gene Targeting ; Granulocytes/cytology ; Hematopoiesis ; Hematopoietic Stem Cells/cytology ; Leukemia, Promyelocytic, Acute/pathology ; Male ; Mice ; Monocytes/cytology ; Neoplasm Proteins/genetics/*physiology ; Neoplasms, Experimental/etiology ; *Nuclear Proteins ; Oncogene Proteins, Fusion/physiology ; Transcription Factors/genetics/*physiology ; Transcriptional Activation ; Tretinoin/pharmacology/*physiology ; Tumor Suppressor Proteins
    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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    Role of dynamin in the formation of transport vesicles from the trans-Golgi network (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-07
    Description: Dynamin guanosine triphosphatases support the scission of clathrin-coated vesicles from the plasmalemma during endocytosis. By fluorescence microscopy of cultured rat hepatocytes, a green fluorescent protein-dynamin II fusion protein localized with clathrin-coated vesicles at the Golgi complex. A cell-free assay was utilized to demonstrate the role of dynamin in vesicle formation at the trans-Golgi. Addition of peptide-specific anti-dynamin antibodies to the assay mixture inhibited both constitutive exocytic and clathrin-coated vesicle formation. Immunodepletion of dynamin proteins also inhibited vesicle formation, and budding efficiency was restored upon readdition of purified dynamin. These data suggest that dynamin participates in the formation of distinct transport vesicles from the trans-Golgi network.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, S M -- Howell, K E -- Henley, J R -- Cao, H -- McNiven, M A -- P30 CA-46934/CA/NCI NIH HHS/ -- P30 DK-34914/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 23;279(5350):573-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Basic Research in Digestive Diseases, Mayo Clinic and Foundation, Rochester, MN 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9438853" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Biological Transport ; Cell Membrane/chemistry ; Cells, Cultured ; Clathrin/analysis ; Coated Vesicles/chemistry/*metabolism/ultrastructure ; Cytosol/metabolism ; Dynamins ; GTP Phosphohydrolases/analysis/immunology/*metabolism ; Golgi Apparatus/chemistry/*metabolism ; Green Fluorescent Proteins ; Guanosine 5'-O-(3-Thiotriphosphate)/metabolism ; Liver/ultrastructure ; Luminescent Proteins ; Microscopy, Fluorescence ; Organelles/chemistry/*metabolism/ultrastructure ; Rats ; Recombinant Fusion Proteins/analysis
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Neurodegeneration. Huntington's research points to possible new therapies (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):43-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy ; Brain-Derived Neurotrophic Factor/metabolism ; Cells, Cultured ; Clinical Trials as Topic ; Corpus Striatum/pathology ; Disease Models, Animal ; Gene Expression Regulation ; Humans ; Huntington Disease/*drug therapy/genetics/pathology/*physiopathology ; Mice ; Mitochondria/metabolism ; Mutation ; Nerve Tissue Proteins/chemistry/*genetics/metabolism/*physiology ; Neurons/*physiology ; Nuclear Proteins/chemistry/*genetics/metabolism/*physiology ; Peptides ; Transcription Factors/metabolism ; Trinucleotide Repeat Expansion
    Print ISSN: 0036-8075
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  • 29
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    Achieving stability of lipopolysaccharide-induced NF-kappaB activation (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-17
    Description: The activation dynamics of the transcription factor NF-kappaB exhibit damped oscillatory behavior when cells are stimulated by tumor necrosis factor-alpha (TNFalpha) but stable behavior when stimulated by lipopolysaccharide (LPS). LPS binding to Toll-like receptor 4 (TLR4) causes activation of NF-kappaB that requires two downstream pathways, each of which when isolated exhibits damped oscillatory behavior. Computational modeling of the two TLR4-dependent signaling pathways suggests that one pathway requires a time delay to establish early anti-phase activation of NF-kappaB by the two pathways. The MyD88-independent pathway required Inferon regulatory factor 3-dependent expression of TNFalpha to activate NF-kappaB, and the time required for TNFalpha synthesis established the delay.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Covert, Markus W -- Leung, Thomas H -- Gaston, Jahlionais E -- Baltimore, David -- GM039458-21/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 16;309(5742):1854-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16166516" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Adaptor Proteins, Vesicular Transport/deficiency/physiology ; Animals ; Antigens, Differentiation/physiology ; Cell Line ; Cells, Cultured ; Computer Simulation ; Cycloheximide/pharmacology ; DNA-Binding Proteins/genetics/physiology ; Gene Expression Profiling ; Gene Expression Regulation ; I-kappa B Kinase ; I-kappa B Proteins/biosynthesis/genetics/metabolism ; Interferon Regulatory Factor-3 ; Kinetics ; Lipopolysaccharides/*immunology/metabolism ; Mice ; Models, Biological ; Myeloid Differentiation Factor 88 ; NF-kappa B/*metabolism ; Oligonucleotide Array Sequence Analysis ; Protein Synthesis Inhibitors/pharmacology ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Immunologic/deficiency/metabolism/physiology ; Signal Transduction ; Time Factors ; Toll-Like Receptor 4 ; Transcription Factors/genetics/physiology ; Tumor Necrosis Factor-alpha/biosynthesis/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Self-propagating, molecular-level polymorphism in Alzheimer's beta-amyloid fibrils (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-18
    Description: Amyloid fibrils commonly exhibit multiple distinct morphologies in electron microscope and atomic force microscope images, often within a single image field. By using electron microscopy and solid-state nuclear magnetic resonance measurements on fibrils formed by the 40-residue beta-amyloid peptide of Alzheimer's disease (Abeta(1-40)), we show that different fibril morphologies have different underlying molecular structures, that the predominant structure can be controlled by subtle variations in fibril growth conditions, and that both morphology and molecular structure are self-propagating when fibrils grow from preformed seeds. Different Abeta(1-40) fibril morphologies also have significantly different toxicities in neuronal cell cultures. These results have implications for the mechanism of amyloid formation, the phenomenon of strains in prion diseases, the role of amyloid fibrils in amyloid diseases, and the development of amyloid-based nano-materials.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petkova, Aneta T -- Leapman, Richard D -- Guo, Zhihong -- Yau, Wai-Ming -- Mattson, Mark P -- Tycko, Robert -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):262-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health (NIH), Bethesda, MD 20892-0520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653506" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amyloid beta-Peptides/*chemistry/toxicity/*ultrastructure ; Animals ; Cells, Cultured ; Chemistry, Physical ; Hippocampus/cytology ; Humans ; Hydrogen Bonding ; Microscopy, Atomic Force ; Microscopy, Electron, Transmission ; Molecular Structure ; Neurons/cytology/drug effects ; Nuclear Magnetic Resonance, Biomolecular ; Peptide Fragments/*chemistry/toxicity/*ultrastructure ; Physicochemical Phenomena ; Protein Conformation ; Protein Structure, Secondary ; Rats
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    Stimulus specificity of gene expression programs determined by temporal control of IKK activity (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-17
    Description: A small number of mammalian signaling pathways mediate a myriad of distinct physiological responses to diverse cellular stimuli. Temporal control of the signaling module that contains IkappaB kinase (IKK), its substrate inhibitor of NF-kappaB (IkappaB), and the key inflammatory transcription factor NF-kappaB can allow for selective gene activation. We have demonstrated that different inflammatory stimuli induce distinct IKK profiles, and we examined the underlying molecular mechanisms. Although tumor necrosis factor-alpha (TNFalpha)-induced IKK activity was rapidly attenuated by negative feedback, lipopolysaccharide (LPS) signaling and LPS-specific gene expression programs were dependent on a cytokine-mediated positive feedback mechanism. Thus, the distinct biological responses to LPS and TNFalpha depend on signaling pathway-specific mechanisms that regulate the temporal profile of IKK activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Werner, Shannon L -- Barken, Derren -- Hoffmann, Alexander -- GM071573/GM/NIGMS NIH HHS/ -- GM72024/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 16;309(5742):1857-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Signaling Systems Laboratory, Department of Chemistry and Biochemistry, 9500 Gilman Drive, Mailcode 0375, La Jolla, CA 92093-0375, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16166517" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Autocrine Communication ; Cell Line ; Cells, Cultured ; Computer Simulation ; Cytokines/genetics ; Feedback, Physiological ; Gene Expression Profiling ; *Gene Expression Regulation ; I-kappa B Kinase ; I-kappa B Proteins/metabolism ; Lipopolysaccharides/immunology/metabolism/pharmacology ; Mice ; Models, Biological ; NF-kappa B/deficiency/metabolism ; Oligonucleotide Array Sequence Analysis ; Protein-Serine-Threonine Kinases/*metabolism ; Receptors, Immunologic/metabolism ; Signal Transduction ; Toll-Like Receptor 4 ; Transcriptional Activation ; Tumor Necrosis Factor-alpha/deficiency/immunology/metabolism/pharmacology
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    Endosomal proteolysis of the Ebola virus glycoprotein is necessary for infection (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-16
    Description: Ebola virus (EboV) causes rapidly fatal hemorrhagic fever in humans and there is currently no effective treatment. We found that the infection of African green monkey kidney (Vero) cells by vesicular stomatitis viruses bearing the EboV glycoprotein (GP) requires the activity of endosomal cysteine proteases. Using selective protease inhibitors and protease-deficient cell lines, we identified an essential role for cathepsin B (CatB) and an accessory role for cathepsin L (CatL) in EboV GP-dependent entry. Biochemical studies demonstrate that CatB and CatL mediate entry by carrying out proteolysis of the EboV GP subunit GP1 and support a multistep mechanism that explains the relative contributions of these enzymes to infection. CatB and CatB/CatL inhibitors diminish the multiplication of infectious EboV-Zaire in cultured cells and may merit investigation as anti-EboV drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandran, Kartik -- Sullivan, Nancy J -- Felbor, Ute -- Whelan, Sean P -- Cunningham, James M -- R01 AI059371/AI/NIAID NIH HHS/ -- R01 AI059371-01A1/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 Jun 10;308(5728):1643-5. Epub 2005 Apr 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15831716" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cathepsin B/antagonists & inhibitors/*metabolism ; Cathepsin L ; Cathepsins/antagonists & inhibitors/*metabolism ; Cell Line ; Cells, Cultured ; Cercopithecus aethiops ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Ebolavirus/metabolism/*physiology ; Endosomes/*metabolism ; Hydrogen-Ion Concentration ; Mice ; Vero Cells ; Vesicular stomatitis Indiana virus/genetics/physiology ; Viral Envelope Proteins/*metabolism ; Virion/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The beta-glucuronidase klotho hydrolyzes and activates the TRPV5 channel (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-22
    Description: Blood calcium concentration is maintained within a narrow range despite large variations in dietary input and body demand. The Transient Receptor Potential ion channel TRPV5 has been implicated in this process. We report here that TRPV5 is stimulated by the mammalian hormone klotho. Klotho, a beta-glucuronidase, hydrolyzes extracellular sugar residues on TRPV5, entrapping the channel in the plasma membrane. This maintains durable calcium channel activity and membrane calcium permeability in kidney. Thus, klotho activates a cell surface channel by hydrolysis of its extracellular N-linked oligosaccharides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, Q -- Hoefs, S -- van der Kemp, A W -- Topala, C N -- Bindels, R J -- Hoenderop, J G -- New York, N.Y. -- Science. 2005 Oct 21;310(5747):490-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, 6500 HB Nijmegen, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16239475" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; Glucuronidase/antagonists & inhibitors/metabolism ; Glycosylation ; Humans ; Hydrolysis ; Kidney/cytology/metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Inbred C57BL ; Mutation ; Patch-Clamp Techniques ; Protein Transport ; Rabbits ; Sodium/metabolism ; TRPV Cation Channels/genetics/*metabolism ; Transfection
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    Glial membranes at the node of Ranvier prevent neurite outgrowth (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-19
    Description: Nodes of Ranvier are regularly placed, nonmyelinated axon segments along myelinated nerves. Here we show that nodal membranes isolated from the central nervous system (CNS) of mammals restricted neurite outgrowth of cultured neurons. Proteomic analysis of these membranes revealed several inhibitors of neurite outgrowth, including the oligodendrocyte myelin glycoprotein (OMgp). In rat spinal cord, OMgp was not localized to compact myelin, as previously thought, but to oligodendroglia-like cells, whose processes converge to form a ring that completely encircles the nodes. In OMgp-null mice, CNS nodes were abnormally wide and collateral sprouting was observed. Nodal ensheathment in the CNS may stabilize the node and prevent axonal sprouting.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Jeffrey K -- Phillips, Greg R -- Roth, Alejandro D -- Pedraza, Liliana -- Shan, Weisong -- Belkaid, Wiam -- Mi, Sha -- Fex-Svenningsen, Asa -- Florens, Laurence -- Yates, John R 3rd -- Colman, David R -- NS20147/NS/NINDS NIH HHS/ -- P41 RR11823/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1813-7. Epub 2005 Nov 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16293723" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/analysis ; Axons/*physiology/ultrastructure ; Cattle ; Cell Surface Extensions/chemistry/*physiology/ultrastructure ; Cells, Cultured ; GPI-Linked Proteins ; Ganglia, Spinal/physiology/ultrastructure ; Humans ; Mice ; Myelin Proteins ; Myelin Sheath/chemistry ; Myelin-Associated Glycoprotein/analysis ; Myelin-Oligodendrocyte Glycoprotein ; Neurites/*physiology/ultrastructure ; Neuroglia/chemistry/*physiology/*ultrastructure ; Oligodendroglia/chemistry/physiology/ultrastructure ; Proteoglycans/analysis ; Proteomics ; Ranvier's Nodes/chemistry/*physiology/ultrastructure ; Rats ; Spinal Cord/cytology
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    Neuroscience. Brain under surveillance: the microglia patrol (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fetler, Luc -- Amigorena, Sebastian -- New York, N.Y. -- Science. 2005 Jul 15;309(5733):392-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire Physico-Chimie Curie, CNRS UMR 168, Institut Curie, Paris, France. luc.fetler@curie.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16020721" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Astrocytes/metabolism ; Brain/blood supply/*cytology/pathology/*physiology ; Brain Injuries/immunology/pathology/*physiopathology ; Capillaries/injuries ; Cell Surface Extensions/physiology/ultrastructure ; Cells, Cultured ; Mice ; Mice, Transgenic ; Microglia/cytology/*physiology/*ultrastructure ; Microscopy/methods ; Movement ; Phagocytosis ; Photons ; Receptors, Purinergic P2/metabolism
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    Neuroscience. Making synapses: a balancing act (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hussain, Natasha K -- Sheng, Morgan -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1207-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Picower Center for Learning and Memory, RIKEN-MIT Neuroscience Research Center, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. natashah@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15731430" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion Molecules, Neuronal ; Cells, Cultured ; Glutamic Acid/metabolism ; Hippocampus/cytology ; Membrane Proteins/*metabolism ; Nerve Tissue Proteins/*metabolism ; Neural Inhibition ; Neurons/physiology ; Presynaptic Terminals/*physiology ; Protein Binding ; Rats ; Synapses/*physiology ; Synaptic Membranes/*physiology ; gamma-Aminobutyric Acid/metabolism
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    Cell signaling. Stat acetylation--a key facet of cytokine signaling? (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Shea, John J -- Kanno, Yuka -- Chen, Xiaomin -- Levy, David E -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):217-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653493" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acetyltransferases/metabolism ; Active Transport, Cell Nucleus ; Cell Nucleus/metabolism ; Cells, Cultured ; Cytokines/*physiology ; Cytoplasm/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Dimerization ; Histone Acetyltransferases ; Histone Deacetylases/metabolism ; Lysine/*metabolism ; Mutation ; NF-kappa B/metabolism ; Nuclear Proteins/metabolism ; Phosphorylation ; Protein Processing, Post-Translational ; STAT3 Transcription Factor ; *Signal Transduction ; Trans-Activators/chemistry/genetics/*metabolism ; Transcriptional Activation ; src Homology Domains
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    Cell biology. Ras on the roundabout (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-03-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meder, Doris -- Simons, Kai -- New York, N.Y. -- Science. 2005 Mar 18;307(5716):1731-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany. meder@mpi-cbg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15774748" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Animals ; Cell Differentiation ; Cell Membrane/*metabolism ; Cell Proliferation ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cytosol/metabolism ; Dogs ; Fluorescence Resonance Energy Transfer ; Genes, ras ; Golgi Apparatus/*metabolism ; Guanosine Triphosphate/metabolism ; Humans ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinases/metabolism ; Models, Biological ; Palmitic Acid/metabolism ; Protein Isoforms/chemistry/metabolism ; Proto-Oncogene Proteins p21(ras)/chemistry/*metabolism ; ras Proteins
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    Stem cells. Scientists chase after immortality in a petri dish (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2005 Sep 23;309(5743):1982-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16179446" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication ; Cell Differentiation ; Cell Line ; Cells, Cultured ; Embryo, Mammalian/*cytology ; Female ; Genomic Imprinting ; Humans ; Male ; Meiosis ; *Oocytes/cytology/physiology ; Ovary/cytology/physiology ; *Spermatozoa/cytology/physiology ; *Stem Cells/cytology/physiology ; Testis/cytology/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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    Bone marrow stromal cells generate muscle cells and repair muscle degeneration (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-09
    Description: Bone marrow stromal cells (MSCs) have great potential as therapeutic agents. We report a method for inducing skeletal muscle lineage cells from human and rat general adherent MSCs with an efficiency of 89%. Induced cells differentiated into muscle fibers upon transplantation into degenerated muscles of rats and mdx-nude mice. The induced population contained Pax7-positive cells that contributed to subsequent regeneration of muscle upon repetitive damage without additional transplantation of cells. These MSCs represent a more ready supply of myogenic cells than do the rare myogenic stem cells normally found in muscle and bone marrow.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dezawa, Mari -- Ishikawa, Hiroto -- Itokazu, Yutaka -- Yoshihara, Tomoyuki -- Hoshino, Mikio -- Takeda, Shin-ichi -- Ide, Chizuka -- Nabeshima, Yo-ichi -- New York, N.Y. -- Science. 2005 Jul 8;309(5732):314-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Kyoto University Graduate School of Medicine, Yoshidakonoecho, Sakyo-ku, Kyoto, 606-8501 Japan. dezawa@anat2.med.kyoto-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16002622" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/*cytology/physiology ; Bone Marrow Transplantation ; *Cell Differentiation ; Cell Fusion ; Cell Lineage ; Cell Proliferation ; Cell Separation ; Cells, Cultured ; Colforsin/pharmacology ; Fibroblast Growth Factor 2/pharmacology ; Gene Expression Profiling ; Homeodomain Proteins/analysis ; Humans ; Mice ; Mice, Inbred mdx ; Mice, Nude ; Muscle Cells/*cytology ; Muscle Development/genetics ; Muscle Fibers, Skeletal/*cytology ; Muscle Proteins/analysis ; Muscle, Skeletal/cytology ; Muscular Diseases/*therapy ; Muscular Dystrophy, Duchenne/therapy ; Neuregulins/pharmacology ; PAX7 Transcription Factor ; Platelet-Derived Growth Factor/pharmacology ; Rats ; Regeneration ; Satellite Cells, Skeletal Muscle/cytology/physiology ; Stem Cells/cytology/physiology ; Stromal Cells/*cytology/physiology/transplantation ; Transfection
    Print ISSN: 0036-8075
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    Altered TCR signaling from geometrically repatterned immunological synapses (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-19
    Description: The immunological synapse is a specialized cell-cell junction that is defined by large-scale spatial patterns of receptors and signaling molecules yet remains largely enigmatic in terms of formation and function. We used supported bilayer membranes and nanometer-scale structures fabricated onto the underlying substrate to impose geometric constraints on immunological synapse formation. Analysis of the resulting alternatively patterned synapses revealed a causal relation between the radial position of T cell receptors (TCRs) and signaling activity, with prolonged signaling from TCR microclusters that had been mechanically trapped in the peripheral regions of the synapse. These results are consistent with a model of the synapse in which spatial translocation of TCRs represents a direct mechanism of signal regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mossman, Kaspar D -- Campi, Gabriele -- Groves, Jay T -- Dustin, Michael L -- GM64900/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Nov 18;310(5751):1191-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biophysics Graduate Group, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16293763" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Antigen-Presenting Cells/metabolism ; Cells, Cultured ; Lipid Bilayers ; Mice ; Models, Immunological ; Receptors, Antigen, T-Cell/chemistry/*metabolism ; *Signal Transduction ; Structure-Activity Relationship ; T-Lymphocytes/immunology/*metabolism
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    Axonopathy and transport deficits early in the pathogenesis of Alzheimer's disease (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-26
    Description: We identified axonal defects in mouse models of Alzheimer's disease that preceded known disease-related pathology by more than a year; we observed similar axonal defects in the early stages of Alzheimer's disease in humans. Axonal defects consisted of swellings that accumulated abnormal amounts of microtubule-associated and molecular motor proteins, organelles, and vesicles. Impairing axonal transport by reducing the dosage of a kinesin molecular motor protein enhanced the frequency of axonal defects and increased amyloid-beta peptide levels and amyloid deposition. Reductions in microtubule-dependent transport may stimulate proteolytic processing of beta-amyloid precursor protein, resulting in the development of senile plaques and Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokin, Gorazd B -- Lillo, Concepcion -- Falzone, Tomas L -- Brusch, Richard G -- Rockenstein, Edward -- Mount, Stephanie L -- Raman, Rema -- Davies, Peter -- Masliah, Eliezer -- Williams, David S -- Goldstein, Lawrence S B -- EY12598/EY/NEI NIH HHS/ -- EY13408/EY/NEI NIH HHS/ -- P50 AG05131/AG/NIA NIH HHS/ -- R01 EY007042/EY/NEI NIH HHS/ -- R01 EY007042-19/EY/NEI NIH HHS/ -- R01 EY013408/EY/NEI NIH HHS/ -- R01 EY013408-02/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1282-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Cellular and Molecular Medicine, School of Medicine, University of California San Diego (UCSD), 9500 Gilman Drive, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15731448" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Alzheimer Disease/genetics/*metabolism/*pathology ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Animals ; *Axonal Transport ; Axons/*pathology/physiology ; Basal Nucleus of Meynert/pathology ; Brain/*metabolism/*pathology ; Cells, Cultured ; Cytoplasmic Vesicles/ultrastructure ; Female ; Hippocampus ; Humans ; Kinesin/metabolism ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Microtubule-Associated Proteins/genetics/metabolism ; Neurons/metabolism ; Organelles/ultrastructure ; Plaque, Amyloid/pathology ; Time Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Recognition of host immune activation by Pseudomonas aeruginosa (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-30
    Description: It is generally reasoned that lethal infections caused by opportunistic pathogens develop permissively by invading a host that is both physiologically stressed and immunologically compromised. However, an alternative hypothesis might be that opportunistic pathogens actively sense alterations in host immune function and respond by enhancing their virulence phenotype. We demonstrate that interferon-gamma binds to an outer membrane protein in Pseudomonas aeruginosa, OprF, resulting in the expression of a quorum-sensing dependent virulence determinant, the PA-I lectin. These observations provide details of the mechanisms by which prokaryotic organisms are directly signaled by immune activation in their eukaryotic host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Licheng -- Estrada, Oscar -- Zaborina, Olga -- Bains, Manjeet -- Shen, Le -- Kohler, Jonathan E -- Patel, Nachiket -- Musch, Mark W -- Chang, Eugene B -- Fu, Yang-Xin -- Jacobs, Michael A -- Nishimura, Michael I -- Hancock, Robert E W -- Turner, Jerrold R -- Alverdy, John C -- 2-RO1 GM062344-05/GM/NIGMS NIH HHS/ -- DK-38510/DK/NIDDK NIH HHS/ -- DK-47722/DK/NIDDK NIH HHS/ -- R01DK61931/DK/NIDDK NIH HHS/ -- R01DK68271/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2005 Jul 29;309(5735):774-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, University of Chicago, Pritzker School of Medicine, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16051797" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesins, Bacterial/*biosynthesis ; Animals ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; Cytokines/immunology/metabolism/pharmacology ; Humans ; Interferon-gamma/immunology/*metabolism/pharmacology ; Lectins/*biosynthesis ; Lymphocyte Activation ; Porins/isolation & purification/*metabolism ; Protein Binding ; Pseudomonas aeruginosa/growth & development/*immunology/metabolism/*pathogenicity ; Pyocyanine/biosynthesis ; Recombinant Proteins/pharmacology ; Signal Transduction ; T-Lymphocytes/*immunology ; Up-Regulation ; Virulence
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    Control of excitatory and inhibitory synapse formation by neuroligins (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-01
    Description: The normal function of neural networks depends on a delicate balance between excitatory and inhibitory synaptic inputs. Synapse formation is thought to be regulated by bidirectional signaling between pre- and postsynaptic cells. We demonstrate that members of the Neuroligin family promote postsynaptic differentiation in cultured rat hippocampal neurons. Down-regulation of neuroligin isoform expression by RNA interference results in a loss of excitatory and inhibitory synapses. Electrophysiological analysis revealed a predominant reduction of inhibitory synaptic function. Thus, neuroligins control the formation and functional balance of excitatory and inhibitory synapses in hippocampal neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chih, Ben -- Engelman, Holly -- Scheiffele, Peter -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1324-8. Epub 2005 Jan 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Cellular Biophysics, Center for Neurobiology and Behavior, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15681343" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Cell Adhesion Molecules, Neuronal ; Cell Line ; Cells, Cultured ; Dendrites/physiology/ultrastructure ; Down-Regulation ; Evoked Potentials ; Excitatory Postsynaptic Potentials ; Hippocampus/cytology ; Membrane Proteins/genetics/*metabolism ; Membrane Transport Proteins/metabolism ; Mutation ; Nerve Tissue Proteins/genetics/*metabolism ; Neural Inhibition ; Neurons/physiology ; Presynaptic Terminals/*physiology ; Protein Isoforms ; RNA Interference ; Rats ; Receptors, AMPA/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/*physiology ; Synaptic Membranes/*physiology ; Synaptic Transmission ; Transfection ; Vesicular Glutamate Transport Protein 1 ; Vesicular Inhibitory Amino Acid Transport Proteins
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  • 45
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    Equivalent effects of snake PLA2 neurotoxins and lysophospholipid-fatty acid mixtures (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-13
    Description: Snake presynaptic phospholipase A2 neurotoxins (SPANs) paralyze the neuromuscular junction (NMJ). Upon intoxication, the NMJ enlarges and has a reduced content of synaptic vesicles, and primary neuronal cultures show synaptic swelling with surface exposure of the lumenal domain of the synaptic vesicle protein synaptotagmin I. Concomitantly, these neurotoxins induce exocytosis of neurotransmitters. We found that an equimolar mixture of lysophospholipids and fatty acids closely mimics all of the biological effects of SPANs. These results draw attention to the possible role of local lipid changes in synaptic vesicle release and provide new tools for the study of exocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rigoni, Michela -- Caccin, Paola -- Gschmeissner, Steve -- Koster, Grielof -- Postle, Anthony D -- Rossetto, Ornella -- Schiavo, Giampietro -- Montecucco, Cesare -- GP0272Y01/Telethon/Italy -- New York, N.Y. -- Science. 2005 Dec 9;310(5754):1678-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Sciences and Consiglio Nazionale Ricerche Institute of Neuroscience, University of Padova, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16339444" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Elapid Venoms/toxicity ; Esterification ; Exocytosis ; Fatty Acids/*metabolism/toxicity ; Glutamic Acid/metabolism ; Hydrolysis ; Kinetics ; Lipid Bilayers ; Lysophospholipids/*metabolism/toxicity ; Male ; Mass Spectrometry ; Membrane Fusion ; Membrane Lipids/metabolism ; Mice ; Neuromuscular Junction/drug effects/metabolism/physiology ; Neurons/drug effects/metabolism/ultrastructure ; Neurotoxins/*metabolism/toxicity ; Neurotransmitter Agents/metabolism ; Phospholipases A/*metabolism/toxicity ; Phospholipases A2 ; Synapses/drug effects/ultrastructure ; Synaptic Membranes/metabolism/*physiology ; Synaptic Vesicles/drug effects/physiology/ultrastructure
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    Nod2 mutation in Crohn's disease potentiates NF-kappaB activity and IL-1beta processing (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-02-05
    Description: Variants of NOD2, an intracellular sensor of bacteria-derived muramyl dipeptide (MDP), increase susceptibility to Crohn's disease (CD). These variants are thought to be defective in activation of nuclear factor kappaB (NF-kappaB) and antibacterial defenses, but CD clinical specimens display elevated NF-kappaB activity. To illuminate the pathophysiological function of NOD2, we introduced such a variant to the mouse Nod2 locus. Mutant mice exhibited elevated NF-kappaB activation in response to MDP and more efficient processing and secretion of the cytokine interleukin-1beta (IL-1beta). These effects are linked to increased susceptibility to bacterial-induced intestinal inflammation and identify NOD2 as a positive regulator of NF-kappaB activation and IL-1beta secretion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maeda, Shin -- Hsu, Li-Chung -- Liu, Hongjun -- Bankston, Laurie A -- Iimura, Mitsutoshi -- Kagnoff, Martin F -- Eckmann, Lars -- Karin, Michael -- AI43477/AI/NIAID NIH HHS/ -- AI56075/AI/NIAID NIH HHS/ -- DK07202/DK/NIDDK NIH HHS/ -- DK35108/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 4;307(5710):734-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0723, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15692052" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylmuramyl-Alanyl-Isoglutamine/immunology ; Animals ; Anti-Bacterial Agents/pharmacology ; Apoptosis ; Bacteria/immunology ; Cells, Cultured ; Colitis/immunology/pathology ; Colon/*immunology/microbiology ; Crohn Disease/genetics/*immunology ; Cytokines/biosynthesis/genetics ; Dextran Sulfate/pharmacology ; Interleukin-1/*metabolism ; Intestinal Mucosa/immunology ; Intracellular Signaling Peptides and Proteins/*genetics/*physiology ; Lipopolysaccharides/immunology ; Macrophage Activation ; Macrophages/*immunology/metabolism ; Mice ; Mutation ; NF-kappa B/*metabolism ; Nod2 Signaling Adaptor Protein ; Peptidoglycan/immunology ; Signal Transduction
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    Obligate role of anti-apoptotic MCL-1 in the survival of hematopoietic stem cells (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-19
    Description: Apoptosis is important in controlling hematopoietic stem cell (HSC) numbers. However, the specific BCL-2 family member(s) that regulate HSC homeostasis are not precisely defined. We tested myeloid leukemia-1 (MCL-1) as an attractive candidate that is highly expressed in HSCs and regulated by growth factor signals. Inducible deletion of Mcl-1 in mice resulted in ablation of bone marrow. This resulted in the loss of early bone marrow progenitor populations, including HSCs. Moreover, growth factors including stem cell factor increased transcription of the Mcl-1 gene and required MCL-1 to augment survival of purified bone marrow progenitors. Deletion of Mcl-1 in other tissues, including liver, did not impair survival. Thus, MCL-1 is a critical and specific regulator essential for ensuring the homeostasis of early hematopoietic progenitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Opferman, Joseph T -- Iwasaki, Hiromi -- Ong, Christy C -- Suh, Heikyung -- Mizuno, Shin-ichi -- Akashi, Koichi -- Korsmeyer, Stanley J -- CA072009/CA/NCI NIH HHS/ -- DK061320/DK/NIDDK NIH HHS/ -- R37CA50239/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 18;307(5712):1101-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Cancer Immunology and AIDS, Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15718471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Bone Marrow Cells/cytology/physiology ; Cell Count ; Cell Lineage ; Cell Shape ; Cell Survival ; Cells, Cultured ; Colony-Forming Units Assay ; Gene Deletion ; Gene Expression ; Hematopoietic Stem Cells/cytology/*physiology ; Homeostasis ; Interleukin-6/pharmacology ; Liver/cytology/physiology ; Mice ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins/genetics/*physiology ; Poly I-C/pharmacology ; Polymerase Chain Reaction ; Proto-Oncogene Proteins c-bcl-2/genetics/*physiology ; RNA, Messenger/genetics/metabolism ; Signal Transduction ; Stem Cell Factor/pharmacology ; Transduction, Genetic
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    Astrocytic purinergic signaling coordinates synaptic networks (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-10-08
    Description: To investigate the role of astrocytes in regulating synaptic transmission, we generated inducible transgenic mice that express a dominant-negative SNARE domain selectively in astrocytes to block the release of transmitters from these glial cells. By releasing adenosine triphosphate, which accumulates as adenosine, astrocytes tonically suppressed synaptic transmission, thereby enhancing the dynamic range for long-term potentiation and mediated activity-dependent, heterosynaptic depression. These results indicate that astrocytes are intricately linked in the regulation of synaptic strength and plasticity and provide a pathway for synaptic cross-talk.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pascual, Olivier -- Casper, Kristen B -- Kubera, Cathryn -- Zhang, Jing -- Revilla-Sanchez, Raquel -- Sul, Jai-Yoon -- Takano, Hajime -- Moss, Stephen J -- McCarthy, Ken -- Haydon, Philip G -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):113-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Conte Center for Integration at the Tripartite Synapse, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210541" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/*metabolism ; Adenosine A1 Receptor Antagonists ; Adenosine Triphosphatases/antagonists & inhibitors ; Adenosine Triphosphate/analogs & derivatives/metabolism/pharmacology ; Animals ; Astrocytes/drug effects/*physiology ; Cells, Cultured ; Excitatory Postsynaptic Potentials ; Hippocampus/drug effects/physiology ; In Vitro Techniques ; Long-Term Potentiation/drug effects ; Mice ; Mice, Transgenic ; Neuronal Plasticity/drug effects ; Purinergic P1 Receptor Antagonists ; Purinergic P2 Receptor Antagonists ; Receptor, Adenosine A1/metabolism ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Receptors, Purinergic P1/metabolism ; Receptors, Purinergic P2/metabolism ; Synapses/*physiology ; *Synaptic Transmission/drug effects ; Xanthines/pharmacology
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    Neuroscience. Cancer drugs may help injured nerve cells regrow their axons (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210503" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*pharmacology ; Axons/drug effects/*physiology ; Cells, Cultured ; Erlotinib Hydrochloride ; Mice ; Nerve Crush ; *Nerve Regeneration/drug effects ; Neurons/drug effects/physiology ; Optic Nerve Injuries/drug therapy ; Quinazolines/*pharmacology ; Rats ; Receptor, Epidermal Growth Factor/*antagonists & inhibitors/metabolism ; Signal Transduction/*drug effects ; Spinal Cord Injuries/drug therapy
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    American Chemical Society meeting. Nanofibers seed blood vessels (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, Robert F -- New York, N.Y. -- Science. 2005 Apr 1;308(5718):44-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15802582" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/*growth & development ; Cells, Cultured ; Fibroblast Growth Factors/chemistry/metabolism ; Heparin/chemistry/metabolism ; *Nanostructures ; *Neovascularization, Physiologic ; Peptides/*chemistry/metabolism ; Vascular Endothelial Growth Factor A/chemistry/metabolism
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    Differential lysosomal proteolysis in antigen-presenting cells determines antigen fate (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-03-12
    Description: Antigen-presenting cells (APCs) internalize antigens and present antigen-derived peptides to T cells. Although APCs have been thought to exhibit a well-developed capacity for lysosomal proteolysis, here we found that they can exhibit two distinct strategies upon antigen encounter. Whereas macrophages contained high levels of lysosomal proteases and rapidly degraded internalized proteins, dendritic cells (DCs) and B lymphocytes were protease-poor, resulting in a limited capacity for lysosomal degradation. Consistent with these findings, DCs in vivo degraded internalized antigens slowly and thus retained antigen in lymphoid organs for extended periods. Limited lysosomal proteolysis also favored antigen presentation. These results help explain why DCs are able to efficiently accumulate, process, and disseminate antigens and microbes systemically for purposes of tolerance and immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delamarre, Lelia -- Pack, Margit -- Chang, Henry -- Mellman, Ira -- Trombetta, E Sergio -- R37-AI34098/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 Mar 11;307(5715):1630-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Department of Immunobiology, Ludwig Institute for Cancer Research, Yale University School of Medicine, 333 Cedar Street, Post Office Box 208002, New Haven, CT 06520-8002, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15761154" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigen-Presenting Cells/*enzymology/*immunology/metabolism ; Antigens/*metabolism ; B-Lymphocytes/enzymology/immunology/metabolism ; Cells, Cultured ; Dendritic Cells/*enzymology/immunology/metabolism ; Endocytosis ; Green Fluorescent Proteins/immunology/metabolism ; Histocompatibility Antigens Class II/immunology ; Horseradish Peroxidase/immunology/metabolism ; Lymphoid Tissue/cytology/enzymology/immunology ; Lysosome-Associated Membrane Glycoproteins ; Lysosomes/*enzymology/ultrastructure ; Macrophages/enzymology/immunology/metabolism ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Inbred C3H ; Peptide Hydrolases/*metabolism ; Ribonuclease, Pancreatic/immunology/metabolism ; Ribonucleases/immunology/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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    Direct isolation of satellite cells for skeletal muscle regeneration (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-06
    Description: Muscle satellite cells contribute to muscle regeneration. We have used a Pax3(GFP/+) mouse line to directly isolate (Pax3)(green fluorescent protein)-expressing muscle satellite cells, by flow cytometry from adult skeletal muscles, as a homogeneous population of small, nongranular, Pax7+, CD34+, CD45-, Sca1- cells. The flow cytometry parameters thus established enabled us to isolate satellite cells from wild-type muscles. Such cells, grafted into muscles of mdx nu/nu mice, contributed both to fiber repair and to the muscle satellite cell compartment. Expansion of these cells in culture before engraftment reduced their regenerative capacity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montarras, Didier -- Morgan, Jennifer -- Collins, Charlotte -- Relaix, Frederic -- Zaffran, Stephane -- Cumano, Ana -- Partridge, Terence -- Buckingham, Margaret -- New York, N.Y. -- Science. 2005 Sep 23;309(5743):2064-7. Epub 2005 Sep 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS Unite de Recherche Associee 2578, Department of Developmental Biology, INSERM, Pasteur Institute, 75724 Paris Cedex 15, France. dmontarr@pasteur.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16141372" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/analysis ; *Cell Separation ; Cells, Cultured ; DNA-Binding Proteins/analysis/biosynthesis ; Diaphragm ; Dystrophin/biosynthesis ; Flow Cytometry ; Green Fluorescent Proteins/analysis ; Homeodomain Proteins/analysis/biosynthesis ; Mice ; Mice, Inbred mdx ; Mice, Nude ; Muscle Development ; Muscle Fibers, Skeletal/metabolism ; Muscle, Skeletal/cytology/*physiology ; PAX7 Transcription Factor ; Paired Box Transcription Factors ; *Regeneration ; Satellite Cells, Skeletal Muscle/*cytology/physiology/transplantation ; Stem Cell Transplantation ; Transcription Factors/analysis/biosynthesis
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    Impaired thermosensation in mice lacking TRPV3, a heat and camphor sensor in the skin (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-03-05
    Description: Environmental temperature is thought to be directly sensed by neurons through their projections in the skin. A subset of the mammalian transient receptor potential (TRP) family of ion channels has been implicated in this process. These "thermoTRPs" are activated at distinct temperature thresholds and are typically expressed in sensory neurons. TRPV3 is activated by heat (〉33 degrees C) and, unlike most thermoTRPs, is expressed in mouse keratinocytes. We found that TRPV3 null mice have strong deficits in responses to innocuous and noxious heat but not in other sensory modalities; hence, TRPV3 has a specific role in thermosensation. The natural compound camphor, which modulates sensations of warmth in humans, proved to be a specific activator of TRPV3. Camphor activated cultured primary keratinocytes but not sensory neurons, and this activity was abolished in TRPV3 null mice. Therefore, heat-activated receptors in keratinocytes are important for mammalian thermosensation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moqrich, Aziz -- Hwang, Sun Wook -- Earley, Taryn J -- Petrus, Matt J -- Murray, Amber N -- Spencer, Kathryn S R -- Andahazy, Mary -- Story, Gina M -- Patapoutian, Ardem -- New York, N.Y. -- Science. 2005 Mar 4;307(5714):1468-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15746429" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bradykinin/pharmacology ; CHO Cells ; Camphor/pharmacology ; Cation Transport Proteins/genetics/*physiology ; Cells, Cultured ; Cricetinae ; Dermis/anatomy & histology/innervation/ultrastructure ; Epidermis/anatomy & histology/innervation/ultrastructure ; Ganglia, Spinal/cytology/metabolism ; *Hot Temperature ; Humans ; Ion Channels/genetics/*physiology ; Keratinocytes/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons, Afferent/physiology ; Patch-Clamp Techniques ; TRPV Cation Channels ; Temperature ; Thermoreceptors/*physiology ; *Thermosensing ; Time Factors
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    PUMA couples the nuclear and cytoplasmic proapoptotic function of p53 (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-10
    Description: The Trp53 tumor suppressor gene product (p53) functions in the nucleus to regulate proapoptotic genes, whereas cytoplasmic p53 directly activates proapoptotic Bcl-2 proteins to permeabilize mitochondria and initiate apoptosis. Here, we demonstrate that a tripartite nexus between Bcl-xL, cytoplasmic p53, and PUMA coordinates these distinct p53 functions. After genotoxic stress, Bcl-xL sequestered cytoplasmic p53. Nuclear p53 caused expression of PUMA, which then displaced p53 from Bcl-xL, allowing p53 to induce mitochondrial permeabilization. Mutant Bcl-xL that bound p53, but not PUMA, rendered cells resistant to p53-induced apoptosis irrespective of PUMA expression. Thus, PUMA couples the nuclear and cytoplasmic proapoptotic functions of p53.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chipuk, Jerry E -- Bouchier-Hayes, Lisa -- Kuwana, Tomomi -- Newmeyer, Donald D -- Green, Douglas R -- New York, N.Y. -- Science. 2005 Sep 9;309(5741):1732-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16151013" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Cell Line, Tumor ; Cell Nucleus/*metabolism ; Cells, Cultured ; Cytoplasm/*metabolism ; DNA Damage ; Gene Expression Regulation ; Humans ; Immunoprecipitation ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism ; Models, Biological ; Permeability ; Protein Binding ; Protein Structure, Tertiary ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Recombinant Proteins/metabolism ; Tumor Suppressor Protein p53/*metabolism ; Tumor Suppressor Proteins/chemistry/*metabolism ; Ultraviolet Rays ; bcl-2-Associated X Protein ; bcl-X Protein
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Synapses form in skeletal muscles lacking neuregulin receptors (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-06-25
    Description: The formation of the neuromuscular junction (NMJ) is directed by reciprocal interactions between motor neurons and muscle fibers. Neuregulin (NRG) and Agrin from motor nerve terminals are both implicated. Here, we demonstrate that NMJs can form in the absence of the NRG receptors ErbB2 and ErbB4 in mouse muscle. Postsynaptic differentiation is, however, induced by Agrin. We therefore conclude that NRG signaling to muscle is not required for NMJ formation. The effects of NRG signaling to muscle may be mediated indirectly through Schwann cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Escher, P -- Lacazette, E -- Courtet, M -- Blindenbacher, A -- Landmann, L -- Bezakova, G -- Lloyd, K C -- Mueller, U -- Brenner, H R -- New York, N.Y. -- Science. 2005 Jun 24;308(5730):1920-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Physiology, Biozentrum, University of Basel, 4056 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15976301" target="_blank"〉PubMed〈/a〉
    Keywords: Agrin/physiology ; Animals ; Animals, Newborn ; Cells, Cultured ; Genes, erbB ; Genes, erbB-2 ; Membrane Potentials ; Mice ; Motor Endplate/metabolism/physiology/ultrastructure ; Muscle, Skeletal/*innervation/ultrastructure ; Mutation ; Neuregulins/*metabolism ; Neuromuscular Junction/embryology/metabolism/*physiology/ultrastructure ; Presynaptic Terminals/physiology ; RNA, Messenger/genetics/metabolism ; Receptor, Epidermal Growth Factor/genetics/*physiology ; Receptor, ErbB-2/genetics/*physiology ; Receptor, ErbB-4 ; Receptors, Cholinergic/chemistry/genetics/metabolism ; Recombination, Genetic ; Schwann Cells/physiology ; *Signal Transduction ; Synaptic Transmission
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    Stem cell depletion through epidermal deletion of Rac1 (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-08-06
    Description: Mammalian epidermis is maintained by self-renewal of stem cells, but the underlying mechanisms are unknown. Deletion of Rac1, a Rho guanosine triphosphatase, in adult mouse epidermis stimulated stem cells to divide and undergo terminal differentiation, leading to failure to maintain the interfollicular epidermis, hair follicles, and sebaceous glands. Rac1 exerts its effects in the epidermis by negatively regulating c-Myc through p21-activated kinase 2 (PAK2) phosphorylation. We conclude that a pleiotropic regulator of cell adhesion and the cytoskeleton plays a critical role in controlling exit from the stem cell niche and propose that Rac and Myc represent a global stem cell regulatory axis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benitah, Salvador Aznar -- Frye, Michaela -- Glogauer, Michael -- Watt, Fiona M -- New York, N.Y. -- Science. 2005 Aug 5;309(5736):933-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Keratinocyte Laboratory, Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16081735" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Differentiation/metabolism ; Apoptosis ; Carcinoma, Squamous Cell/metabolism ; Cell Differentiation/*physiology ; Cells, Cultured ; Epidermis/*cytology ; Gene Deletion ; Humans ; Keratinocytes ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neuropeptides/genetics/*physiology ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins c-myc/metabolism ; Skin Neoplasms/metabolism ; Stem Cells/*cytology ; Tamoxifen/*analogs & derivatives ; p21-Activated Kinases ; rac GTP-Binding Proteins/genetics/*physiology ; rac1 GTP-Binding Protein
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    Mammalian SAD kinases are required for neuronal polarization (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-12
    Description: Electrical activity in neurons is generally initiated in dendritic processes then propagated along axons to synapses, where it is passed to other neurons. Major structural features of neurons-their dendrites and axons-are thus related to their fundamental functions: the receipt and transmission of information. The acquisition of these distinct properties by dendrites and axons, called polarization, is a critical step in neuronal differentiation. We show here that SAD-A and SAD-B, mammalian orthologs of a kinase needed for presynaptic differentiation in Caenorhabditis elegans, are required for neuronal polarization. These kinases will provide entry points for unraveling signaling mechanisms that polarize neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kishi, Masashi -- Pan, Y Albert -- Crump, Justin Gage -- Sanes, Joshua R -- New York, N.Y. -- Science. 2005 Feb 11;307(5711):929-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Washington University Medical School, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15705853" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Axons/physiology/ultrastructure ; Brain/*cytology/embryology/metabolism ; Brain Chemistry ; Cell Differentiation ; Cell Line ; *Cell Polarity ; Cell Shape ; Cells, Cultured ; Cerebral Cortex/cytology/embryology/metabolism ; Dendrites/physiology/ultrastructure ; Hippocampus/cytology ; Mice ; Microtubule-Associated Proteins/metabolism ; Mutation ; Neurons/*cytology/*physiology/ultrastructure ; Phosphorylation ; Prosencephalon/cytology/embryology/metabolism ; Protein-Serine-Threonine Kinases/genetics/*physiology ; Spinal Cord/chemistry/embryology ; tau Proteins/metabolism
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    EGFR activation mediates inhibition of axon regeneration by myelin and chondroitin sulfate proteoglycans (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-08
    Description: Inhibitory molecules associated with myelin and the glial scar limit axon regeneration in the adult central nervous system (CNS), but the underlying signaling mechanisms of regeneration inhibition are not fully understood. Here, we show that suppressing the kinase function of the epidermal growth factor receptor (EGFR) blocks the activities of both myelin inhibitors and chondroitin sulfate proteoglycans in inhibiting neurite outgrowth. In addition, regeneration inhibitors trigger the phosphorylation of EGFR in a calcium-dependent manner. Local administration of EGFR inhibitors promotes significant regeneration of injured optic nerve fibers, pointing to a promising therapeutic avenue for enhancing axon regeneration after CNS injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koprivica, Vuk -- Cho, Kin-Sang -- Park, Jong Bae -- Yiu, Glenn -- Atwal, Jasvinder -- Gore, Bryan -- Kim, Jieun A -- Lin, Estelle -- Tessier-Lavigne, Marc -- Chen, Dong Feng -- He, Zhigang -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):106-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/drug effects/*physiology ; Calcium/metabolism ; Cells, Cultured ; Chondroitin Sulfate Proteoglycans/*metabolism ; Enzyme Inhibitors/pharmacology ; Erlotinib Hydrochloride ; GPI-Linked Proteins ; Humans ; Mice ; Myelin Proteins/*metabolism/pharmacology ; Nerve Crush ; *Nerve Regeneration/drug effects ; Neurites/drug effects/physiology ; Optic Nerve/drug effects/physiology ; Optic Nerve Injuries/drug therapy ; Phosphorylation ; Quinazolines/pharmacology ; Receptor, Epidermal Growth Factor/*antagonists & inhibitors/*metabolism ; Receptors, Cell Surface/metabolism ; Retinal Ganglion Cells/drug effects/physiology ; Signal Transduction/drug effects ; Tyrphostins/pharmacology
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    Nucleus accumbens long-term depression and the expression of behavioral sensitization (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-29
    Description: Drug-dependent neural plasticity related to drug addiction and schizophrenia can be modeled in animals as behavioral sensitization, which is induced by repeated noncontingent or self-administration of many drugs of abuse. Molecular mechanisms that are critical for behavioral sensitization have yet to be specified. Long-term depression (LTD) of alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor (AMPAR)-mediated synaptic transmission in the brain has been proposed as a cellular substrate for learning and memory. The expression of LTD in the nucleus accumbens (NAc) required clathrin-dependent endocytosis of postsynaptic AMPARs. NAc LTD was blocked by a dynamin-derived peptide that inhibited clathrin-mediated endocytosis or by a GluR2-derived peptide that blocked regulated AMPAR endocytosis. Systemic or intra-NAc infusion of the membrane-permeable GluR2 peptide prevented the expression of amphetamine-induced behavioral sensitization in the rat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brebner, Karen -- Wong, Tak Pan -- Liu, Lidong -- Liu, Yitao -- Campsall, Paul -- Gray, Sarah -- Phelps, Lindsay -- Phillips, Anthony G -- Wang, Yu Tian -- New York, N.Y. -- Science. 2005 Nov 25;310(5752):1340-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brain Research Centre, University of British Columbia, Vancouver, British Columbia V6T 2B5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16311338" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Addictive ; Behavior, Animal/*drug effects ; Cells, Cultured ; Clathrin/physiology ; Dextroamphetamine/*administration & dosage/pharmacology ; Dynamins/pharmacology ; Endocytosis ; Excitatory Postsynaptic Potentials ; *Long-Term Synaptic Depression/drug effects ; Male ; Membrane Potentials ; Models, Animal ; Motor Activity/*drug effects ; Nucleus Accumbens/drug effects/*physiology ; Patch-Clamp Techniques ; Peptides/pharmacology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/metabolism ; Recombinant Fusion Proteins/pharmacology ; Stereotyped Behavior/*drug effects ; Synaptic Transmission/drug effects ; Ventral Tegmental Area/drug effects/physiology
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    Genetics. Jumping DNA mixes it up in the developing brain (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-06-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2005 Jun 17;308(5729):1729.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15961641" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*cytology/*growth & development ; Cell Differentiation ; Cells, Cultured ; *Gene Expression Regulation ; Humans ; *Long Interspersed Nucleotide Elements ; Mice ; Mice, Transgenic ; Neurons/*cytology/physiology ; Rats ; Stem Cells/*cytology/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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    Nota bene: triplet repeat diseases. Innocent inclusions (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelner, K L -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):643.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9841418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death ; Cells, Cultured ; Huntington Disease/*genetics/pathology ; Inclusion Bodies/*physiology ; Mice ; Neurons/*pathology ; Spinocerebellar Degenerations/*genetics/pathology ; *Trinucleotide Repeats
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    A method in Ebola's madness (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1998 Feb 13;279(5353):983-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9490485" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Ebolavirus/metabolism/*pathogenicity ; Endothelium, Vascular/metabolism/virology ; Genetic Therapy ; Genetic Vectors ; Glycoproteins/*metabolism/secretion ; Hemorrhagic Fever, Ebola/*virology ; Humans ; Membrane Glycoproteins/*metabolism/secretion ; Neutrophils/metabolism ; Retroviridae/physiology ; Viral Matrix Proteins/*metabolism/secretion ; Viral Proteins/*metabolism/secretion
    Print ISSN: 0036-8075
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    Quiescence in nuclear transfer (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilmut, I -- Campbell, K H -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9767023" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle/embryology/*genetics ; Cells, Cultured ; *Cloning, Organism ; Fetus ; Fibroblasts/*cytology ; *G0 Phase ; G1 Phase ; *Nuclear Transfer Techniques
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    Claim of human-cow embryo greeted with skepticism (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1998 Nov 20;282(5393):1390-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9867634" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioethics ; Cattle ; Cell Culture Techniques ; Cells, Cultured ; Dna ; Embryo Research ; Embryo, Mammalian/*cytology ; *Genetic Research ; Humans ; Hybrid Cells/*cytology ; *Nuclear Transfer Techniques ; Stem Cells/*cytology ; *Transplantation, Heterologous
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    Developmental options (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shortman, K -- Maraskovsky, E -- New York, N.Y. -- Science. 1998 Oct 16;282(5388):424-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. van_es@wehi.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9841399" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Cell Movement ; Cells, Cultured ; Cytokines/pharmacology ; Dendritic Cells/cytology/immunology/*physiology ; Endothelium, Vascular/cytology/*physiology ; Humans ; Macrophages/cytology/physiology ; Mice ; Monocytes/cytology/*physiology ; Phagocytosis
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    Can IL-2 smoke out HIV reservoirs? (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉WIlliams, N -- New York, N.Y. -- Science. 1998 Nov 20;282(5393):1394-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9867636" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-HIV Agents/*therapeutic use ; Cells, Cultured ; Controlled Clinical Trials as Topic ; Drug Therapy, Combination ; HIV/drug effects/*physiology ; HIV Infections/*drug therapy/virology ; Humans ; Interleukin-2/*therapeutic use ; T-Lymphocytes/*virology ; Viremia/drug therapy
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    Homeostasis of the antibody response: immunoregulation by NK cells (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-11-11
    Description: When injected into mice, the synthetic double-stranded polynucleotide poly(inosinic) X poly(cytidylic) acid induces high natural killer (NK) cell activity within 4 to 12 hours. Induction of NK activity in mice immunized 2 or 3 days previously, or the addition of NK cells to cultures immunized in vitro 2 or 3 days previously, promotes early termination of the ongoing primary immunoglobulin M antibody response. A target for NK cells is a population of accessory cells that has interacted with antigen and is necessary for sustaining the antibody response. The inference is strong that NK cells induced normally by immunization also terminate the usual antibody response in vivo by elimination of antigen-exposed accessory cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abruzzo, L V -- Rowley, D A -- 5-T32-CA-09267/CA/NCI NIH HHS/ -- R01-10242/PHS HHS/ -- New York, N.Y. -- Science. 1983 Nov 11;222(4624):581-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6685343" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody Formation ; Antibody-Producing Cells/immunology ; Cells, Cultured ; Homeostasis ; Killer Cells, Natural/*immunology/radiation effects ; Lymphocyte Cooperation ; Lymphocytes/*immunology ; Mice ; Poly I-C/immunology ; Spleen/immunology
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    Primary murine bone marrow cultures support continuous growth of infectious human trypanosomes (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-04-22
    Description: The human parasite Trypanosoma brucei gambiense grew continuously at 37 degrees C in primary cultures of murine bone marrow. Cultured parasites remained virulent for mice. Rapid parasite growth coincided with the appearance of adherent adipocyte-epitheloid cell aggregates that also promoted hematopoiesis. This culture system should permit studies of host cell control of trypanosome proliferation, pathogenic effects of trypanosomes on blood cell development, and the relative trypanocidal and marrow suppressive activities of drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balber, A E -- CA 14049/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Apr 22;220(4595):421-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6836284" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Marrow ; Cells, Cultured ; Culture Media ; Humans ; Mice ; Mice, Inbred BALB C ; Trypanosoma brucei brucei/growth & development ; Trypanosoma brucei gambiense/*growth & development ; Trypanosomiasis, African/parasitology
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    Collagen formation by the hepatocyte in primary monolayer culture and in vivo (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-03-18
    Description: Immunohistochemical techniques were used to confirm biochemical evidence that parenchymal cells isolated from adult rat liver and maintained in nonreplicating monolayer culture for 2 days synthesized type IV basement membrane collagen. On continued incubation in serum-free medium, the hepatocytes also synthesized the interstitial collagens, types I and III. Consistent with these results in culture, type IV collagen was localized to the hepatocytes in slices of pathologic rat liver. Hence collagen formation is a previously unrecognized function of the hepatocyte that may be important in the pathogenesis of liver fibrosis or cirrhosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diegelmann, R F -- Guzelian, P S -- Gay, R -- Gay, S -- AM18976/AM/NIADDK NIH HHS/ -- DE02570/DE/NIDCR NIH HHS/ -- HL11310/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 Mar 18;219(4590):1343-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828863" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basement Membrane/metabolism ; Cells, Cultured ; Collagen/*biosynthesis/immunology ; Liver/cytology/*metabolism ; Molecular Weight ; Rats
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    Transformation of Bloom's syndrome fibroblasts by DNA transfection (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-12-09
    Description: Nonmalignant diploid human fibroblast cells (GM3498B) derived from a skin biopsy of a patient with Bloom's syndrome have been transformed by transfection with DNA from a tumorigenic mouse cell line (Ha-8) carrying a single copy of the Harvey murine sarcoma virus (Ha-MuSV) genome. The transformed cell lines have an extended life-span, form colonies in agarose, and proliferate in nude mice--characteristics of neoplastic transformation. Like the parental cells, they also exhibit a high spontaneous level of sister chromatid exchanges. Finally, the transformed cells contain most, if not all, of the Ha-MuSV genome as well as the human rasH sequence. These experiments show that these diploid nonmalignant human cells can be used as recipients in transfection experiments for studying the genetic control of neoplastic transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doniger, J -- Di Paolo, J A -- Popescu, N C -- New York, N.Y. -- Science. 1983 Dec 9;222(4628):1144-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6648529" target="_blank"〉PubMed〈/a〉
    Keywords: Bloom Syndrome/*genetics ; Cell Adhesion ; *Cell Transformation, Neoplastic ; Cells, Cultured ; DNA, Neoplasm/*genetics ; Humans ; Oncogenes ; Transfection
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    Formaldehyde damage to DNA and inhibition of DNA repair in human bronchial cells (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-04-08
    Description: Cultured bronchial epithelial and fibroblastic cells from humans were used to study DNA damage and toxicity caused by formaldehyde. Formaldehyde caused the formation of cross-links between DNA and proteins, caused single-strand breaks in DNA, and inhibited the resealing of single-strand breaks produced by ionizing radiation. Formaldehyde also inhibited the unscheduled DNA synthesis that occurs after exposure of cells to ultraviolet irradiation or to benzo[a]pyrene diolexpoxide but at doses substantially higher than those required to inhibit the resealing of x-ray-induced single-strand breaks. Therefore, formaldehyde could exert its mutagenic and carcinogenic effects by both damaging DNA and inhibiting DNA repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grafstrom, R C -- Fornace, A J Jr -- Autrup, H -- Lechner, J F -- Harris, C C -- New York, N.Y. -- Science. 1983 Apr 8;220(4593):216-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828890" target="_blank"〉PubMed〈/a〉
    Keywords: Bronchi/*cytology/drug effects ; Cells, Cultured ; *DNA/biosynthesis ; DNA Repair/*drug effects ; Epithelium/drug effects ; Fibroblasts/drug effects ; Formaldehyde/*pharmacology ; Humans
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    Neuron-glia adhesion is inhibited by antibodies to neural determinants (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-10-07
    Description: Suspensions of embryonic chick neuronal cells adhered to monolayers of glial cells, but few neurons bound to control monolayers of fibroblastic cells from meninges or skin. Neuronal cell-glial cell adhesion was inhibited by prior incubation of the neurons with Fab' fragments of antibodies to neuronal membranes. In contrast, antibodies to the neural cell adhesion molecule (N-CAM) did not inhibit the binding. These results suggest that a specific adhesive mechanism between neurons and glial cells exists and that it is mediated by CAM's that differ from those so far identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grumet, M -- Rutishauser, U -- Edelman, G M -- AI-11378/AI/NIAID NIH HHS/ -- HD-09635/HD/NICHD NIH HHS/ -- HD-16550/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 Oct 7;222(4619):60-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6194561" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigen-Antibody Complex ; *Cell Adhesion ; Cell Membrane/immunology ; Cells, Cultured ; Chick Embryo ; Epitopes ; Immunoglobulin Fab Fragments ; Neuroglia/*physiology ; Neurons/immunology/*physiology
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    Tumor-derived growth factor increases bone resorption in a tumor associated with humoral hypercalcemia of malignancy (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-09-23
    Description: Evidence is presented that a tumor-derived transforming growth factor is responsible for stimulating bone resorption and causing hypercalcemia in an animal tumor model of the hypercalcemia of malignancy. Both conditioned medium harvested from cultured tumor cells and tumor extracts of the transplantable rat Leydig cell tumor associated with hypercalcemia contained a macromolecular bone resorbing factor with the chemical characteristics of a tumor-derived transforming growth factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ibbotson, K J -- D'Souza, S M -- Ng, K W -- Osborne, C K -- Niall, M -- Martin, T J -- Mundy, G R -- AM-28149/AM/NIADDK NIH HHS/ -- CA-29537/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 23;221(4617):1292-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6577602" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Resorption ; Calcium ; Cells, Cultured ; Culture Media ; Growth Substances/*physiology ; Hypercalcemia/*etiology ; Leydig Cell Tumor/complications/*physiopathology ; Male ; Neoplasm Proteins/*physiology ; Neoplasms, Experimental/complications/physiopathology ; Peptides/*physiology ; Rats ; Transforming Growth Factors
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    Fragile sites in chromosomes: possible model for the study of spontaneous chromosome breakage (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-04-01
    Description: The tissue culture condition that is required for the type of chromosome breakage seen at most fragile sites, namely, the absence of folic acid and thymidine in the medium, greatly enhanced micronucleus formation in proliferating lymphocyte cultures from normal individuals. This suggests that chromosome breakage at fragile sites and the apparently spontaneous damage that gives rise to micronuclei are controlled by the same mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jacky, P B -- Beek, B -- Sutherland, G R -- New York, N.Y. -- Science. 1983 Apr 1;220(4592):69-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828880" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Cell Nucleus/drug effects/ultrastructure ; Cells, Cultured ; Child ; *Chromosome Aberrations ; Chromosome Fragile Sites ; *Chromosome Fragility ; Culture Media ; Dose-Response Relationship, Drug ; Female ; Folic Acid/pharmacology ; Humans ; Lymphocytes/ultrastructure ; Male ; Middle Aged ; Thymidine/pharmacology
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    Oxygen tension regulates the expression of angiogenesis factor by macrophages (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-09-23
    Description: When cultured in a hypoxic environment similar to that found in the center of a wound, macrophages secreted active angiogenesis factor into the medium. Under conditions similar to those of well-oxygenated tissue, macrophages did not secrete active angiogenesis factor. Macrophages that secreted the factor at hypoxic conditions stopped secreting it when returned to room air. Thus the control of angiogenesis in wound healing may be the result of macrophages responding to tissue oxygen tension without the necessity of interacting with other cell types or biochemical signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knighton, D R -- Hunt, T K -- Scheuenstuhl, H -- Halliday, B J -- Werb, Z -- Banda, M J -- GM27345/GM/NIGMS NIH HHS/ -- HL26323/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 23;221(4617):1283-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6612342" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inducing Agents/*biosynthesis ; Animals ; Anoxia/physiopathology ; Cells, Cultured ; Cornea ; Growth Substances/*biosynthesis ; Macrophages/*physiology ; Models, Biological ; Oxygen/*physiology ; Rabbits ; *Wound Healing
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    Drug-induced alterations of cytokeratin organization in cultured epithelial cells (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-02-04
    Description: The distribution of keratin intermediate filaments, previously considered static in organization and imperturbable by conventional drugs used to alter the structure and organization of the cytoskeleton, can be altered significantly by treatment with colchicine and cytochalasin D. The loss of microfilaments and microtubules converts the keratin cytoskeleton from a branching, even distribution to a series of starlike structures whose filaments are maintained by multiple membrane attachment sites. These findings provide a means for manipulating cytokeratin organization to investigate the role of keratins in cytoskeletal structure and function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knapp, L W -- O'Guin, W M -- Sawyer, R H -- New York, N.Y. -- Science. 1983 Feb 4;219(4584):501-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6186022" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Colchicine/*pharmacology ; Cytochalasin D ; Cytochalasins/*pharmacology ; Cytoskeleton/*drug effects ; Epithelium ; *Keratins ; Mice ; Microtubules/drug effects
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    Human endothelial cells: use of heparin in cloning and long-term serial cultivation (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-11-11
    Description: Endothelial cells from human blood vessels were cultured in vitro, with doubling times of 17 to 21 hours for 42 to 79 population doublings. Cloned human endothelial cell strains were established for the first time and had similar proliferative capacities. This vigorous cell growth was achieved by addition of heparin to culture medium containing reduced concentrations of endothelial cell growth factor. The routine cloning and long-term culture of human endothelial cells will facilitate studying the human endothelium in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thornton, S C -- Mueller, S N -- Levine, E M -- AG-00839/AG/NIA NIH HHS/ -- T32-CA-09171/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Nov 11;222(4624):623-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6635659" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division/drug effects ; Cells, Cultured ; Clone Cells/enzymology ; Endothelium/*cytology ; Growth Substances/pharmacology ; Heparin/*pharmacology ; Humans ; Time Factors
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    Interaction with membrane remnants of target myotubes maintains transmitter sensitivity of cultured neurons (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-05-27
    Description: Parasympathetic neurons, when cultured alone, lose sensitivity to acetylcholine, but if striated muscle is included in the culture, neuronal chemosensitivity is maintained. The membrane remnants of myotubes ruptured by osmotic shock also supported the responsiveness of the cultured neurons to transmitter, whereas muscle-conditioned medium or membrane remnants of nonmuscle embryonic skin cells did not support this responsiveness. The regulation of chemosensitivity by contact of neurons with the target cell membrane may be important in the formation and maintenance of neuronal circuitry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tuttle, J B -- NS-10338/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 May 27;220(4600):977-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6133352" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/physiology ; Animals ; Cell Membrane/physiology ; Cells, Cultured ; Chick Embryo ; Fibroblasts/physiology ; Muscles/*physiology ; Nervous System/growth & development ; Neurons/*physiology ; Neurotransmitter Agents/*physiology ; Synapses/physiology
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    High-frequency transfection and cytopathology of the hepatitis B virus core antigen gene in human cells (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-10-28
    Description: A protoplast fusion method was developed to stably transfect human cells with pSV2-derived plasmids at frequencies greater than 10(-3). This procedure made it possible to test the biological effect of a hepatitis B virus (HBV) gene independent of the viral structures required for infection. A pSV2gpt+ plasmid constructed to carry a subgenomic fragment of HBV that contained the core antigen gene (HBc gene) was transfected into human cells. A human epithelial cell line was stably transfected with the HBc+ gene by selecting recipient cells for expression of guanine phosphoribosyl transferase expression. With this gpt+/HBc+ cell line it was shown that growth in serum-free medium or treatment with 5'-azacytidine stimulates the production of the HBV core antigen. A hepatocellular carcinoma carrying the entire HBV genome was stimulated to produce the HBc gene product in response to the same factors that stimulated HBcAg production in the gpt+/HBc+ cell line constructed by transfection. The temporal relation between the cytopathologic response and HBc gene expression was similar for both cell types, indicating a primary role for HBc gene expression in the cytopathology of HBV-infected human liver.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoakum, G H -- Korba, B E -- Lechner, J F -- Tokiwa, T -- Gazdar, A F -- Seeley, T -- Siegel, M -- Leeman, L -- Autrup, H -- Harris, C C -- New York, N.Y. -- Science. 1983 Oct 28;222(4622):385-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6194563" target="_blank"〉PubMed〈/a〉
    Keywords: Azacitidine/pharmacology ; Cell Fusion ; *Cell Transformation, Viral ; Cells, Cultured ; Cytopathogenic Effect, Viral ; Gene Expression Regulation/drug effects ; Genes, Viral ; Hepatitis B Core Antigens/*genetics ; Humans ; Transfection
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    Insulin receptor: evidence that it is a protein kinase (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-01-21
    Description: Highly purified preparations of insulin receptor catalyzed the phosphorylation of the 95,000-dalton subunit of the insulin receptor. This subunit of the insulin receptor was also labeled with [alpha-32P]8-azidoadenosine 5'-triphosphate, a photoaffinity label for adenosine triphosphate binding sites. The identity of the 95,000-dalton band was confirmed in both cases by precipitation with a monoclonal antibody to the insulin receptor. These results suggest that the insulin receptor is itself a protein kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roth, R A -- Cassell, D J -- New York, N.Y. -- Science. 1983 Jan 21;219(4582):299-301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6849137" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Cell Line ; Cells, Cultured ; Lymphocytes ; Molecular Weight ; Phosphoproteins/physiology ; Protein Kinases/*physiology ; Receptor, Insulin/*physiology
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    Recombination during gene transfer into mouse cells can restore the function of deleted genes (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-01-14
    Description: Two plasmids containing nonoverlapping deletions of the herpes simplex virus thymidine kinase gene were introduced into thymidine kinase-deficient mouse L cells by DNA-mediated gene transfer. Thymidine kinase-producing transformants were generated by a mixture of the two plasmids at a frequency significantly greater than that generated by either plasmid alone. Southern blot analyses demonstrated that functional thymidine kinase genes were generated by homologous recombination between the two deletion mutants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Small, J -- Scangos, G -- New York, N.Y. -- Science. 1983 Jan 14;219(4581):174-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6294829" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cells, Cultured ; Chromosome Deletion ; *Genetic Engineering ; Mice ; Mutation ; *Plasmids ; *Recombination, Genetic ; Simplexvirus ; Thymidine Kinase/*genetics
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  • 82
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    Human macrophages armed with murine immunoglobulin G2a antibodies to tumors destroy human cancer cells (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-08-26
    Description: Macrophages isolated from tumor-bearing patients as well as cultured human monocytes express Fc receptors that cross-react strongly with murine immunoglobulins of the G2a but only slightly or not at all with the G1, G2b, or G3 subclasses. Such macrophages in the presence of murine immunoglobulin G2a monoclonal antibodies to tumors mediated the killing of tumor cells in vitro. These data suggest that monoclonal antibodies of the G2a subclass may be useful in the immunotherapy of human cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steplewski, Z -- Lubeck, M D -- Koprowski, H -- CA-10815/CA/NCI NIH HHS/ -- CA-21124/CA/NCI NIH HHS/ -- CA-25874/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 Aug 26;221(4613):865-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6879183" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*immunology ; Cells, Cultured ; Cytotoxicity, Immunologic ; Humans ; *Immunity, Cellular ; Immunoglobulin G/immunology ; Immunotherapy ; Macrophages/*immunology ; Mice ; Monocytes/immunology ; Neoplasms, Experimental/immunology/therapy ; Receptors, Fc/*immunology ; Species Specificity
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 83
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    Hepatitis B virus infection in cultured human lymphoblastoid cells (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-08-12
    Description: Since it has been postulated that liver hepatocytes may become infected by hepatitis B virus (HBV) in vivo through direct contact with infected macrophages, the possibility that a circulating cell of hematopoietic origin might be susceptible to infection with HBV was investigated. Cells positive for HBV surface antigen were identified in aspirates of bone marrow cells from people infected with HBV. These cells were used to prepare a lymphoblastoid suspension culture that contains HBV-infected cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Romet-Lemonne, J L -- McLane, M F -- Elfassi, E -- Haseltine, W A -- Azocar, J -- Essex, M -- New York, N.Y. -- Science. 1983 Aug 12;221(4611):667-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6867736" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Hepatitis B/*microbiology/pathology ; Hepatitis B Surface Antigens/immunology ; Hepatitis B virus/growth & development ; Humans ; Liver/pathology ; Lymphocytes/*microbiology/pathology ; Male ; Middle Aged
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  • 84
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    Synaptic activity mediates death of hypoxic neurons (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-04-29
    Description: Cultured hippocampal neurons, when exposed to cyanide or an anoxic atmosphere in the early stages of differentiation, were not visibly affected. However, neurons in the mature cultures died when exposed to cyanide or anoxia. Cell death could be prevented by treatment with magnesium, which eliminates synaptic activity. These observations suggest that damage in hypoxic neurons is mediated by synaptic activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rothman, S M -- 5 K07 N500568-02/PHS HHS/ -- New York, N.Y. -- Science. 1983 Apr 29;220(4596):536-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6836300" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Anoxia/*metabolism/physiopathology ; Cells, Cultured ; Hippocampus/cytology ; Magnesium/pharmacology ; Magnesium Chloride ; Membrane Potentials/drug effects ; Neurons/metabolism/*physiology ; Rats ; Sodium Cyanide/pharmacology ; Synapses/drug effects/*physiology
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  • 85
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    Infection of normal human epithelial cells by Epstein-Barr virus (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-03-11
    Description: Primary cultures of epithelial cells were grown from the tonsils and adenoids of patients with diseases not related to Epstein-Barr virus. The cells could not be infected by Epstein-Barr virus. Fluorescein-labeled Epstein-Barr virus and a cytofluorograph were then used to show that the epithelial cells do not have detectable receptors for the virus. However, implantation with Epstein-Barr virus receptors gave the cells the ability to bind the labeled virus. One to 5 percent of receptor-implanted cells exposed to the transforming B95-8 substrain of the virus expressed Epstein-Barr nuclear antigen. The early and viral capsid Epstein-Barr virus-determined antigens were not detected in the virus-infected cultures. The results show that normal human epithelial cells from the nasopharynx become susceptible to infection by Epstein-Barr virus when the membrane barrier resulting from the lack of viral receptors is overcome by receptor implantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shapiro, I M -- Volsky, D J -- 1R01 CA33386-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Mar 11;219(4589):1225-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6298935" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Epithelium/*microbiology ; Herpesviridae Infections/*microbiology ; Herpesvirus 4, Human/growth & development ; Humans ; Receptors, Virus/metabolism ; Virus Replication
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  • 86
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    Axonal proteins of presynaptic neurons during synaptogenesis (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-09-23
    Description: Changes occur in the synthesis and axonal transport of neuronal proteins in dorsal-root ganglia axons as a result of contact with cells from the spinal cord during synapse formation. Dorsal-root ganglia cells were cultured in a compartmental cel culture system that allows separate access to neuronal cell bodies and their axons. When cells from the ventral spinal cord were cultured with the dorsal-root ganglia axons, synapses were established within a few days. Metabolic labeling and two-dimensional electrophoresis revealed that four of more than 300 axonal proteins had changed in their expression by the time synapses were established. The highly selective nature of these changes suggests that the proteins involved may be important in the processes of axon growth and synapse formation and their regulation by the regional environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sonderegger, P -- Fishman, M C -- Bokoum, M -- Bauer, H C -- Nelson, P G -- New York, N.Y. -- Science. 1983 Sep 23;221(4617):1294-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6612344" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*metabolism ; Cells, Cultured ; Chick Embryo ; Isoelectric Point ; Molecular Weight ; Nerve Tissue Proteins/*biosynthesis ; Synapses/*metabolism
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  • 87
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    Latrunculins: novel marine toxins that disrupt microfilament organization in cultured cells (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-02-04
    Description: Two toxins, latrunculins A and B, which contain a new class of 16- and 14-membered marine macrolides attached to the rare 2-thiazolidinone moiety, were purified recently from the Red Sea sponge Latrunculia magnifica. The effects of these toxins on cultured mouse neuroblastoma and fibroblast cells have been evaluated. In both types of cells, submicromolar toxin concentrations rapidly induce striking changes in cell morphology that are reversible upon removal of the toxin. Immunofluorescence studies with antibodies specific for cytoskeletal proteins reveal that the toxins cause major alterations in the organization of microfilaments without obvious effects on the organization of the microtubular system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spector, I -- Shochet, N R -- Kashman, Y -- Groweiss, A -- New York, N.Y. -- Science. 1983 Feb 4;219(4584):493-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6681676" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; *Bicyclo Compounds, Heterocyclic ; Cells, Cultured ; Cytoskeleton/*drug effects ; Fibroblasts/ultrastructure ; Marine Toxins/*pharmacology ; Microscopy, Fluorescence ; Microtubules/drug effects ; Neuroblastoma/ultrastructure ; Thiazoles/*pharmacology ; Thiazolidines
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  • 88
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    Glucose stimulation of the antilipolytic effect of insulin in humans (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-06-03
    Description: Dose-response studies of the inhibition of lipolysis by insulin in isolated human adipocytes were conducted with the use of a sensitive bioluminescent assay of glycerol release. The addition of glucose to the incubation medium was associated with an increase in insulin sensitivity and an increase in the maximum insulin effect. The results suggest that glucose plays an important role in regulating the antilipolytic action of insulin in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arner, P -- Bolinder, J -- Ostman, J -- New York, N.Y. -- Science. 1983 Jun 3;220(4601):1057-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6342138" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/cytology ; Cells, Cultured ; Dose-Response Relationship, Drug ; Drug Synergism ; Glucose/*pharmacology ; Humans ; Insulin/*pharmacology ; Isoproterenol/pharmacology ; Lipolysis/*drug effects
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  • 89
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    Fluoride directly stimulates proliferation and alkaline phosphatase activity of bone-forming cells (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-10-21
    Description: Fluoride is one of the most potent but least well understood stimulators of bone formation in vivo. Bone formation was shown to arise from direct effects on bone cells. Treatment with sodium fluoride increased proliferation and alkaline phosphatase activity of bone cells in vitro and increased bone formation in embryonic calvaria at concentrations that stimulate bone formation in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farley, J R -- Wergedal, J E -- Baylink, D J -- AM31061/AM/NIADDK NIH HHS/ -- AM31062/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1983 Oct 21;222(4621):330-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6623079" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaline Phosphatase/*metabolism ; Animals ; Bone Development/*drug effects ; Bone and Bones/*cytology/embryology/enzymology ; Cell Division/drug effects ; Cells, Cultured ; Chick Embryo ; Dose-Response Relationship, Drug ; Fluorides/*pharmacology ; Parathyroid Hormone/pharmacology
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  • 90
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    Cell growth on liquid microcarriers (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-03-25
    Description: Anchorage-dependent cell growth is demonstrated on microcarriers of fluorocarbon fluid formed by emulsification and stabilized with polylysine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keese, C R -- Giaever, I -- New York, N.Y. -- Science. 1983 Mar 25;219(4591):1448-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828872" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion ; Cell Division ; *Cell Physiological Phenomena ; Cells, Cultured ; Culture Media ; Emulsions ; Fluorocarbons ; Kinetics
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  • 91
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    Substance P and somatostatin regulate sympathetic noradrenergic function (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-09-09
    Description: Peptidergic-noradrenergic interactions were examined in explants of rat sympathetic superior cervical ganglia and in cultures of dissociated cells. The putative peptide transmitters substance P and somatostatin each increased the activity of the catecholamine-synthesizing enzyme tyrosine hydroxylase after 1 week of exposure in culture. Maximal increases occurred at 10(-7) molar for each peptide, and either increasing or decreasing the concentration reduced the effects. Similar increases in tyrosine hydroxylase were produced by a metabolically stable agonist of substance P, while a substance P antagonist prevented the effects of the agonist. The data suggest that the increased tyrosine hydroxylase activity was mediated by peptide interaction with specific substance P receptors and that peptides may modulate sympathetic catecholaminergic function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kessler, J A -- Adler, J E -- Black, I B -- New York, N.Y. -- Science. 1983 Sep 9;221(4615):1059-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6192502" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacitracin/pharmacology ; Captopril/pharmacology ; Cells, Cultured ; Culture Techniques ; Dose-Response Relationship, Drug ; Ganglia, Sympathetic/*enzymology ; Rats ; Somatostatin/*pharmacology ; Substance P/*pharmacology ; Tyrosine 3-Monooxygenase/*metabolism
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  • 92
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    Action potentials in macrophages derived from human monocytes (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-02-25
    Description: The electrical activity of macrophages derived from human blood monocytes was recorded in vitro with intracellular microelectrodes and was analyzed with computer-assisted data acquisition and analysis techniques. In cells impaled 6 to 8 days after the cultures were prepared, the resting potentials reached a maximum value of -72 millivolts. The cells were electrically excitable; spikes exhibited a slow upstroke, a fast downstroke, a discrete threshold, a large overshoot, and a brief undershoot. Repetitive firing was induced by a maintained depolarizing current. A positive relation was observed between transmembrane currents and resting potential. Voltage-current relations were nonrectifying for subthreshold current injections. Since these cells had not been treated with any specific activation factors, the electrical activity recorded is evidence for the presence of voltage-dependent inward and outward currents in the membranes of mature macrophages. The electrical signals generated by these cells may be useful for the assay of sensor and effector functions of macrophages, such as chemotaxis, receptor-ligand interactions, and phagocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCann, F V -- Cole, J J -- Guyre, P M -- Russell, J A -- AM0535/AM/NIADDK NIH HHS/ -- BRSG05392/RS/DRS NIH HHS/ -- CA17323/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Feb 25;219(4587):991-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6823563" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Cell Differentiation ; Cells, Cultured ; Humans ; Macrophages/*physiology ; Monocytes/cytology
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  • 93
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    Cooperation between oncogenes. Investigators focus on cooperation between two or more oncogenes to help explain the multistep development of human cancers (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1983 Nov 11;222(4624):602-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6635658" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cells, Cultured ; Mice ; *Oncogenes ; Platelet-Derived Growth Factor/*genetics
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  • 94
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    RNA splice site selection: evidence for a 5' leads to 3' scanning model (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-06-24
    Description: Human G gamma-globin genes containing tandem duplications of the donor (5') or acceptor (3') RNA splice sites of the second intervening sequence were constructed in order to ascertain the directionality of RNA splice site selection. These genes were introduced into cultured monkey cells, and their transcripts were analyzed. Transcripts of these duplication variants were spliced only at the proximal copy of the duplicated splice sites. These data are consistent with a 5' leads to 3' model of splice site selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lang, K M -- Spritz, R A -- AM28598/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1983 Jun 24;220(4604):1351-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6304877" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cells, Cultured ; Globins/genetics ; Haplorhini ; Humans ; Plasmids ; *RNA Splicing ; RNA, Messenger/genetics/physiology ; Simian virus 40/genetics ; Transcription, Genetic
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  • 95
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    Vasoactive intestinal peptide alters membrane potential and cyclic nucleotide levels in retinal horizontal cells (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-09-09
    Description: Vasoactive intestinal peptide stimulated the synthesis of adenosine 3',5'-monophosphate in fractions of isolated carp horizontal cells. When applied extracellularly to isolated and cultured horizontal cells, the peptide also induced a slow depolarization (30 to 40 millivolts) accompanied by a decrease in membrane resistance. However, analogs of adenosine 3',5'-monophosphate applied extracellularly or intracellularly, and forscolin applied extracellularly, had no effect on the membrane potential of cultured horizontal cells, indicating that the induced depolarization was not related to the accumulation of adenosine 3',5'-monophosphate in these cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lasater, E M -- Watling, K J -- Dowling, J E -- EY-00811/EY/NEI NIH HHS/ -- EY-00824/EY/NEI NIH HHS/ -- EY-05476/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 9;221(4615):1070-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6308770" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carps ; Cells, Cultured ; Cyclic AMP/*metabolism ; Dopamine/pharmacology ; Gastrointestinal Hormones/*pharmacology ; Kainic Acid/pharmacology ; Membrane Potentials/*drug effects ; Retina/*drug effects/physiology ; Vasoactive Intestinal Peptide/*pharmacology
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  • 96
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    Evidence for the recessive nature of cellular immortality (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-09-02
    Description: Fusion of immortal cell lines with normal human fibroblasts or certain other immortal cell lines yields hybrids having limited division potential. Cellular immortality was found to be a recessive phenotype in hybrids. It was also found that at least two separate events in the normal cell genome can result in immortality. In fusions involving certain immortal parent cells, these events can be complemented to result in hybrids with finite division capacity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pereira-Smith, O M -- Smith, J R -- AG 03262/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 2;221(4614):964-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6879195" target="_blank"〉PubMed〈/a〉
    Keywords: *Cell Division ; Cell Line ; *Cell Survival ; Cells, Cultured ; Genes, Recessive ; Humans ; Hybrid Cells/*physiology ; Phenotype
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  • 97
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    Activation of 2-aminofluorene by cultured plant cells (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-03-25
    Description: Cultured tobacco plant cells activated 2-aminofluorene to an agent mutagenic to Salmonella typhimurium strain TA98. The plant activation of 2-aminofluorene is heat-inactivated and may not involve solely cytochrome P-450. The kinetics of activation demonstrated both time- and concentration-dependent responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Plewa, M J -- Weaver, D L -- Blair, L C -- Gentile, J M -- ES02384/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1983 Mar 25;219(4591):1427-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6338591" target="_blank"〉PubMed〈/a〉
    Keywords: Biotransformation ; Cells, Cultured ; Fluorenes/*metabolism/pharmacology ; Kinetics ; Mutagenicity Tests ; Mutagens/*metabolism ; *Mutation ; *Plants, Toxic ; Salmonella typhimurium/drug effects ; Tobacco/*metabolism
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  • 98
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    Isolation and transmission of human retrovirus (human t-cell leukemia virus) (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-02-18
    Description: Nine new isolates of human T-cell leukemia-lymphoma virus (HTLV) were obtained from cells of seven patients with malignancies of mature T cells and from two clinically normal relatives of a T-cell leukemia patient. These people were from the United States, Israel, the West Indies, and Japan. The virus was detected in the fresh T cells and was isolated from the established T-cell lines. Each isolate is closely related to the first HTLV isolate, and all the new HTLV isolates were transmitted into normal human T cells obtained from the umbilical cord blood of newborns.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Popovic, M -- Sarin, P S -- Robert-Gurroff, M -- Kalyanaraman, V S -- Mann, D -- Minowada, J -- Gallo, R C -- New York, N.Y. -- Science. 1983 Feb 18;219(4586):856-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6600519" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cells, Cultured ; Female ; Humans ; Leukemia/*microbiology ; Male ; Retroviridae/growth & development/*isolation & purification ; T-Lymphocytes/*microbiology
    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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  • 99
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    Mobilization of cellular calcium-45 and lead-210: effect of physiological stimuli (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-04-15
    Description: Isolated rat hepatocytes in primary culture were used as a model system to evaluate the effects of selected hormones and culture conditions on the efflux of calcium-45 and lead-210 from cells labeled with these isotopes. Alpha-adrenergic stimuli, angiotensin, vasopressin, dibutyryl adenosine 3',5'-monophosphate, and reduced phosphate concentrations in the medium increased the efflux of calcium-45 and lead-210. Glucagon and insulin had no effect, but increased phosphate concentrations decreased the efflux of both isotopes. Experiments with hepatocytes cultured in a medium free of calcium and lead demonstrated that the increased efflux of calcium-45 and lead-210 induced by hormones was the result of mobilization of the ions from intracellular stores. The data indicate that the physiological stimuli that mobilized calcium ions also mobilized lead ions, and that the mobilized lead would be available to interact with calcium-mediated cell functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pounds, J G -- Mittelstaedt, R A -- New York, N.Y. -- Science. 1983 Apr 15;220(4594):308-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6301003" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/pharmacology ; Animals ; Bucladesine/pharmacology ; Calcium Radioisotopes/*metabolism ; Cells, Cultured ; Epinephrine/pharmacology ; Insulin/pharmacology ; Lead/*metabolism ; Liver/cytology ; Phosphates/pharmacology ; Propranolol/pharmacology ; Radioisotopes ; Rats ; Vasopressins/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 100
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    Irreversible ligands with high selectivity toward delta and mu opiate receptors (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-04-15
    Description: Alkylating agents that display strong selectivity for opiate receptor types delta or mu were prepared by appropriate modification of the structures of the strong analgesics fentanyl, etonitazene, and endoethenotetrahydrooripavine. The availability of these substances should facilitate studies of the structural basis of receptor specificity and of the physiologic roles of these receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rice, K C -- Jacobson, A E -- Burke, T R Jr -- Bajwa, B S -- Streaty, R A -- Klee, W A -- New York, N.Y. -- Science. 1983 Apr 15;220(4594):314-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6132444" target="_blank"〉PubMed〈/a〉
    Keywords: Alkylation ; Animals ; Benzimidazoles/analogs & derivatives/metabolism ; Brain/physiology ; Cells, Cultured ; Chemical Phenomena ; Chemistry ; Enkephalin, Methionine/analogs & derivatives/metabolism ; Fentanyl/analogs & derivatives/metabolism ; *Isothiocyanates ; Ligands ; Rats ; Receptors, Opioid/*metabolism/physiology ; Thebaine/analogs & derivatives/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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