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  • 1
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    Requirement for type 2 NO synthase for IL-12 signaling in innate immunity (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-13
    Description: Interleukin-12 (IL-12) and type 2 NO synthase (NOS2) are crucial for defense against bacterial and parasitic pathogens, but their relationship in innate immunity is unknown. In the absence of NOS2 activity, IL-12 was unable to prevent spreading of Leishmania parasites, did not stimulate natural killer (NK) cells for cytotoxicity or interferon-gamma (IFN-gamma) release, and failed to activate Tyk2 kinase and to tyrosine phosphorylate Stat4 (the central signal transducer of IL-12) in NK cells. Activation of Tyk2 in NK cells by IFN-alpha/beta also required NOS2. Thus, NOS2-derived NO is a prerequisite for cytokine signaling and function in innate immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diefenbach, A -- Schindler, H -- Rollinghoff, M -- Yokoyama, W M -- Bogdan, C -- New York, N.Y. -- Science. 1999 May 7;284(5416):951-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Klinische Mikrobiologie, Immunologie und Hygiene, Universitat Erlangen, Wasserturmstrasse 3, D-91054 Erlangen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10320373" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cyclic GMP/metabolism ; Cytotoxicity, Immunologic ; DNA-Binding Proteins/metabolism ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Immunity, Innate ; Interferon-gamma/biosynthesis/genetics ; Interferons/pharmacology ; Interleukin-12/pharmacology/*physiology ; Janus Kinase 2 ; Killer Cells, Natural/*immunology/metabolism ; *Leishmania major ; Leishmaniasis, Cutaneous/*immunology/metabolism ; Lysine/analogs & derivatives/pharmacology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/antagonists & inhibitors/*metabolism ; Nitric Oxide Synthase Type II ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Proteins/metabolism ; *Proto-Oncogene Proteins ; STAT4 Transcription Factor ; *Signal Transduction ; TYK2 Kinase ; Trans-Activators/metabolism ; Up-Regulation
    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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    Vital involvement of a natural killer cell activation receptor in resistance to viral infection (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-05-08
    Description: Natural killer (NK) cells are lymphocytes that can be distinguished from T and B cells through their involvement in innate immunity and their lack of rearranged antigen receptors. Although NK cells and their receptors were initially characterized in terms of tumor killing in vitro, we have determined that the NK cell activation receptor, Ly-49H, is critically involved in resistance to murine cytomegalovirus in vivo. Ly-49H requires an immunoreceptor tyrosine-based activation motif (ITAM)-containing transmembrane molecule for expression and signal transduction. Thus, NK cells use receptors functionally resembling ITAM-coupled T and B cell antigen receptors to provide vital innate host defense.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, M G -- Dokun, A O -- Heusel, J W -- Smith, H R -- Beckman, D L -- Blattenberger, E A -- Dubbelde, C E -- Stone, L R -- Scalzo, A A -- Yokoyama, W M -- New York, N.Y. -- Science. 2001 May 4;292(5518):934-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Rheumatology Division, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11340207" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; *Antigens, Ly ; Crosses, Genetic ; Cytotoxicity, Immunologic ; Female ; Haplotypes ; Herpesviridae Infections/*immunology ; Histocompatibility Antigens Class I/immunology ; Humans ; *Immunity, Innate ; Killer Cells, Natural/*immunology ; Lectins, C-Type ; Ligands ; *Lymphocyte Activation ; Male ; Membrane Glycoproteins/genetics/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Muromegalovirus/*immunology ; Phenotype ; Receptors, Immunologic/*immunology ; Receptors, NK Cell Lectin-Like ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Embryological evidence identifies wing digits in birds as digits 1, 2, and 3 (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-12
    Description: The identities of the digits of the avian forelimb are disputed. Whereas paleontological findings support the position that the digits correspond to digits one, two, and three, embryological evidence points to digit two, three, and four identities. By using transplantation and cell-labeling experiments, we found that the posteriormost digit in the wing does not correspond to digit four in the hindlimb; its progenitor segregates early from the zone of polarizing activity, placing it in the domain of digit three specification. We suggest that an avian-specific shift uncouples the digit anlagen from the molecular mechanisms that pattern them, resulting in the imposition of digit one, two, and three identities on the second, third, and fourth anlagens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tamura, Koji -- Nomura, Naoki -- Seki, Ryohei -- Yonei-Tamura, Sayuri -- Yokoyama, Hitoshi -- New York, N.Y. -- Science. 2011 Feb 11;331(6018):753-7. doi: 10.1126/science.1198229.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology and Neurosciences, Graduate School of Life Sciences, Tohoku University, Aobayama, Aoba-ku, Sendai 980-8578, Japan. tam@m.tohoku.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21311019" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Chick Embryo/*embryology ; Coturnix/*embryology ; Forelimb/embryology/transplantation ; Hedgehog Proteins/metabolism ; Hindlimb/embryology/transplantation ; Limb Buds/embryology ; Mice ; Signal Transduction ; Toes/embryology ; Wings, Animal/*embryology
    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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    A small-molecule AdipoR agonist for type 2 diabetes and short life in obesity (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-11-01
    Description: Adiponectin secreted from adipocytes binds to adiponectin receptors AdipoR1 and AdipoR2, and exerts antidiabetic effects via activation of AMPK and PPAR-alpha pathways, respectively. Levels of adiponectin in plasma are reduced in obesity, which causes insulin resistance and type 2 diabetes. Thus, orally active small molecules that bind to and activate AdipoR1 and AdipoR2 could ameliorate obesity-related diseases such as type 2 diabetes. Here we report the identification of orally active synthetic small-molecule AdipoR agonists. One of these compounds, AdipoR agonist (AdipoRon), bound to both AdipoR1 and AdipoR2 in vitro. AdipoRon showed very similar effects to adiponectin in muscle and liver, such as activation of AMPK and PPAR-alpha pathways, and ameliorated insulin resistance and glucose intolerance in mice fed a high-fat diet, which was completely obliterated in AdipoR1 and AdipoR2 double-knockout mice. Moreover, AdipoRon ameliorated diabetes of genetically obese rodent model db/db mice, and prolonged the shortened lifespan of db/db mice on a high-fat diet. Thus, orally active AdipoR agonists such as AdipoRon are a promising therapeutic approach for the treatment of obesity-related diseases such as type 2 diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okada-Iwabu, Miki -- Yamauchi, Toshimasa -- Iwabu, Masato -- Honma, Teruki -- Hamagami, Ken-ichi -- Matsuda, Koichi -- Yamaguchi, Mamiko -- Tanabe, Hiroaki -- Kimura-Someya, Tomomi -- Shirouzu, Mikako -- Ogata, Hitomi -- Tokuyama, Kumpei -- Ueki, Kohjiro -- Nagano, Tetsuo -- Tanaka, Akiko -- Yokoyama, Shigeyuki -- Kadowaki, Takashi -- England -- Nature. 2013 Nov 28;503(7477):493-9. doi: 10.1038/nature12656. Epub 2013 Oct 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan [2] Department of Integrated Molecular Science on Metabolic Diseases, 22nd Century Medical and Research Center, The University of Tokyo, Tokyo 113-0033, Japan [3] Department of Molecular Medicinal Sciences on Metabolic Regulation, 22nd Century Medical and Research Center, The University of Tokyo, Tokyo 113-0033, Japan [4].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24172895" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylate Kinase/metabolism ; Adiponectin/metabolism/pharmacology ; Adipose Tissue, White/drug effects/metabolism/pathology ; Administration, Oral ; Animals ; Diabetes Mellitus, Type 2/complications/*drug therapy/metabolism/prevention & ; control ; Diet, High-Fat ; Drug Evaluation, Preclinical ; Dyslipidemias/drug therapy ; Enzyme Activation/drug effects ; Glucose Intolerance/drug therapy ; Inflammation/drug therapy ; Insulin Resistance ; Liver/drug effects/metabolism/pathology ; Longevity/*drug effects ; Mice ; Mitochondria/drug effects/metabolism ; Muscle Fibers, Skeletal/cytology/drug effects ; Muscles/cytology ; Obesity/complications/drug therapy/genetics/*physiopathology ; Oxidative Stress/drug effects ; PPAR alpha/metabolism ; Piperidines/administration & dosage/metabolism/*pharmacology/therapeutic use ; Receptors, Adiponectin/*agonists/deficiency/genetics/metabolism ; Signal Transduction/drug effects ; Small Molecule Libraries/chemistry ; Transcription Factors/biosynthesis ; Triglycerides/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Reversal of left-right asymmetry: a situs inversus mutation (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-30
    Description: A recessive mutation was identified in a family of transgenic mice that resulted in a reversal of left-right polarity (situs inversus) in 100 percent of the homozygous transgenic mice tested. Sequences that flanked the transgenic integration site were cloned and mapped to mouse chromosome 4, between the Tsha and Hxb loci. During early embryonic development, the direction of postimplantation turning, one of the earliest manifestations of left-right asymmetry, was reversed in homozygous transgenic embryos. This insertional mutation identifies a gene that controls embryonic turning and visceral left-right polarity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yokoyama, T -- Copeland, N G -- Jenkins, N A -- Montgomery, C A -- Elder, F F -- Overbeek, P A -- HD25340/HD/NICHD NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):679-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8480178" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Chromosome Mapping ; Cloning, Molecular ; Embryonic and Fetal Development/*genetics ; Female ; *Genes, Recessive ; Homozygote ; Male ; Mice ; Mice, Transgenic ; Mutagenesis, Insertional ; Situs Inversus/*genetics
    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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  • 6
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    Altered growth of human colon cancer cell lines disrupted at activated Ki-ras (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-02
    Description: Point mutations that activate the Ki-ras proto-oncogene are presented in about 50 percent of human colorectal tumors. To study the functional significance of these mutations, the activated Ki-ras genes in two human colon carcinoma cell lines, DLD-1 and HCT 116, were disrupted by homologous recombination. Compared with parental cells, cells disrupted at the activated Ki-ras gene were morphologically altered, lost the capacity for anchorage-independent growth, grew more slowly both in vitro and in nude mice, and showed reduced expression of c-myc. Thus, the activated Ki-ras gene plays a key role in colorectal tumorigenesis through altered cell differentiation and cell growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shirasawa, S -- Furuse, M -- Yokoyama, N -- Sasazuki, T -- New York, N.Y. -- Science. 1993 Apr 2;260(5104):85-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Kyushu University, Fukuoka, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8465203" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Differentiation ; Cell Division ; Codon ; Colonic Neoplasms/*genetics/pathology ; Gene Expression Regulation, Neoplastic ; Genes, myc/genetics ; Genes, ras/*genetics ; Humans ; Infant ; Mice ; Mice, Nude ; Molecular Sequence Data ; Mutagenesis, Insertional ; Nucleic Acid Hybridization ; Plasmids ; *Point Mutation ; Polymerase Chain Reaction ; Restriction Mapping ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Pan-viral specificity of IFN-induced genes reveals new roles for cGAS in innate immunity (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-11-29
    Description: The type I interferon (IFN) response protects cells from viral infection by inducing hundreds of interferon-stimulated genes (ISGs), some of which encode direct antiviral effectors. Recent screening studies have begun to catalogue ISGs with antiviral activity against several RNA and DNA viruses. However, antiviral ISG specificity across multiple distinct classes of viruses remains largely unexplored. Here we used an ectopic expression assay to screen a library of more than 350 human ISGs for effects on 14 viruses representing 7 families and 11 genera. We show that 47 genes inhibit one or more viruses, and 25 genes enhance virus infectivity. Comparative analysis reveals that the screened ISGs target positive-sense single-stranded RNA viruses more effectively than negative-sense single-stranded RNA viruses. Gene clustering highlights the cytosolic DNA sensor cyclic GMP-AMP synthase (cGAS, also known as MB21D1) as a gene whose expression also broadly inhibits several RNA viruses. In vitro, lentiviral delivery of enzymatically active cGAS triggers a STING-dependent, IRF3-mediated antiviral program that functions independently of canonical IFN/STAT1 signalling. In vivo, genetic ablation of murine cGAS reveals its requirement in the antiviral response to two DNA viruses, and an unappreciated contribution to the innate control of an RNA virus. These studies uncover new paradigms for the preferential specificity of IFN-mediated antiviral pathways spanning several virus families.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4077721/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4077721/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schoggins, John W -- MacDuff, Donna A -- Imanaka, Naoko -- Gainey, Maria D -- Shrestha, Bimmi -- Eitson, Jennifer L -- Mar, Katrina B -- Richardson, R Blake -- Ratushny, Alexander V -- Litvak, Vladimir -- Dabelic, Rea -- Manicassamy, Balaji -- Aitchison, John D -- Aderem, Alan -- Elliott, Richard M -- Garcia-Sastre, Adolfo -- Racaniello, Vincent -- Snijder, Eric J -- Yokoyama, Wayne M -- Diamond, Michael S -- Virgin, Herbert W -- Rice, Charles M -- 099220/Wellcome Trust/United Kingdom -- AI057158/AI/NIAID NIH HHS/ -- AI057160/AI/NIAID NIH HHS/ -- AI083025/AI/NIAID NIH HHS/ -- AI091707/AI/NIAID NIH HHS/ -- AI095611/AI/NIAID NIH HHS/ -- AI104972/AI/NIAID NIH HHS/ -- DK095031/DK/NIDDK NIH HHS/ -- G0801822/Medical Research Council/United Kingdom -- GM076547/GM/NIGMS NIH HHS/ -- GM103511/GM/NIGMS NIH HHS/ -- HHSN266200700010C/PHS HHS/ -- HHSN272200900041CU19/CU/CSP VA/ -- K01 DK095031/DK/NIDDK NIH HHS/ -- R00 AI095320/AI/NIAID NIH HHS/ -- R01 AI032972/AI/NIAID NIH HHS/ -- R01 AI091707/AI/NIAID NIH HHS/ -- R01 AI102597/AI/NIAID NIH HHS/ -- R01 AI104972/AI/NIAID NIH HHS/ -- T32 AI005284/AI/NIAID NIH HHS/ -- T32 AR007279/AR/NIAMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Jan 30;505(7485):691-5. doi: 10.1038/nature12862. Epub 2013 Nov 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, New York 10065, USA [2] Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA (J.W.S.); MRC-University of Glasgow Centre for Virus Research, Glasgow, Scotland G61 1QH, UK (R.M.E.). ; Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, New York 10065, USA. ; Rheumatology Division, Department of Medicine, and Howard Hughes Medical Institute, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; Infectious Diseases Division, Department of Medicine and Department of Molecular Microbiology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; 1] Seattle Biomedical Research Institute, Seattle, Washington 98109, USA [2] Institute for Systems Biology, Seattle, Washington 98109, USA. ; Seattle Biomedical Research Institute, Seattle, Washington 98109, USA. ; Department of Microbiology and Immunology, Columbia University, New York, New York 10032, USA. ; Department of Microbiology, University of Chicago, Chicago, Illinois 60637, USA. ; 1] School of Biology, University of St Andrews, St Andrews, Scotland KY16 9ST, UK [2] Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA (J.W.S.); MRC-University of Glasgow Centre for Virus Research, Glasgow, Scotland G61 1QH, UK (R.M.E.). ; 1] Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA [2] Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA [3] Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA. ; Department of Medical Microbiology, Leiden University Medical Center, Leiden 2300 RC, The Netherlands. ; 1] Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA [2] Infectious Diseases Division, Department of Medicine and Department of Molecular Microbiology, Washington University School of Medicine, St Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24284630" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cluster Analysis ; DNA Viruses/immunology/pathogenicity ; Flow Cytometry ; Gene Library ; Immunity, Innate/*genetics/*immunology ; Interferon Regulatory Factor-3/immunology/metabolism ; Interferons/*immunology/metabolism ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; Nucleotidyltransferases/deficiency/genetics/*immunology/*metabolism ; RNA Viruses/immunology/pathogenicity ; STAT1 Transcription Factor/metabolism ; Substrate Specificity ; Viruses/classification/*immunology/pathogenicity
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Identification of a T3-associated gamma delta T cell receptor on Thy-1+ dendritic epidermal Cell lines (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-15
    Description: The murine epidermis contains a subpopulation of bone marrow-derived lymphocytes that have a dendritic morphology and that express Thy-1 and T3 cell-surface antigens but not other markers (L3T4 or Lyt-2) characteristic of mature peripheral T lymphocytes. An alternative type of T cell receptor was earlier identified on a subpopulation of murine thymocytes with a similar phenotype (T3+, L3T4-, Lyt-2-), but not on peripheral murine T lymphocytes. Two independently derived Thy-1+, L3T4-, and Lyt-2- dendritic cell lines of epidermal origin that express a T3-associated disulfide-linked heterodimer composed of a 34-kilodalton gamma-chain and 46-kilodalton partner (the delta chain) have now been identified. Analysis of N-linked glycosylation revealed that this receptor is similar to that detected on thymocytes. These results demonstrate that Thy-1+ dendritic epidermal cell lines can express gamma delta T cell receptors in vitro and suggest that Thy-1+ dendritic epidermal cells express such receptors in vivo. The localization of these gamma delta T cell receptor-expressing cells in the epidermis may be of importance for understanding the function of these receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koning, F -- Stingl, G -- Yokoyama, W M -- Yamada, H -- Maloy, W L -- Tschachler, E -- Shevach, E M -- Coligan, J E -- F32AM07219-03/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 May 15;236(4803):834-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2883729" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/*analysis ; Antigens, Thy-1 ; Bone Marrow/immunology ; Cell Line ; Mice ; Molecular Weight ; Receptors, Antigen, T-Cell/*analysis ; T-Lymphocytes/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Conversion of normal behavior to shiverer by myelin basic protein antisense cDNA in transgenic mice (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-29
    Description: Myelin basic proteins (MBPs) are coded by the single gene necessary for myelin formation in the central nervous system of the mouse. An antisense MBP mini-gene was constructed and used to determine the function of antisense DNA in transgenic mice. Several transgenic offspring of a founder transgenic mouse, AS100, were converted from the normal to mutant shiverer phenotype. Antisense MBP messenger RNA was expressed in these mice, and the endogenous MBP messenger RNA, the MBP, and the myelination in the central nervous system were reduced.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Katsuki, M -- Sato, M -- Kimura, M -- Yokoyama, M -- Kobayashi, K -- Nomura, T -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):593-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of DNA Biology, School of Medicine, Tokai University, Isehara, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2456614" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Brain/physiology ; DNA/genetics ; Gene Expression Regulation ; Mice ; Mice, Neurologic Mutants/*physiology ; Mice, Transgenic ; Molecular Sequence Data ; Myelin Basic Protein/genetics/*physiology ; Myelin Sheath/physiology ; Phenotype ; RNA/*genetics ; RNA, Antisense
    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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