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  • Molecular Sequence Data  (3)
  • American Association for the Advancement of Science (AAAS)  (3)
  • 2000-2004
  • 1990-1994  (3)
  • 1940-1944
  • 2003
  • 1992  (3)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (3)
Years
  • 2000-2004
  • 1990-1994  (3)
  • 1940-1944
Year
  • 1
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    The skeletal muscle chloride channel in dominant and recessive human myotonia (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-07
    Description: Autosomal recessive generalized myotonia (Becker's disease) (GM) and autosomal dominant myotonia congenita (Thomsen's disease) (MC) are characterized by skeletal muscle stiffness that is a result of muscle membrane hyperexcitability. For both diseases, alterations in muscle chloride or sodium currents or both have been observed. A complementary DNA for a human skeletal muscle chloride channel (CLC-1) was cloned, physically localized on chromosome 7, and linked to the T cell receptor beta (TCRB) locus. Tight linkage of these two loci to GM and MC was found in German families. An unusual restriction site in the CLC-1 locus in two GM families identified a mutation associated with that disease, a phenylalanine-to-cysteine substitution in putative transmembrane domain D8. This suggests that different mutations in CLC-1 may cause dominant or recessive myotonia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koch, M C -- Steinmeyer, K -- Lorenz, C -- Ricker, K -- Wolf, F -- Otto, M -- Zoll, B -- Lehmann-Horn, F -- Grzeschik, K H -- Jentsch, T J -- New York, N.Y. -- Science. 1992 Aug 7;257(5071):797-800.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Center for Human Genetics, Marburg University, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1379744" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Southern ; Chloride Channels ; *Chromosomes, Human, Pair 7 ; Cloning, Molecular ; DNA/genetics ; Female ; *Genes, Dominant ; *Genes, Recessive ; Genetic Linkage ; Humans ; Ion Channels/*genetics ; Lod Score ; Male ; Membrane Proteins/*genetics ; Molecular Sequence Data ; Muscular Dystrophies/*genetics ; Myotonia Congenita/*genetics ; Pedigree ; Polymorphism, Restriction Fragment Length ; Receptors, Antigen, T-Cell/genetics ; Recombination, Genetic ; Sequence Homology, Nucleic Acid
    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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  • 2
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    Reciprocal regulation of adipogenesis by Myc and C/EBP alpha (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-04-17
    Description: 3T3-L1 adipoblasts that express large amounts of c-Myc cannot terminally differentiate, raising the possibility that Myc inhibits the expression of genes that promote adipogenesis. The CCAAT/enhancer binding protein (C/EBP alpha) is induced during 3T3-L1 adipogenesis when cells commit to the differentiation pathway. Transfection of 3T3-L1 adipoblasts with the gene that encodes C/EBP alpha caused overt expression of the adipocyte morphology. Expression of Myc prohibited the normal induction of C/EBP alpha and prevented adipogenesis. Enforced expression of C/EBP alpha overcame the Myc-induced block to differentiation. These results provide a molecular basis for the regulation of adipogenesis and implicate Myc and C/EBP alpha as pivotal controlling elements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freytag, S O -- Geddes, T J -- CA51748/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Apr 17;256(5055):379-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Research Program, Henry Ford Hospital, Detroit, MI 48202.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1566086" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*cytology/metabolism ; Animals ; Base Sequence ; CCAAT-Enhancer-Binding Proteins ; Cell Differentiation ; Cell Division ; Cell Line ; DNA-Binding Proteins/genetics/*physiology ; *Gene Expression Regulation ; Molecular Sequence Data ; Nuclear Proteins/genetics/*physiology ; Plasmids ; Polymerase Chain Reaction ; Proto-Oncogene Proteins c-myc/genetics/*physiology ; RNA, Messenger/analysis ; Rats ; Transfection
    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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  • 3
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    Identification of envelope V3 loop as the major determinant of CD4 neutralization sensitivity of HIV-1 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-24
    Description: Laboratory isolates of human immunodeficiency virus type-1 (HIV-1) such as HTLV-IIIB are generally T cell line-tropic and highly sensitive to neutralization by soluble CD4 (sCD4), a potential antiviral agent that is undergoing clinical trial. However, many primary HIV-1 isolates are macrophage-tropic and sCD4-resistant. Envelope V3 loop sequences derived from primary HIV-1 isolates were sufficient to confer on HTLV-IIIB not only the tissue tropism but also the degree of sCD4 neutralization resistance characteristic of their HIV-1 strains of origin. Single amino acid changes in the V3 loop enhanced sCD4 resistance by up to tenfold. These observations suggest that the tissue tropism and sCD4 neutralization sensitivity of HIV-1 isolates are regulated by similar mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hwang, S S -- Boyle, T J -- Lyerly, H K -- Cullen, B R -- AI28233/AI/NIAID NIH HHS/ -- AI28662/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 24;257(5069):535-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1636088" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD4/*immunology ; Cell Line ; Cells, Cultured ; Gene Products, gag/*immunology ; HIV Envelope Protein gp120/*immunology ; HIV-1/*immunology/isolation & purification ; Humans ; Kinetics ; Molecular Sequence Data ; Neutralization Tests ; Proviruses/immunology ; T-Lymphocyte Subsets/*immunology ; Transfection ; Virion/immunology
    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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