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  • 1
    Electronic Resource
    Electronic Resource
    Plasmid macro-evolution: selection of deletions during adaptation in a nutrient-limited environment (1991)
    Springer
    Genetica 84 (1991), S. 195-202 
    Details
    ISSN: 1573-6857
    Keywords: Coevolution ; tetracycline-resistance ; Escherichia coli ; pBR322 ; plasmid deletion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Under conditions where plasmid-carriage is deleterious to the cell, evolutionary changes may be expected which result in an attenuation of the deleterious effect of the plasmid. During long-term growth in glucose-limited continuous culture, initiated with a single clone of Escherichia coli containing a derivative of the plasmid pBR322, a structural change arose in the plasmid and predominated in the plasmid-containing sector of the population. This variant possessed a 2.25 kb deletion encompassing the tetracycline resistance operon as well as a region of about 1.5 kb upstream from this operon. Competition experiments involving strains carrying the plasmid with the spontancous deletion, and strains carrying plasmids with artificially constructed deletions, revealed that deletion of this region of the plasmid, involving loss of tetracycline resistance, resulted in an increment in fitness of between 10 and 20%. From the magnitude of the growth advantage, we conclude that the attenuation of the deleterious effect of the plasmid was mainly due to a reduction in the plasmid mediated interference in the metabolism of the cell caused by a deletion of the tetracycline resistance gene.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00127247
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    Paper (German National Licenses)
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  • 2
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    Shared human T cell receptor V beta usage to immunodominant regions of myelin basic protein (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-25
    Description: Multiple sclerosis (MS) may be an autoimmune disease mediated by T cells specific for a myelin protein. Investigations have demonstrated myelin basic protein (MBP)-reactive T cells that were activated in vivo in MS patients, suggesting that MBP may be a target antigen in MS. The variable (V) region of the T cell receptor (TCR) beta chain was examined among 83 T cell lines from both MS patients and healthy subjects that were reactive with the immunodominant region of human MBP (residues 84 to 102) or with a second immunodominant region of MBP (143 to 168). V beta 17 and to a lesser extent V beta 12 were frequently used in recognition of MBP(84-102) among different individuals. In contrast, V beta 17 was very infrequent among lines reactive with MBP (143-168). These data demonstrate shared TCR V beta gene usage for the recognition of immunodominant regions of the human autoantigen MBP. Such TCR structures may be used as targets for specific immunotherapy in MS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wucherpfennig, K W -- Ota, K -- Endo, N -- Seidman, J G -- Rosenzweig, A -- Weiner, H L -- Hafler, D A -- 1 K11 HL 02228-01/HL/NHLBI NIH HHS/ -- NS 00981/NS/NINDS NIH HHS/ -- R01 NS 24247/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 May 25;248(4958):1016-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1693015" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Blotting, Southern ; Epitopes ; Gene Rearrangement, beta-Chain T-Cell Antigen Receptor ; Humans ; Molecular Sequence Data ; Multiple Sclerosis/immunology ; Myelin Basic Protein/*immunology ; Polymerase Chain Reaction ; Receptors, Antigen, T-Cell/*genetics ; Receptors, Antigen, T-Cell, alpha-beta ; T-Lymphocytes/*physiology
    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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    Progression to diabetes in nonobese diabetic (NOD) mice with transgenic T cell receptors (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-19
    Description: The T cell receptor (TCR) requirements in the pathogenesis of insulin-dependent diabetes were examined with transgenic NOD mice bearing nondisease-related TCR alpha and beta chains. In both TCR beta and TCR alpha beta transgenic NOD mice the beta chain transgene was expressed by 〉 98% of peripheral T cells. The alpha chain transgene was also highly expressed. Insulitis developed in both sets of transgenic animals with most of the lymphocytes in the lesion expressing the transgenic beta chain and with depletion of the endogenous TCR V beta genes. Nonetheless, NOD animals transgenic for TCR beta and TCR alpha beta developed diabetes similar to controls. Thus, skewing the TCR repertoire did not diminish autoimmune susceptibility in NOD mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lipes, M A -- Rosenzweig, A -- Tan, K N -- Tanigawa, G -- Ladd, D -- Seidman, J G -- Eisenbarth, G S -- New York, N.Y. -- Science. 1993 Feb 19;259(5098):1165-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joslin Diabetes Center, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8267690" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/physiology ; Animals ; Base Sequence ; Crosses, Genetic ; Diabetes Mellitus, Type 2/genetics/immunology/*physiopathology ; Female ; Gene Rearrangement, T-Lymphocyte ; Islets of Langerhans/immunology/pathology ; Male ; Mice ; Mice, Inbred NOD/*physiology ; Mice, Transgenic ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Pancreatic Diseases/genetics/immunology/pathology ; Polymerase Chain Reaction/methods ; Receptors, Antigen, T-Cell, alpha-beta/genetics/*physiology ; T-Lymphocytes/*immunology/pathology
    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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