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  • 1
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 306 (1983), S. 599-601 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Mta is unique in its non-mendelian pattern of inheritance. The Mta phenotype of any mouse is determined solely by the phenotype of the mother; the father has no influence on transmission of Mta1. Most inbred strains of mice are Mta+, with the exception of certain substrains of NZB1. Thus, ...
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  • 2
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Mechanisms to account for the unusual properties of a DR1αβ complex (designated DRgp50) that is resistant to dissociation under normal conditions utilized were investigated. Expression of this DRgp50 complex is highly correlated with the failure of cells from certain DR1 individuals (DR1x) to stimulate specific DR1-restricted or alloreactive T-cell clones. Pulse/chase experiments demonstrated that this DRgp50 complex was not detectable until approximately 1 h of chase. The DR1 α and β chains associated into the heterodimer in the absence of glycosylation and alterations in the number of oligosaccharides or sialylation of cell surface forms were not evident when compared with normal DR1 α and β chains. Restriction fragment length polymorphism patterns of DR β genes from normal (DR1n) and DR1x individuals were indistinguishable. However, a difference in the α chain genes between DR1n and DR1x individuals was revealed using Bgl II. This Bgl II restriction site mapped to the 3′ untranslated region of DR α and represents a new genomic marker to distinguish this functional and biochemical variant of DR1.
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Immunogenetics 28 (1988), S. 334-344 
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract We examined the regulation of cell surface expression of the Qa-1 alloantigens using a panel of monoclonal anti-Qa-1 cytotoxic T-lymphocyte (mCTL) lines. In contrast to previous reports of tissue-specific expression, we found that Qa-1 was widely expressed, resembling the prototypical class I H-2K/D molecules. We further found that an H-2D-linked gene, which we termed Qdm for Qa-1 determinant modifier, controlled expression of certain CTL-defined Qa-1 antigenic determinants. H-2D khomozygous haplotypes expressed a recessive allele of the modifier, Qdm k, whereas all other H-2 haplotypes tested expressed a dominant allele, Qdm +. The Qdm + allele regulated in trans Qa-1 epitope expression from a Qdm kchromosome, modifying expression of particular CTL-defined Qa-1 antigenic determinants rather than affecting levels of cell surface expression. Mechanisms of Qdm function may include either a novel protein modification system or an unprecedented case of antigen recognition restricted by a nonclassical major histocompatibility complex molecule.
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Immunogenetics 21 (1985), S. 511-516 
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Previous studies of HLA-restricted antigen recognition by cloned T cells have frequently demonstrated reactivity that did not correlate precisely with the expression of serologically defined HLA specificities. To further explore such discrepancies, we utilized monoclonal antibody (MoAb) blocking, partial NH2-terminal amino acid sequencing, and Southern blot hybridization techniques to analyze the fine specificity of four autologous trinitrophenyl-specific T cell lines restricted to DR2-linked epitopes. MoAb blocking studies demonstrated that two of these lines recognized determinants on DR molecules while the other two recognized determinants on the same molecule that expresses the DQw1 determinant. However, these latter two lines appeared to recognize a DQw1-related determinant found primarily in association with DR2, but not the other DQw1-associated DR alleles, DR1 and DRw6. To ascertain whether these lines were defining a functional split of DQw1, we performed partial NH2-terminal amino acid sequencing of the molecules precipitated with a DQw1-specific MoAb (Genox 3.53) from different stimulator lines. The results showed that these T cell lines recognized a subtype of DQw1 that is in linkage disequilibrium with DR2. Moreover, we identified characteristic restriction fragment length polymorphisms with a DQ β -specific cDNA that correlated with stimulatory capacity for the DQw1-restricted lines. These results demonstrate that: (1) DQ molecules may provide restriction determinants that are incorrectly assigned to DR molecules on stimulator panel analyses; (2) cloned antigen-specific T cell lines recognize polymorphic regions of class II molecules not distinguished by either conventional typing antisera or xenogeneic MoAb; and (3) the DQw1 epitope(s) is located on a heterogeneous group of DQ molecules that differ from each other in the primary sequence of their β chains.
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Immunogenetics 25 (1987), S. 234-240 
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Antigenic polymorphism of the class I-like maternally transmitted antigen (Mta) is controlled by a maternally transmitted factor (Mtf) thought to reside in mitochondria. However, the mechanisms by which Mtf generates antigenic polymorphism are not known. To address this issue, we investigated a possible role of post-translational oligosaccharide addition in the formation of Mta determinants. We examined the expression of Mta on cytotoxic T lymphocyte (CTL) target cells cultured in tunicamycin (TM), a known inhibitor of asparagine(N)-linked glycosylation. Of 18 Mtab-specific CTL lines, 8 lysed TM-treated Mtaa targets. Furthermore, a subclone of one of these eight lines, 17D5.G2, lysed TM-treated targets from all Mtaa strains tested, regardless of H-2K/D haplotype. On the other hand, this CTL clone did not lyse TM-treated target cells from the Mta null, but H-2 expressing strain B10. CAS2. Therefore expression of this Mtab-like determinant is concordant with the expression of Mtaa and seems unlikely to represent a cross-reactive H-2K/D epitope. Our data suggest that an Mtab-like determinant is expressed on unglycosylated Mtaa molecules. Thus, N-linked oligosaccharides probably prevent the expression of an Mtab-like determinant on the Mtaa molecule. We discuss how Mtf may contribute to Mta polymorphism through glycosylation.
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  • 7
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Cytotoxic T lymphocytes (CTL) activated in H-2 identical, Qa-1 disparate mixed leukocyte cultures recognize H-2-nonrestricted target antigens indistinguishable by strain or tissue distribution from serologically defined Qa-1 antigens. Cloned Qa-l-specific CTL define determinants encoded by four Qa-1 genotypes; we used anti-Qa-1 sera in antibody blocking experiments to determine if these determinants reside on molecules recognized by Qa-1-specific antibodies. Antisera containing Qa-1.1-specific and TL-specific antibodies blocked recognition of two CTL-defined determinants associated with Qa-1 a . Although both Qa-1 and TL molecules are expressed on activated T cells from appropriate strains, our studies indicated that the CTL recognized Qa-1, not TL. In addition, anti-Qa-1.2 serum inhibited CTL recognition of Qa-1b- and Qa-1c-encoded determinants. Qa-1 d target cells are unique in that they express determinants recognized by anti-Qa-1a CTL and by anti-Qa-1b CTL. Killing of Qa-1 d targets by anti-Qa-1a CTL was not inhibited by anti-Qa-1.1 serum, but was partially inhibited by anti-Qa-1.2 serum. Cytotoxicity of Qa-1 d cells by one anti-Qa-1b CTL clone was inhibited by both anti-Qa-1.2 and anti-Qa-1.1 sera, indicating close association of both serological determinants with the determinants recognized by the CTL. Thus, all of the CTL-defined Qa-1 determinants resided on molecules recognized by Qa-1-specific antibodies, but anti-Qa-1a CTL and Qa-1.1-specific antibodies did not have identical specificities.
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Immunogenetics 29 (1989), S. 258-264 
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Maternally transmitted antigen (Mta) is a mouse major histocompatibility antigen recognized by cytotoxic T lymphocytes. A role for mitochondria in expression of this class I-like cell surface antigen has been previously established. We now show that a labile product of mitochondrial protein synthesis is required for Mta expression. Reexpression of Mta determinants after enzymatic removal occurred within 24 h, and the regeneration process was sensitive to chloramphenicol (CAP), a selective inhibitor of mitochondrial protein synthesis. Additionally, target cells treated with CAP for as little as 18 h showed diminished expression of Mta. The estimated half-life for Mtf products ranged from 6 to 15 h, less than the half-lives of known mitochondrial translation products. This suggests that the Mtf product is not generated by the normal turnover of stable mitochondrial respiratory proteins. Instead, these results indicate the existence of either labile unknown mitochondrially encoded peptides or a rapid turnover pathway for known mitochondrial products.
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  • 9
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 10
    Publication Date: 2001-11-19
    Print ISSN: 0009-2347
    Electronic ISSN: 1520-605X
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
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