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  • 1
    Electronic Resource
    Electronic Resource
    MECHANISMS OF INTERFERON-MEDIATED INHIBITION OF PROTEIN SYNTHESIS (1980)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 350 (1980), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1980.tb20650.x
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  • 2
    Electronic Resource
    Electronic Resource
    FVB/N (H2 q ) mouse is resistant to arthritis induction and exhibits a genomic deletion of T-cell receptor V beta gene segments (1999)
    Springer
    Immunogenetics 49 (1999), S. 851-859 
    Details
    ISSN: 1432-1211
    Keywords: Key words FVB/NJ mouse strain ; Animal model ; Arthritis ; Autoimmune disease ; T-cell receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract  Animal models of autoimmune diseases have been instrumental in advancing our understanding of autoimmunity in humans. Collagen-induced arthritis (CIA) in mice is an autoimmune disease model of rheumatoid arthritis. Susceptibility to CIA in mice is linked to genes of the major histocompatibility complex (MHC). CD4+ T cells that express the T-cell receptor (TCR) Tcra-V11.1 and/or Tcrb-V8.2 play a key role in the pathogenesis of arthritis in the DBA/1 mouse (H2 q ). We identified an inbred mouse strain, FVB/NJ (H2 q ), that is resistant to arthritis induction and exhibits a genomic deletion of certain Tcrb-V gene segments. We report a novel polymerase chain reaction-based method for the rapid identification of new mouse strains that exhibit germline Tcrb-V gene deletions. We mapped for the first time both the 5′ and 3′ breakpoints of the Tcrb-V deletion in the FVB/NJ, SWR, SJL, C57L, and C57BR strains to within 1.1 kilobases. Since there is an association between a particular Tcra-V allele (Tcra-V11.1 d ) and arthritis susceptibility in H2 q mouse strains, we examined the allelic polymorphisms of the Tcra-V11 gene subfamily members between the arthritis-susceptible DBA/1 mouse and the arthritis-resistant FVB/NJ mouse strain. The amino acid sequences of the Tcra-V11.1 alleles differ at two positions (codons 18 and 68). Therefore, the resistance of FVB/NJ mouse to arthritis induction may be due in part to Tcra-V11.1 coding sequence polymorphism and Tcrb-V8.2 gene segment deletion, as we have recently demonstrated in the case of SWR mouse strain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002510050564
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  • 3
    Electronic Resource
    Electronic Resource
    T-cell receptor Vbeta deletion and Valpha polymorphism are responsible for the resistance of SWR mouse to arthritis induction (1999)
    Springer
    Immunogenetics 49 (1999), S. 764-772 
    Details
    ISSN: 1432-1211
    Keywords: Key words Animal model ; Arthritis ; Autoimmune disease ; T-cell receptor polymorphism ; Transgenic mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract  Collagen type II-induced arthritis (CIA) develops in susceptible mouse strains after intradermal injections of type II collagen (CII) in complete Freund's adjuvant (CFA). Susceptibility to CIA in mice is linked to genes of the major histocompatibility complex (MHC). Although the SWR mouse has a susceptible MHC haplotype (H2 q ), it is resistant to CIA. SWR exhibits at least two known immunological defects: (1) it contains a germline deletion of about 50% of T-cell receptor (TCR) Vβ-chain gene segments, and (2) SWR is deficient in complement component C5. It has been shown that T cells that express TCRVα11.1 and TCRVβ8.2 play a substantial role in the pathogenesis of arthritis in the DBA/1 mouse (H2 q ). We generated SWR transgenic (tg) mice to determine whether the expression of pathogenic Vα11.1 and/or Vβ8.2 transgenes would confer arthritis susceptibility. Arthritis was induced in the SWR TCRαβ tg mice, but not in SWR TCRβ tg mice. To address the role of Vα11.1 in arthritis susceptibility, we examined the allelic polymorphisms of the Tcra-V11-gene subfamily members between the arthritis susceptible DBA/1 mouse and the arthritis-resistant SWR mouse strain. The amino acid sequences of the Vα11.1 alleles differ at two positions (codons 18 and 68). Accordingly, these two amino acid changes are sufficient to allow the production of pathogenic T cells in SWR mice. This is the first demonstration of the association of a particular Tcra-V allele and arthritis susceptibility in mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002510050550
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  • 4
    Electronic Resource
    Electronic Resource
    Effects of analogs of 1,25(OH)2 Vitamin D3 on the proliferation and differentiation of the human chronic myelogenous leukemia cell line, RWLeu-4 (1992)
    Springer
    Journal of cancer research and clinical oncology 118 (1992), S. 190-194 
    Details
    ISSN: 1432-1335
    Keywords: Vitamin D3 ; Analogs ; Chronic myelogenous leukemia cells ; Differentiation ; Proliferation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We evaluated the proliferative and differentiative effects of analogs of 1,25(OH)2 vitamin D3 [1,25(OH)2D3] on a chronic myelogenous leukemia cell line, RWLeu-4, which is growth-inhibited and differentiates in response to 1,25(OH)2D3 (ED50-3-10 nM). Side-chain-fluorinated analogs were more potent (ED50=0.7–2 nM) while most of those with altered saturation of the D ring or side-chain carbon-carbon bonds were equally or less effective than 1,25(OH)2D3. However, the two analogs with either two additional double bonds or an extra double and triple bond in the D ring had greater antiproliferatiive activity [1,25(OH)2-16,23-diene D3 (ED50=2.7 nM) and 1,25(OH)2-16-ene-23-yne D3 (ED50=0.7 nM)]. Since the latter of these has been reported to be less potent at mobilizing calcium than 1,25(OH)2D3, it (or a similar compound) may be a candidate for clinical use as an antineoplastic agent.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01410133
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