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  • 1985-1989  (2)
Material
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Year
  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 43 (1988), S. 0 
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In this study, we investigated the role of calcium and phospholipid-dependent protein kinase (protein kinase C, PKC) in the modulation of histamine release from human basophils. A novel and potent inhibitor of PKC, K-252a, inhibited the release of histamine induced by anti-IgE in a dose-dependent manner with ID50 (the dose required for 50% inhibition of histamine release) of 2.2 × 10-8M. Histamine release stimulated with 12-0-tetradecanoyl-phorbol-13-acetate(TPA) was also suppressed by K-252a with maximal inhibition of 48.0 ± 9.3% at lO-7M. In contrast, K-252a did not inhibit the release of histamine in response to FMLP and ionophore A23187. Another inhibitor of PKC, H-7, exhibited a dose-dependent inhibition of anti-IgE-induced histamine release with ID50 of 8.6 × 10-4M. H-8 and HA1004, which closely resemble H-7 in chemical structure but are less potent in inhibiting PKC, did not inhibit histamine release stimulated with anti-IgE, but rather enhanced the release at higher concentrations. These results strongly suggest that PKC activation plays a crucial role in the mediation of IgE-mediated histamine release from human basophils.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation 11 (1987), S. 365-369 
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of adenosine analogs on human polymorphonuclear leukocyte (PMN) phagocytosis to latex beads or sheep red blood cells were investigated in an in vitro experiment. The purine compounds such asN 6-phenylisopropyladenosine (PIA), 5′-N-ethylcarboxamido-adenosine (NECA), an A2 adenosine receptor agonist, and adenosine as high as 2 mM had no effect on PMN phagocytosis. In contrast, 2′,5′-dideoxyadenosine (DDA), a P-site adenosine receptor agonist, and 5′-methylthioadenosine (MTA), a naturally occuring purine nucleoside, caused profound inhibition of phagocytic function of PMNs in a dose-dependent manner. Dipyridamole, which blocks purine nucleoside uptake, reversed the suppression due to MTA. Theophylline, an R-site receptor antagonist did not prevent the effect of MTA. These results suggested that phagocytosis of PMNs is suppressed by stimulation of the P-site adenosine receptors.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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