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  • chemotherapy of malaria  (1)
  • conformational changes  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Binding of rat α1-inhibitor-3-methylamine to the α2-macroglobulin signaling receptor induces second messengers (1996)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 61 (1996), S. 61-71 
    Details
    ISSN: 0730-2312
    Keywords: α2M* ; cAMP synthesis ; IP3 synthesis ; α1I3 ; conformational changes ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Binding of receptor-recognized forms of tetrameric human α2-macroglobulin (α2M*) to a macrophage signaling receptor induces cAMP synthesis, increases in inositol 1,4,5-triphosphate (IP3) synthesis, and a concomitant rise in cytosolic free calcium ([Ca2+]i). The α2M* signaling receptor is coupled to a pertussis-toxin insensitive G protein. Binding of α2M* also occurs to the low density lipoprotein receptor-related protein/α2M receptor (LRP/α2MR), but this binding does not induce signal transduction. Rat α1-inhibitor-3 (α1I3) is a monomeric member of the α-macroglobulin/complement superfamily. Like α2M, it can react with proteinases or methylamine which induces a conformational change causing activated α1I3 to bind to LRP/α2MR. We now report that α1I3-methylamine binds to the macrophage α2M* signaling receptor inducing a rapid rise in the synthesis of IP3 with a subsequent 1.5- to 3-fold rise in [Ca2+]i. α1I3-methylamine binding to macrophages also caused a statistically significant elevation in cAMP. Native α1I3, like α2M, was unable to induce signal transduction. α1I3 forms a complex with α1-microglobulin, which has a distinct conformation from α1I3 and is recognized by LRP/α2MR. This complex also induces an increase in [Ca2+]i comparable to the effect of α1I3-methylamine on macrophages. It is concluded that activation of α1I3 by methylamine or binding of α1-microglobulin causes similar conformational changes in the inhibitor, exposing the receptor recognition site for the α2M* signaling receptor, as well as for LRP/α2MR. © 1996 Wiley-Liss, Inc.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
  • 2
    Electronic Resource
    Electronic Resource
    Chloroquine, quinine and quinidine inhibit calcium release from macrophage intracellular stores by blocking inositol 1,4,5-trisphosphate binding to its receptor (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 64 (1997), S. 225-232 
    Details
    ISSN: 0730-2312
    Keywords: chemotherapy of malaria ; inositol trisphosphate receptors ; chloroquine ; cytosolic calcium ; endocytosis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The binding of many ligands to cellular receptors induces a signaling cascade which generates inositol 1,4,5-trisphosphate (IP3). IP3 binding to its receptors in various internal compartments causes a rapid Ca2+ efflux into the cytosol. We now demonstrate that chloroquine blocks ligand-induced Ca2+ mobilization without affecting IP3 synthesis. The effect is independent of the ligand employed and occurred with five unrelated ligands; namely, α2-macroglobulin-methylamine, angiotensin II, bradykinin, carbachol, and epidermal growth factor. Chloroquine, quinidine, and quinine, however, block binding of [3H]IP3 to its receptors by 90%, 88%, and 71%, respectively. These observations suggest a previously undetected mechanism by which these agents may in part function as antimalarials. J. Cell. Biochem. 64:225-232. © 1997 Wiley-Liss, Inc.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
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