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  • Title: Changes in Ca2+ concentration in phorbol ester and thapsigargin treated glioma C6 cells. The role of protein kinase C in regulation of Ca2+ entry.
    Author: Barańska J, Chaban V, Czarny M, Sabała P.
    Journal: Cell Calcium; 1995 Mar; 17(3):207-15. PubMed ID: 7621533.
    Abstract:
    Glioma C6 cells treated with 12-0-tetradecanoyl-phorbol-13-acetate, TPA (10 nM and 100 nM) manifested slow increase in intracellular calcium concentration ([Ca2+]i), dependent upon both Ca2+ release from intracellular stores and Ca2+ entry, and ranging from 50 to 500 nM in different cells. The effect of TPA was abolished by the down-regulation procedure and by protein kinase C inhibitors, such as staurosporine (100 nM), suramin (100 microM), and sphingosine (100 microM), pointing to a role of protein kinase C (PKC) in this process. On the other hand, thapsigargin (100 nM), a selective inhibitor of the endoplasmic reticulum Ca(2+)-ATPase, produced a rapid increase in [Ca2+]i (up to 800 nM). This increase consisted of a transient initial phase followed by sustained elevation in [Ca2+]i, typical of Ca2+ release from intracellular stores and of Ca2+ entry, respectively. However, when the cells were exposed to TPA (100 nM) prior to thapsigargin (100 nM), then thapsigargin produced only a transient rise in [Ca2+]i. We suggest that TPA, a PKC activator, affects thapsigargin-induced Ca2+ entry, probably by PKC-mediated changes in cytoskeleton structures.
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