Activation of adenylate cyclase results in down-regulation of c-jun mRNA expression in rat C6 glioma cells
To investigate the possible mechanisms involved in forskolin-induced c-jun mRNA decrease in rat C6 glioma cells, we examined effects of a PKA inhibitor (H-89), a l-type Ca 2+ channel blocker (nimodipine), a calmodulin activation inhibitor (calmidazolium chloride) and a Ca 2+/calmodulin-dependent pro...
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Veröffentlicht in: | Neuroscience letters 1999-11, Vol.276 (1), p.53-56 |
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Sprache: | eng |
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Zusammenfassung: | To investigate the possible mechanisms involved in forskolin-induced
c-jun mRNA decrease in rat C6 glioma cells, we examined effects of a PKA inhibitor (H-89), a
l-type Ca
2+ channel blocker (nimodipine), a calmodulin activation inhibitor (calmidazolium chloride) and a Ca
2+/calmodulin-dependent protein kinase II inhibitor (KN-62) on forskolin-induced
c-jun mRNA down-regulation. H-89 caused a reversal of forskolin-induced
c-jun mRNA decrease. Furthermore, nimodipine, KN-62 and calmidazolium chloride partially blocked forskolin-induced
c-jun mRNA down-regulation. Our results suggest that activation of adenylate cyclase appears to be involved in a down-regulation of
c-jun mRNA expression through a PKA pathway. In addition,
l-type calcium channels, calmodulin and Ca
2+/calmodulin-dependent protein kinase II may be partially involved in
c-jun mRNA down-regulation induced by forskolin. |
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ISSN: | 0304-3940 1872-7972 |
DOI: | 10.1016/S0304-3940(99)00780-6 |