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Mol Cell Neurosci. 2003 Feb;22(2):135-45.

Ca(2+)-dependent prodynorphin transcriptional derepression in neuroblastoma cells is exerted through DREAM protein activity in a kinase-independent manner.

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Centro Nacional de Biotecnologia (CNB), Universidad Autónoma de Madrid, Cantoblanco, E-28049, Madrid, Spain

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  • Mol Cell Neurosci. 2003 Oct;24(2):524.


Prodynorphin transcription has been postulated as an important molecular mechanism involved in adaptation/repair processes. Expression of prodynorphin is modulated according to the levels of the second messengers cAMP and Ca(2+). In the neuroblastoma cell lines, the increase of prodynorphin mRNA levels is coupled to an elevation of intracellular cAMP levels. Promoter analyses have revealed that the DRE site, a silencer element present in the prodynorphin promoter, is involved in PKA-dependent prodynorphin derepression. In this way, DREAM, a calcium-dependent repressor, plays an outstanding role. In this study, Ca(2+) release from internal stores has been found to promote an increase of prodynorphin mRNA levels in NB69 cells. Surprisingly, Ca(2+)-dependent prodynorphin gene transcription was insensitive to the broad-spectrum kinase inhibitors and sensitive to agents that alter internal Ca(2+) accumulation. Moreover, we demonstrate that in NB69 cells, the Ca(2+) signaling pathway uses DREAM as an effector to evoke prodynorphin transcription derepression in a kinase-independent manner.

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