Altiok, NedretChangeux, Jean-Pierre2019-06-272019-06-272001110014-57930014-5793https://hdl.handle.net/20.500.12469/246https://doi.org/10.1016/S0014-5793(00)02311-5Electrical activity of myotubes represses nicotinic acetylcholine receptor (AChR) gene expression. This effect is mimicked by okadaic acid and blocked by tetrodotoxin (TTX) or staurosporine in cultured myocytes [Altiok et al. EMBO J. 16 (1997) 717-725]. In this study we investigated the mechanism of this repression. We show that addition of exogenous phospholipase D (PLD) and C inhibits AChR expression in a manner which parallels that of okadaic acid. Furthermore okadaic acid caused an increase of the threonine phosphorylation of protein kinase C zeta (PKC zeta) and activator of transcription factor (ATF2) and a decrease of the phosphorylation of Sp1. All these effects were reversed by staurosporine and TTX also abolished ATF2 phosphorylation. These data reveal a possible involvement of PLD c-jun N-terminal kinase PKC zeta and Sp1 in the repression of AChR genes by electrical activity. (C) 2001 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.eninfo:eu-repo/semantics/openAccessc-jun N-terminal kinasePhospholipase DProtein kinase CSkeletal muscleSp1Article3333383487WOS:00016644110000510.1016/S0014-5793(00)02311-52-s2.0-0035808272Q1Q111163354