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J Biol Chem, Vol. 274, Issue 1, 75-85, January 1, 1999
From the Grup de Neurobiologia Molecular, Departament de
Ciències Mèdiques Bàsiques, Facultat de Medicina,
Universitat de Lleida, 25198 Lleida, Catalonia, Spain
Evidence suggests that membrane depolarization is
able to promote neuronal survival through a sustained, although
moderate, increase in the intracellular calcium. We have used the PC12
cell line to study the possible intracellular pathways that can be activated by calcium influx. Previously, we observed that membrane depolarization-induced calcium influx was able to activate the extracellular-regulated kinase (ERK)/mitogen-activated protein kinase
pathway and most of this activation was
calmodulin-dependent. We demonstrated that a part of the
ERK activation is due to the phosphorylation of the epidermal growth
factor receptor. Here, we show that both the epidermal growth factor
receptor phosphorylation and the Shc-Grb2-Ras activation are not
calmodulin-modulated. Moreover, dominant negative mutant
Ha-ras (Asn-17) prevents the activation on ERKs by membrane
depolarization, suggesting that Ras and calmodulin are both necessaries
to activate ERKs by membrane depolarization. We failed to observe any
significant induction and/or modulation of the A-Raf, B-Raf or
c-Raf-1 kinase activities, thus suggesting the existence of a MEK
kinase different from the classical Raf kinases that directly or
indirectly can be modulated by Ca2+/calmodulin.
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