Abstract
MBP kinase detection assay revealed that acidic FGF (aFGF) augmented MBP kinase activity in a dose-dependent manner in astrocytes (AC). The molar potency of this action of aFGF in dibutyryl cyclic AMP (DBcAMP)-treated AC was significantly higher than that in quiescent AC. Consistently, the molar potency of accumulation of p21ras-GTP by aFGF was significantly higher in DBcAMP-treated AC than in quiescent AC. However, binding study showed that Bmax and KD for [125I]aFGF in DBcAMP-treated AC were quite similar to those in quiescent AC. Furthermore, the expression levels of Grb2, SOS, and p21ras were not changed by treatment of AC with DBcAMP. These results suggest that cytodifferentiation potentiates the p21ras/Erk signaling pathway in AC in response to aFGF without changing the expression levels of signaling molecules mediating from the FGF receptor to p21ras.
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