Department of Physiology, University of Siena, via Aldo Moro 7, Siena, Italy.
In Vitro Cell Dev Biol Anim. 2011 Jan;47(1):73-81. doi: 10.1007/s11626-010-9355-6. Epub 2010 Nov 13.
PKCs can have opposite effects on ERK phosphorylation. Novel (n)PKCs can inhibit ERK by phosphorylation of Raf-1, classical and atypical PKCs can activate ERK by removing an inhibitory protein from Raf-1. The aim of this work was to clarify how PMA-activated PKCs lead to ERK activation in MCF-7 cells expressing mainly nPKCs. Using chemical inhibitors and antibodies against PKCs, delivered into cells by the Chariot transfection system, we found that nPKCs activate ERK through transphosphorylation of PKD1, the blockage of which prevented PMA-stimulated ERK activation. We conclude that the nPKCs/PKD1 cascade is determinant for ERK activation by PMA in MCF-7 cells.
蛋白激酶 C（PKCs）可以对细胞外信号调节激酶（ERK）的磷酸化产生相反的影响。新型（n）PKCs 可以通过磷酸化 Raf-1 来抑制 ERK，而经典和非典型 PKCs 可以通过从 Raf-1 上去除抑制蛋白来激活 ERK。本工作旨在阐明 PMA 激活的 PKCs 如何导致主要表达 nPKCs 的 MCF-7 细胞中 ERK 的激活。我们使用化学抑制剂和针对 PKCs 的抗体，通过 Chariot 转染系统递送到细胞中，发现 nPKCs 通过 PKD1 的转磷酸化来激活 ERK，阻断 PKD1 可防止 PMA 刺激的 ERK 激活。我们得出结论，nPKCs/ PKD1 级联反应是 PMA 在 MCF-7 细胞中激活 ERK 的决定因素。
