Suppr超能文献

蛋白激酶A通过刺激14-3-3结合并阻止Raf-1与Ras相互作用来阻断Raf-1活性。

Protein kinase A blocks Raf-1 activity by stimulating 14-3-3 binding and blocking Raf-1 interaction with Ras.

作者信息

Dumaz Nicolas, Marais Richard

机构信息

Cancer Research UK Centre for Cell and Molecular Biology, Institute of Cancer Research, 237 Fulham Road, London SW3 6JB, United Kingdom.

出版信息

J Biol Chem. 2003 Aug 8;278(32):29819-23. doi: 10.1074/jbc.C300182200. Epub 2003 Jun 11.

Abstract

Cyclic AMP (cAMP) blocks Raf-1 activation by stimulating its phosphorylation on serine 43 (Ser43), serine 233 (Ser233), and serine 259 (Ser259). We show here that phosphorylation of all three sites blocks Raf-1 binding to Ras.GTP in vivo and that cAMP stimulates binding of 14-3-3 proteins to Ser233 and Ser259. We also show that Raf-1 and protein kinase A (PKA) form a complex in vivo that is disrupted by cAMP and that ablation of PKA by use of small interfering RNA blocks phosphorylation by cAMP. The ability of PKA to block Raf-1 activation is ablated by the PKA inhibitor H89. These studies suggest that Raf-1 and cAMP form a signaling complex in cells. Upon activation of PKA, Raf-1 is phosphorylated and 14-3-3 binds, blocking Raf-1 recruitment to the plasma membrane and preventing its activation.

摘要

环磷酸腺苷(cAMP)通过刺激丝氨酸43(Ser43)、丝氨酸233(Ser233)和丝氨酸259(Ser259)的磷酸化来阻断Raf-1的激活。我们在此表明,这三个位点的磷酸化在体内均会阻断Raf-1与Ras.GTP的结合,且cAMP会刺激14-3-3蛋白与Ser233和Ser259的结合。我们还表明,Raf-1与蛋白激酶A(PKA)在体内形成复合物,该复合物会被cAMP破坏,并且使用小干扰RNA消除PKA会阻断cAMP的磷酸化作用。PKA抑制剂H89消除了PKA阻断Raf-1激活的能力。这些研究表明,Raf-1与cAMP在细胞中形成信号复合物。PKA激活后,Raf-1发生磷酸化,14-3-3与之结合,从而阻断Raf-1募集至质膜并阻止其激活。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验