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1
Cyclic AMP blocks cell growth through Raf-1-dependent and Raf-1-independent mechanisms.环磷酸腺苷通过依赖Raf-1和不依赖Raf-1的机制来阻止细胞生长。
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2
Cyclic AMP-dependent kinase regulates Raf-1 kinase mainly by phosphorylation of serine 259.环磷酸腺苷依赖性激酶主要通过磷酸化丝氨酸259来调节Raf-1激酶。
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3
Differential effects on cAMP on the MAP kinase cascade: evidence for a cAMP-insensitive step that can bypass Raf-1.环磷酸腺苷（cAMP）对丝裂原活化蛋白激酶（MAP）激酶级联反应的不同影响：存在一个可绕过Raf-1的对cAMP不敏感步骤的证据。
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4
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本文引用的文献

1
Regulation of Raf-1 activation and signalling by dephosphorylation.通过去磷酸化对Raf-1激活和信号传导的调节。
EMBO J. 2002 Jan 15;21(1-2):64-71. doi: 10.1093/emboj/21.1.64.
2
Protein phosphatases 1 and 2A promote Raf-1 activation by regulating 14-3-3 interactions.蛋白磷酸酶1和2A通过调节14-3-3相互作用促进Raf-1激活。
Oncogene. 2001 Jul 5;20(30):3949-58. doi: 10.1038/sj.onc.1204526.
3
Rap1 signalling: adhering to new models.Rap1信号传导：遵循新模型。
Nat Rev Mol Cell Biol. 2001 May;2(5):369-77. doi: 10.1038/35073073.
4
Embryonic lethality and fetal liver apoptosis in mice lacking the c-raf-1 gene.缺乏c-raf-1基因的小鼠胚胎致死性和胎肝凋亡
EMBO J. 2001 Apr 17;20(8):1952-62. doi: 10.1093/emboj/20.8.1952.
5
MEK kinase activity is not necessary for Raf-1 function.MEK激酶活性对于Raf-1功能并非必需。
EMBO J. 2001 Apr 17;20(8):1940-51. doi: 10.1093/emboj/20.8.1940.
6
S338 phosphorylation of Raf-1 is independent of phosphatidylinositol 3-kinase and Pak3.Raf-1的S338磷酸化独立于磷脂酰肌醇3激酶和Pak3。
Mol Cell Biol. 2001 Apr;21(7):2423-34. doi: 10.1128/MCB.21.7.2423-2434.2001.
7
Ras activation of the Raf kinase: tyrosine kinase recruitment of the MAP kinase cascade.Ras对Raf激酶的激活：丝裂原活化蛋白激酶级联反应的酪氨酸激酶募集
Recent Prog Horm Res. 2001;56:127-55. doi: 10.1210/rp.56.1.127.
8
Activation of B-Raf kinase requires phosphorylation of the conserved residues Thr598 and Ser601.B-Raf激酶的激活需要保守残基苏氨酸598和丝氨酸601的磷酸化。
EMBO J. 2000 Oct 16;19(20):5429-39. doi: 10.1093/emboj/19.20.5429.
9
Meaningful relationships: the regulation of the Ras/Raf/MEK/ERK pathway by protein interactions.有意义的关系：蛋白质相互作用对Ras/Raf/MEK/ERK信号通路的调控
Biochem J. 2000 Oct 15;351 Pt 2(Pt 2):289-305.
10
Cell-type specific integration of cross-talk between extracellular signal-regulated kinase and cAMP signaling.细胞外信号调节激酶与环磷酸腺苷信号之间串扰的细胞类型特异性整合
Mol Pharmacol. 2000 Oct;58(4):659-68.

环磷酸腺苷通过依赖Raf-1和不依赖Raf-1的机制来阻止细胞生长。

Cyclic AMP blocks cell growth through Raf-1-dependent and Raf-1-independent mechanisms.

作者信息

Dumaz Nicolas, Light Yvonne, Marais Richard

机构信息

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

出版信息

Mol Cell Biol. 2002 Jun;22(11):3717-28. doi: 10.1128/MCB.22.11.3717-3728.2002.

DOI:10.1128/MCB.22.11.3717-3728.2002
PMID:11997508
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC133826/
Abstract

It is widely accepted that cyclic AMP (cAMP) can block cell growth by phosphorylating Raf-1 on serine 43 and inhibiting signaling to extracellular signal-regulated protein kinase. We show that the suppression of Raf-1 by cAMP is considerably more complex than previously reported. When cellular cAMP is elevated, Raf-1 is phosphorylated on three residues (S43, S233, and S259), which work independently to block Raf-1. Both Ras-dependent and Ras-independent processes are disrupted. However, when cAMP-insensitive versions of Raf-1 are expressed in NIH 3T3 cells, their growth is still strongly suppressed when cAMP is elevated. Thus, although Raf-1 appears to be an important cAMP target, other pathways are also targeted by cAMP, providing alternative mechanisms that lead to suppression of cell growth.

摘要

普遍认为，环磷酸腺苷（cAMP）可通过使丝氨酸43位点的Raf-1磷酸化并抑制向细胞外信号调节蛋白激酶的信号传导来阻断细胞生长。我们发现，cAMP对Raf-1的抑制作用比先前报道的要复杂得多。当细胞内cAMP升高时，Raf-1在三个位点（S43、S233和S259）发生磷酸化，这些位点独立发挥作用来阻断Raf-1。Ras依赖性和Ras非依赖性过程均被破坏。然而，当在NIH 3T3细胞中表达对cAMP不敏感的Raf-1版本时，cAMP升高时其生长仍会受到强烈抑制。因此，尽管Raf-1似乎是cAMP的一个重要靶点，但cAMP也靶向其他途径，提供了导致细胞生长抑制的替代机制。