Identification of a nerve growth factor- and epidermal growth factor-regulated protein kinase that phosphorylates the protooncogene product c-Fos.
Identification of a nerve growth factor- and epidermal growth factor-regulated protein kinase that phosphorylates the protooncogene product c-Fos.
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鉴定神经生长因子和表皮生长因子调节的蛋白激酶，该蛋白激酶磷酸化原癌基因产物 c-Fos。
DOI：
10.1073/pnas.90.2.368
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发表时间：
1993
影响因子：
11.1
通讯作者：
Landreth,GE
中科院分区：
文献类型：
--
作者：
Taylor,LK;Marshak,DR;Landreth,GE
神经生长因子（NGF）治疗大鼠嗜铬细胞瘤（PC 12）细胞诱导的转录因子c-Fos的合成，它变得高度磷酸化相对于作为细胞去极化的结果产生。一个肽衍生自羧基末端的c-Fos（残基359-370，RKGSSSNEPSSD）含有推定的磷酸化位点被用来检测神经生长因子刺激的Fos激酶。NGF处理的PC 12细胞导致蛋白激酶的快速激活，该蛋白激酶磷酸化c-Fos肽和真正的c-Fos在其羧基末端。该激酶被选择性激活的神经生长因子和表皮生长因子，但不诱导的去极化或其他代理商。c-Fos肽在对应于Ser 362的丝氨酸处被磷酸化，Ser 362是与c-Fos表现出反式阻遏活性的能力密切相关的位点[Ofir，R.，Dwarki，V.J.，Rashid，D. & Verma，I. M.（1990）Nature（伦敦）348，80-82）]。NGF刺激的Fos激酶可能在调节c-Fos表达和转化潜能中起重要作用。
Nerve growth factor (NGF) treatment of rat pheochromocytoma (PC12) cells induces the synthesis of the transcription factor c-Fos, which becomes highly phosphorylated relative to that produced as a result of depolarization of the cell. A peptide derived from the carboxyl terminus of c-Fos (residues 359-370, RKGSSSNEPSSD) containing putative phosphorylation sites was used to detect a NGF-stimulated Fos kinase. NGF treatment of PC12 cells resulted in a rapid activation of a protein kinase which phosphorylated both the c-Fos peptide and authentic c-Fos at its carboxyl terminus. The kinase was selectively activated by NGF and epidermal growth factor but was not induced by depolarization or other agents. The c-Fos peptide was phosphorylated at a serine corresponding to Ser362, a site critically implicated in the capacity of c-Fos to exhibit transrepressive activity [Ofir, R., Dwarki, V. J., Rashid, D. & Verma, I. M. (1990) Nature (London) 348, 80-82)]. The NGF-stimulated Fos kinase may play an important role in regulating the expression and transforming potential of c-Fos.
c-fos转录激活的钙和生长因子途径需要不同的上游调控序列
影响因子：
5.3
作者：
M. Sheng;Scott T. Dougan;Grant McFadden;Michael E. Greenberg
通讯作者：
Michael E. Greenberg