Pim-1 kinase and p100 cooperate to enhance c-myb activity
Pim-1 kinase and p100 cooperate to enhance c-myb activity
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DOI：
10.1016/s1097-2765(00)80141-0
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发表时间：
1998-10-01
期刊：
影响因子：
16
通讯作者：
Ness, SA
中科院分区：
文献类型：
--
作者：
Leverson, JD;Koskinen, PJ;Ness, SA
pim-1癌基因受造血细胞因子受体调节，编码丝氨酸/苏氨酸蛋白激酶，并在淋巴细胞转化中与c-myc合作。使用酵母双杂交筛选，我们发现pim-1蛋白结合p100，一种与c-Myb转录因子相互作用的转录辅激活因子。Pim-1在体外磷酸化p100，在动物细胞中与p100形成稳定的复合物，并在Ras下游以p100依赖的方式刺激c-Myb转录活性。因此，pim-1和p100似乎是影响c-Myb活性的新信号转导途径的组成部分，将所有三种与精氨酸调节的造血细胞生长、分化和凋亡控制联系起来。
The pim-1 oncogene is regulated by hematopoietic cytokine receptors, encodes a serine/threonine protein kinase, and cooperates with c-myc in lymphoid cell transformation. Using a yeast two-hybrid screen, we found that pim-1 protein binds to p100, a transcriptional coactivator that interacts with the c-Myb transcription factor. Pim-1 phosphorylated p100 in vitro, formed a stable complex with p100 in animal cells, and functioned downstream of Ras to stimulate c-Myb transcriptional activity in a p100-dependent manner. Thus, pim-1 and p100 appear to be components of a novel signal transduction pathway affecting c-Myb activity, linking all three to the cytokine-regulated control of hematopoietic cell growth, differentiation, and apoptosis.