Deshpande R V, Moore M A
James Ewing Laboratory of Developmental Hematopoiesis, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.
Mol Cell Biochem. 1998 Jan;178(1-2):47-50. doi: 10.1023/a:1006894329316.
Granulocyte colony stimulating factor (G-CSF) regulates survival, proliferation, and differentiation of myeloid precursor cells. One of the signaling mechanisms for the G-CSF receptor (G-CSF-R) involves the activation of Ras/MAP kinase (MEK) pathway. Since Raf is an important, common link between Ras and MEK in the Ras-Raf-MEK cascade, we studied the expression of c-raf mRNA in G-CSF-treated myeloid precursor cell lines--NFS-60 and HL-60. G-CSF did not alter c-raf mRNA expression in these cells up to 24 h, but induced a transient up-regulation of c-fos mRNA expression between 15-60 min post-treatment. Our results show that G-CSF triggers a de novo induction of c-fos but not c-raf mRNA, and suggests that G-CSF-R-mediated activation of Ras/MEK pathway may involve post-transcriptional mechanisms of Raf regulation.
粒细胞集落刺激因子（G-CSF）调节髓系前体细胞的存活、增殖和分化。G-CSF受体（G-CSF-R）的信号传导机制之一涉及Ras/丝裂原活化蛋白激酶（MEK）途径的激活。由于Raf是Ras-Raf-MEK级联反应中Ras和MEK之间重要的共同连接点，我们研究了c-raf mRNA在G-CSF处理的髓系前体细胞系——NFS-60和HL-60中的表达。在长达24小时的时间内，G-CSF未改变这些细胞中c-raf mRNA的表达，但在处理后15-60分钟之间诱导了c-fos mRNA表达的短暂上调。我们的结果表明，G-CSF引发了c-fos的从头诱导，但不是c-raf mRNA，并表明G-CSF-R介导的Ras/MEK途径激活可能涉及Raf调节的转录后机制。
