Hall D J, Jones S D, Kaplan D R, Whitman M, Rollins B J, Stiles C D
Department of Microbiology and Molecular Genetics, Dana Farber Cancer Institute, Boston, Massachusetts.
Mol Cell Biol. 1989 Apr;9(4):1705-13. doi: 10.1128/mcb.9.4.1705-1713.1989.
Platelet-derived growth factor (PDGF) and the synthetic double-stranded RNA poly(I).poly(C) [poly(I.C)] stimulate transcription of the JE gene in BALB/c-3T3 fibroblasts. The response of JE to poly(I.C) does not appear to be channeled through any known component of the PDGF receptor signal transduction apparatus. In addition, JE sequences upstream of the transcription start site are devoid of previously identified poly(I.C)-responsive elements, such as those found in the beta-interferon gene. These data suggest that a novel signal transduction pathway regulates the JE response to PDGF and double-stranded RNA. The c-myc and c-fos proto-oncogenes also respond to this pathway but with poor efficiency. However, this pathway operates very efficiently on other PDGF-inducible genes that encode the secretory proteins KC and M-CSF.
血小板衍生生长因子(PDGF)和合成双链RNA聚肌苷酸-聚胞苷酸[poly(I.C)]可刺激BALB/c-3T3成纤维细胞中JE基因的转录。JE对poly(I.C)的反应似乎并非通过PDGF受体信号转导装置的任何已知成分介导。此外,转录起始位点上游的JE序列缺乏先前鉴定的poly(I.C)反应元件,如在β-干扰素基因中发现的那些元件。这些数据表明,一种新的信号转导途径调节JE对PDGF和双链RNA的反应。原癌基因c-myc和c-fos也对该途径有反应,但效率较低。然而,该途径在其他编码分泌蛋白KC和M-CSF的PDGF诱导基因上非常有效。