- 作者: Jan-Jan Liu; Koichi Nakajima; Toshio Hirano; Hsin-Fang Yang-Yen
- 作者服務機構: a Institute of Molecular Biology,Academia Sinica, ; b Institute of Molecular Medicine. National Taiwan University Medical School, Taipei,Taiwan, ROC, ; c Department of Molecular Oncology,Biomedical Research Center, Osaka University Medical School, Osaka, Japan
- 中文摘要: --
- 英文摘要: V-Src induces tyrosine phosphorylation of various cellular proteins and activates a number of signaling molecules including the Jak family of proteins tyrosine kinases and Stat (signal transducers and activators of transcription) proteins. Many cellular effects elicited by v-Src are mediated through Ras, a molecular switch linking growth factor receptors and non-receptor tyrosine kinases to many downstream effectors. In this report, we demonstrated that v-H-Ras and v-Src both induced cellular transformation. However, the activation of Jak1 and Stat3 were only observed in v-Src transformed cells. Using reporter gene assays, we further showed that activation of Stat3 and possibly of Jakl by v-Src were mediated through a Ras-independent pathway. As Stat3 activation has recently been shown to be required for cellular transformation by v-Src, our results suggest that activation of the Jak-Stat pathway may serve as a modulator in some but not all transformation processes.
- 中文關鍵字: --
- 英文關鍵字: Jak1 ; Ras ; v-Src ; Stat3; Signaling molecules