首页> 外文期刊>Journal of Cellular Physiology >Mitogen activated protein kinase-dependent activation of c-Jun and c-Fos is required for neuronal differentiation but not for growth and stress response in PC12 cells.
【24h】

Mitogen activated protein kinase-dependent activation of c-Jun and c-Fos is required for neuronal differentiation but not for growth and stress response in PC12 cells.

机译:有丝分裂原激活蛋白kinase-dependent激活c-Jun c-Fos所需神经元分化但不是对经济增长和在PC12细胞应激反应。

获取原文
获取原文并翻译 | 示例
           

摘要

MAPK-dependent activation of AP-1 protein c-Jun is involved in PC12 cell differentiation and apoptosis. However, the role of other AP-1 proteins and their connection to MAPKs during growth, differentiation and apoptosis has remained elusive. Here we studied the activation of AP-1 proteins in response to ERK, JNK, and p38 signaling upon NGF, EGF and anisomycin exposures. All treatments caused different kinetics and strength of MAPK and AP-1 activities. NGF induced persistent ERK and AP-1 activities, whereas upon EGF and anisomycin exposures, their activities were only weakly and transiently induced. The sustained AP-1 activity was associated with concomitant c-Fos and c-Jun expression and phoshorylation, which were JNK and ERK dependent. While inhibition of the ERK, JNK, and p38 activities partially prevented AP-1 activity and suppressed differentiation, none of them was required for anisomycin-induced apoptosis. The importance of c-Fos and c-Jun as mediators of differentiation was demonstrated by the findings that the corresponding siRNAs suppressed NGF-induced neurite outgrowth. However, the capacity of c-Fos to promote differentiation required cooperation with Jun proteins. In contrast, Fra-2 expression was not required for the differentiation response. Together, the results show that sustained c-Jun and c-Fos activities mediate MAPK signaling and are essential for differentiation of PC12 cells.
机译:AP-1蛋白质c-Jun MAPK-dependent激活参与PC12细胞分化细胞凋亡。期间MAPKs蛋白质和他们联系生长、分化和凋亡仍然难以捉摸。AP-1蛋白质的兵,物和p38信号在神经生长因子、表皮生长因子和茴香霉素曝光。所有治疗不同的动力学和引起的MAPK和AP-1活动的力量。持续的ERK和AP-1活动,而在EGF和茴香霉素曝光,他们的活动只有弱和瞬变感应。持续AP-1活动联系在一起伴随c-Fos c-Jun表达式和phoshorylation,物和ERK的依赖。物,而抑制ERK和p38部分阻止AP-1活动和活动抑制分化,没有一个人anisomycin-induced所需细胞凋亡。c-Fos和c-Jun作为调停人的重要性分化被发现了相应的siRNAs镇压NGF-induced神经突的产物。c-Fos促进分化的能力与小君蛋白质需要合作。相反,Fra-2表达式没有要求微分响应。结果表明,持续的c-Jun和c-Fos活动调解MAPK信号必不可少的PC12细胞的分化。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号