• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国政府科技报告 >Regulation of PKCdelta Apoptotic Activity in Prostate Cancer Cells by Tyrosine Phosphorylation
【24h】

Regulation of PKCdelta Apoptotic Activity in Prostate Cancer Cells by Tyrosine Phosphorylation

机译：酪氨酸磷酸化调节前列腺癌细胞pKCdelta凋亡活性

获取原文
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The androgen-dependent prostate cancer cell LNCaP undergoes apoptosis in response to PMA treatment, a process primarily mediated by one of the PKC isoforms PKCdelta. Tyrosine phosphorylation, as a unique property and regulatory mechanism of PKCdelta, has been studied over years but never in prostate cancer cells. In this report we identified PKCdelta became Tyr phsophorylated at site Ty311 in response to PMA stimulation. But mutation of Tyr 311 affect neither PKCdelta translocation, nor the apoptotic effect of PMA. By using adenovirus infection approach, we found that the other five sites, Tyr52, Tyr64, Tyr155, Tyr187 and Tyr565 are not relevant to the apoptosis of LNCaP cells. We eventually developed methods to analyze the signaling events controlled by Tyr phosphorylation. Etoposide, an anti-cancer agent whose effect is dependent on PKCdelta, does not induce Tyr phosphorylation of PKCdelta in LNCaP cells, indicating different drug effects might rely on different mechanisms. In summary, in this study we found the Tyr sites we examined so far are irrelevant to the apoptotic effect of PMA in LNCaP cells. However, more study will be needed to make a final conclusion on the role of PKCdelta Tyr phosphorylation in the apoptosis induced by PMA.

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
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