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蛋白激酶 Cα 的下调参与亚硒酸钠诱导的 NB4 细胞凋亡。

Downregulation of protein kinase Cα was involved in selenite-induced apoptosis of NB4 cells.

机构信息

National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Peking Union Medical College, Beijing, China.

出版信息

Oncol Res. 2010;19(2):77-83. doi: 10.3727/096504010x12864748215089.

Abstract

We revealed in our previous research that sodium selenite induced obvious apoptosis of human leukemia NB4 cells, with reactive oxygen species (ROS), mitochondrial apoptosis pathway, and endoplasmic reticulum stress (ER stress) involved. In the present study, we revealed protein kinase Ca (PKCalpha) was dramatically downregulated in selenite-induced apoptosis, which was mediated by ROS. Besides, we confirmed PKCalpha played an antiapoptotic role through its effects on ERK1/2 and Akt, while its downregulation was attributed to caspase-3 and PP2Ac under the regulation of ROS. In summary, we speculated that in apoptosis of NB4 cells induced by selenite, PKCalpha functioned to counteract apoptosis, thus its downregulation seemed a mechanism aggravating apoptosis.

摘要

我们在之前的研究中揭示了亚硒酸钠诱导人白血病 NB4 细胞发生明显的凋亡,其中涉及活性氧(ROS)、线粒体凋亡途径和内质网应激(ER 应激)。在本研究中,我们揭示了蛋白激酶 Ca(PKCalpha)在亚硒酸钠诱导的凋亡中显著下调,这是由 ROS 介导的。此外,我们证实 PKCalpha 通过其对 ERK1/2 和 Akt 的作用发挥抗凋亡作用,而其下调归因于 ROS 调控下的 caspase-3 和 PP2Ac。总之,我们推测在亚硒酸钠诱导的 NB4 细胞凋亡中,PKCalpha 发挥拮抗凋亡的作用,因此其下调似乎是加重凋亡的一种机制。

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