期刊
BIOCHEMICAL JOURNAL
卷 475, 期 -, 页码 1129-1139出版社
PORTLAND PRESS LTD
DOI: 10.1042/BCJ20170756
关键词
-
资金
- Japan Society for the Promotion of Science (JSPS) KAKENHI [JP26460364, JP17K19396, JP26291042, JP26111007, JP16K14723, JP17H04041]
- Grants-in-Aid for Scientific Research [16K14723, 26291042, 17K19396] Funding Source: KAKEN
Phosphatase of regenerating liver (PRL) is highly expressed in malignant cancers and promotes cancer progression. Recent studies have suggested its functional relationship with Mg2+, but the importance and molecular details of this relationship remain unknown. Here, we report that PRL expression is regulated by Mg2+ and PRL protects cells from apoptosis under Mg2+ -depleted conditions. When cultured cells were subjected to Mg2+ depletion, endogenous PRL protein levels increased significantly. siRNA-mediated knock-down of endogenous PRL did not significantly affect cell proliferation under normal culture conditions, but it increased cell death after Mg2+ depletion. Imaging analyses with a fluorescent probe for Mg2+ showed that PRL knockdown severely reduced intracellular Mg2+ levels, indicating a role for PRL in maintaining intracellular Mg2+. We also examined the mechanism of augmented expression of PRL proteins and found that PRL mRNA transcription was stimulated by Mg2+ depletion. A series of analyses revealed the activation and the crucial importance of signal transducer and activator of transcription 1 in this process. Collectively, these results implicate PRL in maintaining cellular Mg2+ homeostasis.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据