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首页> 外文期刊>Physiological Reports >14‐3‐3‐β and ‐ε contribute to activation of the osmoprotective transcription factor NFAT5 by increasing its protein abundance and its transactivating activity
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14‐3‐3‐β and ‐ε contribute to activation of the osmoprotective transcription factor NFAT5 by increasing its protein abundance and its transactivating activity

机译：14-3-3-β和ε通过增加蛋白质丰度和反式激活活性来促进渗透保护性转录因子NFAT5的活化

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AbstractHaving previously found that high NaCl causes rapid exit of 14-3-3 isoforms from the nucleus, we used siRNA-mediated knockdown to test whether 14-3-3s contribute to the high NaCl-induced increase in the activity of the osmoprotective transcription factor NFAT5. We find that, when NaCl is elevated, knockdown of 14-3-3-β and/or 14-3-3-ε decreases NFAT5 transcriptional activity, as assayed both by luciferase reporter and by the mRNA abundance of the NFAT5 target genes aldose reductase and the sodium- and chloride-dependent betaine transporter, BGT1. Knockdown of other 14-3-3 isoforms does not significantly affect NFAT5 activity. 14-3-3-β and/or 14-3-3-ε do not act by affecting the nuclear localization of NFAT5, but by at least two other mechanisms: (1) 14-3-3-β and 14-3-3-ε increase protein abundance of NFAT5 and (2) they increase NFAT5 transactivating activity. When NaCl is elevated, knockdown of 14-3-3-β and/or 14-3-3-ε reduces the protein abundance of NFAT5, as measured by Western blot, without affecting the level of NFAT5 mRNA, and the knockdown also decreases NFAT5 transactivating activity, as measured by luciferase reporter. The 14-3-3s increase NFAT5 protein, not by increasing its translation, but by decreasing the rate at which it is degraded, as measured by cycloheximide chase. It is not clear at this point whether the 14-3-3s affect NFAT5 directly or indirectly through their effects on other proteins that signal activation of NFAT5.
机译：摘要先前发现高NaCl会导致14-3-3亚型从核中快速退出，我们使用siRNA介导的敲低来测试14-3-3是否有助于高NaCl诱导的渗透保护性转录因子活性的增加NFAT5。我们发现，当NaCl升高时，通过荧光素酶报道基因和NFAT5靶基因醛糖的mRNA丰度测定，敲除14-3-3-β和/或14-3-3-ε会降低NFAT5转录活性。还原酶和依赖于钠和氯的甜菜碱转运蛋白BGT1。击倒其他14-3-3亚型不会显着影响NFAT5活性。 14-3-3-β和/或14-3-3-ε不会通过影响NFAT5的核定位而起作用，而是通过至少两种其他机制起作用：（1）14-3-3-β和14-3 -3-ε增加NFAT5的蛋白质​​丰度，（2）它们增加NFAT5的反式激活活性。当NaCl升高时，通过Western blot检测，敲除14-3-3-β和/或14-3-3-ε会降低NFAT5的蛋白质​​丰度，而不会影响NFAT5 mRNA的水平，并且敲除也会降低NFAT5反式激活活性，通过萤光素酶报道分子测定。 14-3-3并不是通过增加NFAT5的翻译，而是通过降低NFAT5的降解速率来增加NFAT5的蛋白质​​，如环己酰亚胺追逐法所测量的。目前尚不清楚14-3-3是否直接或间接通过其对其他信号激活NFAT5的蛋白质​​的作用而影响NFAT5。

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