SII-K1基因敲除小鼠中Sytl 1和Ccdc21表达降低，且氧化应激诱导Mt I的能力受损。
Reduced expression of Sytl 1 and Ccdc21 and impaired induction of Mt I by oxidative stress in SII-K1 knockout mice.
作者信息
Tano K, Hamamoto H, Ito T, Sumiya E, Rakwal R, Shibato J, Masuo Y, Ijiri K, Sekimizu K, Akimitsu N
机构信息
Radioisotope Center, The University of Tokyo, Tokyo, Japan.
出版信息
Drug Discov Ther. 2010 Oct;4(5):368-72.
SII-K1 is a member of the transcription elongation factor S-II family. In the mouse, SII-K1 is expressed exclusively in the liver, kidney, heart, and skeletal muscle. Here, we report that deletion of the SII-K1 gene in mice resulted in the downregulation of the synaptotagmin-like 1 (Sytl 1) gene in liver and of the coiled-coil domain-containing 21 (Ccdc21) gene in liver and kidney. Moreover, the induction of the metallothionein I (Mt I) gene in SII-K1-deficient mice liver was impaired in diethyl maleate-induced oxidative stress conditions. Our results suggest that SII-K1 regulates these genes in vivo.
SII-K1是转录延伸因子S-II家族的成员。在小鼠中，SII-K1仅在肝脏、肾脏、心脏和骨骼肌中表达。在此，我们报告小鼠中SII-K1基因的缺失导致肝脏中突触结合蛋白样1（Sytl 1）基因以及肝脏和肾脏中含卷曲螺旋结构域21（Ccdc21）基因的表达下调。此外，在马来酸二乙酯诱导的氧化应激条件下，SII-K1基因缺陷小鼠肝脏中金属硫蛋白I（Mt I）基因的诱导受到损害。我们的结果表明，SII-K1在体内调节这些基因。
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