Oncogene TRE regulates voltage-gated Na^+ channel remodeling

在心肌细胞中，作为心律失常的长期影响，离子通道如电压依赖性Na^+通道可能遭受重构。由于细胞钙超载，钙调蛋白被高度激活以抑制TRE17去泛素化通道的功能。虽然Na^+通道合成完整，但通道降解率超过蛋白质寿命，导致心脏内Na+通道下调，对心脏兴奋性产生长期影响。

In cardiomyocytes, as a long term influence of the arrhythmias, ion channels such as voltage-dependent Na^+ channel may suffer from remodeling. As a consequence of cellular calcium overload, calmodulin is highly activated to suppress TRE17 functions to deubiquitinate the channel. Although Na^+ channel synthesis was intact, channel degradation ration exceeds the protein life span, which leads the down-regulation of Na+channels in the heart as a long-term impact on the cardiac excitability.