Zhijie Wang, Gang Yu, Yinan Liu, Shiyong Liu, Meir Aridor, Yuan Huang, Yushuang Hu, Longfei Wang, Sisi Li, Hongbo Xiong, Bo Tang, Xia Li, Chen Cheng, Susmita Chakrabarti, Fan Wang, Qingyu Wu, Sadashiva S Karnik, Chengqi Xu, Qiuyun Chen, Qing K Wang
BACKGROUND: The cardiac sodium channel Nav 1.5 is essential for the physiological function of the heart and causes cardiac arrhythmias and sudden death when mutated. Many disease-causing mutations in Nav 1.5 cause defects in protein trafficking, a cellular process critical to the targeting of Nav 1.5 to cell surface. However, the molecular mechanisms underlying the trafficking of Nav 1.5, in particular, the exit from the endoplasmic reticulum (ER) for cell surface trafficking, remain poorly understood...
November 2018: Biochimica et Biophysica Acta. Molecular Basis of Disease