Department of Oncology and Surgical Sciences, University of Padova, I-35128 Padova, Italy.
FEBS Lett. 2010 May 17;584(10):2070-5. doi: 10.1016/j.febslet.2010.02.030. Epub 2010 Feb 17.
Human T-cell leukemia virus type-1 (HTLV-1) encodes a mitochondrial protein named p13. p13 mediates an inward K(+) current in isolated mitochondria that leads to mitochondrial swelling, depolarization, increased respiratory chain activity and reactive oxygen species (ROS) production. These effects trigger the opening of the permeability transition pore and are dependent on the presence of K(+) and on the amphipathic alpha helical domain of p13. In the context of cells, p13 acts as a sensitizer to selected apoptotic stimuli. Although it is not known whether p13 influences the activity of endogenous K(+) channels or forms a channel itself, it shares some structural and functional analogies with viroporins, a class of small integral membrane proteins that form pores and alter membrane permeability.
人类 T 细胞白血病病毒 1 型（HTLV-1）编码一种名为 p13 的线粒体蛋白。p13 介导分离的线粒体中的内向 K(+)电流，导致线粒体肿胀、去极化、呼吸链活性增加和活性氧 (ROS) 产生。这些效应触发通透性转换孔的打开，并且依赖于 K(+)的存在以及 p13 的两亲性α螺旋结构域。在细胞环境中，p13 作为对选定凋亡刺激的敏化剂起作用。虽然尚不清楚 p13 是否影响内源性 K(+)通道的活性或自身形成通道，但它与病毒孔蛋白具有一些结构和功能上的相似性，病毒孔蛋白是一类形成孔并改变膜通透性的小整合膜蛋白。
