Zhu Jing, Watanabe Itaru, Gomez Barbara, Thornhill William B
Department of Biological Sciences, Fordham University, Bronx, NY 10458, USA.
Biochem J. 2003 Nov 1;375(Pt 3):761-8. doi: 10.1042/BJ20030885.
Kv1.4 and Kv1.1 potassium channel homomers have been shown to exhibit different intracellular trafficking programmes and cell-surface expression levels in cell lines: a determinant in the pore region of Kv1.4 and Kv1.1 [Zhu, Watanabe, Gomez and Thornhill (2001) J. Biol. Chem. 276, 39419-39427] and a cytoplasmic C-terminal VXXSL determinant on Kv1.4 [Li, Takimoto and Levitan (2000) J. Biol. Chem. 275, 11597-11602] have been described, which affected trafficking and cell-surface expression levels. In the present study, we examined whether trafficking pore determinants influenced any cytoplasmic C-terminal trafficking determinant. We found that removal of VXXSL from a Kv1.4 chimaera that contained the pore of Kv1.1 did not affect cell-surface trafficking. Therefore removal of the C-terminal VXXSL of Kv1.4 inhibited protein surface levels only in the presence of the Kv1.4 pore. In contrast, truncating the cytoplasmic C-terminus of Kv1.1 or truncating a Kv1.1 chimaera with the pore of Kv1.4, had little effect on surface protein levels. Furthermore, the subregion of the Kv1.4 pore trafficking determinant that was required for the inhibitory effect of VXXSL removal was mapped to a threonine residue in the deep pore region. Therefore the Kv1.4 pore determinant affected the trafficking and cell-surface levels directed by the C-terminal VXXSL determinant. Different Kv1 trafficking programmes would affect cell-surface expression levels either positively or negatively and also cell signalling. Cells may use differential trafficking programmes of membrane proteins as a post-translational mechanism to regulate surface protein levels and cell function.
已证明Kv1.4和Kv1.1钾通道同聚体在细胞系中表现出不同的细胞内运输程序和细胞表面表达水平:Kv1.4和Kv1.1孔区域中的一个决定因素[朱、渡边、戈麦斯和桑希尔(2001年)《生物化学杂志》276卷,39419 - 39427页]以及Kv1.4上的一个胞质C末端VXXSL决定因素[李、泷本和莱维坦(2000年)《生物化学杂志》275卷,11597 - 11602页]已被描述,它们影响运输和细胞表面表达水平。在本研究中,我们研究了运输孔决定因素是否影响任何胞质C末端运输决定因素。我们发现,从包含Kv1.1孔的Kv1.4嵌合体中去除VXXSL并不影响细胞表面运输。因此,仅在存在Kv1.4孔的情况下,去除Kv1.4的C末端VXXSL才会抑制蛋白质表面水平。相反,截断Kv1.1的胞质C末端或截断具有Kv1.4孔的Kv1.1嵌合体对表面蛋白水平影响很小。此外,去除VXXSL的抑制作用所需的Kv1.4孔运输决定因素的亚区域被定位到深孔区域的一个苏氨酸残基。因此,Kv1.4孔决定因素影响由C末端VXXSL决定因素指导的运输和细胞表面水平。不同的Kv1运输程序会对细胞表面表达水平产生正向或负向影响,也会影响细胞信号传导。细胞可能将膜蛋白的差异运输程序用作一种翻译后机制来调节表面蛋白水平和细胞功能。