The Rip11/Rab11-FIP5 and kinesin II complex regulates endocytic protein recycling.
The Rip11/Rab11-FIP5 and kinesin II complex regulates endocytic protein recycling.
复制标题
DOI：
10.1242/jcs.032441
复制
发表时间：
2008-11-15
影响因子：
4
通讯作者：
Prekeris R
中科院分区：
文献类型：
--
作者：
Schonteich E;Wilson GM;Burden J;Hopkins CR;Anderson K;Goldenring JR;Prekeris R
内吞蛋白的分选和再循环是正常细胞功能和生长所必需的。内化的受体遵循快速组成性再循环途径，直接从早期内体返回细胞表面，或涉及通过核周再循环内体转运的缓慢途径。缓慢的再循环途径被认为在将再循环蛋白质引导到细胞表面的特定位置（例如运动细胞的前缘）中起关键作用。这些途径受到各种Rab GTPases（例如Rab 4和Rab 11）的调节。在这里，我们的特点Rip 11/FIP 5，一个已知的Rab 11结合蛋白，在调节内吞循环的作用。我们使用电子显微镜和荧光显微镜与基于siRNA的蛋白质敲除的组合来显示Rip 11/FIP 5存在于外周内体，在那里它调节内化受体的分选到缓慢的再循环途径。我们还确定驱动蛋白II作为Rip 11/FIP 5结合蛋白，并表明它是需要指导内吞蛋白进入相同的回收途径。因此，我们建议Rip 11/FIP 5-驱动蛋白-II复合物在通过核周再循环内体的内化受体的路由中具有关键作用。
Sorting and recycling of endocytosed proteins are required for proper cellular function and growth. Internalized receptors either follow a fast constitutive recycling pathway, returning to the cell surface directly from the early endosomes, or a slow pathway that involves transport via perinuclear recycling endosomes. Slow recycling pathways are thought to play a key role in directing recycling proteins to specific locations on cell surfaces, such as the leading edges of motile cells. These pathways are regulated by various Rab GTPases, such as Rab4 and Rab11. Here we characterize the role of Rip11/FIP5, a known Rab11-binding protein, in regulating endocytic recycling. We use a combination of electron and fluorescent microscopy with siRNA-based protein knockdown to show that Rip11/FIP5 is present at the peripheral endosomes, where it regulates the sorting of internalized receptors to a slow recycling pathway. We also identify kinesin II as a Rip11/FIP5-binding protein and show that it is required for directing endocytosed proteins into the same recycling pathway. Thus, we propose that the Rip11/FIP5-kinesin-II complex has a key role in the routing of internalized receptors through the perinuclear recycling endosomes.
登录
查看更多内容
影响因子：
5.6
作者：
Eathiraj, Sudharshan;Mishra, Ashwini;Lambright, David G.
通讯作者：
Lambright, David G.
影响因子：
3.3
作者：
Bananis, E;Nath, S;Wolkoff, AW
通讯作者：
Wolkoff, AW
影响因子：
4.8
作者：
Lindsay, AJ;Hendrick, AG;McCaffrey, MW
通讯作者：
McCaffrey, MW
影响因子：
4.8
作者：
Hales, CM;Vaerman, JP;Goldenring, JR
通讯作者：
Goldenring, JR
影响因子：
3.3
作者：
Lapierre, LA;Kumar, R;Goldenring, JR
通讯作者：
Goldenring, JR