Odin (ANKS1A) modulates EGF receptor recycling and stability.
Odin (ANKS1A) modulates EGF receptor recycling and stability.
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DOI：
10.1371/journal.pone.0064817
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Moran MF
中科院分区：
文献类型：
--
作者：
Tong J;Sydorskyy Y;St-Germain JR;Taylor P;Tsao MS;Moran MF
ANKS1A基因产物，也称为Odin，首先被鉴定为表皮生长因子受体网络的酪氨酸磷酸化组分。在这里，我们表明Odin是EGFR回收的效应子。在EGF刺激的HEK293细胞中，Odin的酪氨酸磷酸化在EGFR内化之前被诱导，并且独立于EGFR到ERK信号传导。Odin的过表达增加EGF诱导的EGFR运输到再循环内体和再循环回到细胞表面，并减少运输到溶酶体和降解。相反，Odin在HEK293和非小细胞肺癌细胞系RVH6849中的敲除，其表达的EGF受体比HEK293多大约10倍，导致EGFR再循环减少，并加速向溶酶体的运输和降解。通过控制内化受体的内吞命运，Odin可以提供一层调节，使细胞能够与生理学和病理学高度可变的受体细胞密度和配体浓度梯度相抗衡。
The ANKS1A gene product, also known as Odin, was first identified as a tyrosine-phosphorylated component of the epidermal growth factor receptor network. Here we show that Odin functions as an effector of EGFR recycling. In EGF-stimulated HEK293 cells tyrosine phosphorylation of Odin was induced prior to EGFR internalization and independent of EGFR-to-ERK signaling. Over-expression of Odin increased EGF-induced EGFR trafficking to recycling endosomes and recycling back to the cell surface, and decreased trafficking to lysosomes and degradation. Conversely, Odin knockdown in both HEK293 and the non-small cell lung carcinoma line RVH6849, which expresses roughly 10-fold more EGF receptors than HEK293, caused decreased EGFR recycling and accelerated trafficking to the lysosome and degradation. By governing the endocytic fate of internalized receptors, Odin may provide a layer of regulation that enables cells to contend with receptor cell densities and ligand concentration gradients that are physiologically and pathologically highly variable.
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