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PLoS One. 2013 Jun 25;8(6):e64817. doi: 10.1371/journal.pone.0064817. Print 2013.

Odin (ANKS1A) modulates EGF receptor recycling and stability.

Author information

1
Program in Molecular Structure and Function, Hospital for Sick Children, Toronto, Canada.

Abstract

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.

PMID:
23825523
PMCID:
PMC3692516
DOI:
10.1371/journal.pone.0064817
[Indexed for MEDLINE]
Free PMC Article

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