ABSTRACT
Tightly regulated cell surface expression of NTRK2/TrkB provides a mechanism for fine-tuning cellular responses to the neurotrophic factor BDNF. Recently, the degradation of NTRK2 by reticulophagy has been identified as a mechanism to limit its availability for trafficking to the cell membrane. The ER-chaperone CANX (calnexin) delivers NTRK2 to the reticulophagy receptor RETREG1/Fam134b for lysosomal degradation. Upon phosphorylation of CANX, NTRK2 is released from this complex, which facilitates its cell surface transport. These results identify a novel role for CANX in regulating the cell surface expression of NTRK2 and imply a function for reticulophagy that goes beyond regulating the degradation of misfolded proteins within the ER.
Acknowledgements
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Disclosure statement
No potential conflict of interest was reported by the author(s).