ArticleThe Journal of biological chemistry2012
Identification of a key motif that determines the differential surface levels of RET and TrkB tyrosine kinase receptors and controls depolarization enhanced RET surface insertion.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- RET overexpression leads to increased brain metastatic competency in luminal breast cancer.Journal of the National Cancer Institute · 2024Article
- Super-enhancer-controlled positive feedback loop BRD4/ERα-RET-ERα promotes ERα-positive breast cancer.Nucleic acids research · 2022Article
- Optogenetic delivery of trophic signals in a genetic model of Parkinson's disease.PLoS genetics · 2021Article
- Alternative splicing results in RET isoforms with distinct trafficking properties.Molecular biology of the cell · 2012Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RET tyrosine kinase receptor plays an important role in the development and maintenance of the nervous system. Although the ligand-induced RET signaling pathway has been well described, little is known about the regulation of RET surface expression, which is integral to the cell ability to control the response to ligand stimuli. We found that in dorsal root ganglion (DRG) neurons, which co-express RET and TrkB, the receptor surface levels of RET are significantly higher than that of TrkB. Using a sequence substitution strategy, we identified a key motif (Box1), which is necessary and sufficient for the differential RET and TrkB surface levels. Furthermore, pharmacological and mutagenesis assays revealed that protein kinase C (PKC) and high K(+) depolarization increase RET surface levels through phosphorylation of the Thr(675) residue in the Box1 motif. Finally, we found that the phosphorylation status of the Thr(675) residue influences RET mediated response to GDNF stimulation. In all, these findings provide a novel mechanism for the modulation of RET surface expression.
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