ArticleOncogene2020
GGA3-mediated recycling of the RET receptor tyrosine kinase contributes to cell migration and invasion.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- GGAs: Regulation of Multiple Sorting Pathways and Potential Association With Human Diseases.Journal of cellular and molecular medicine · 2026Review
- ARF6 promotes the nuclear translocation of β-catenin to facilitate AFP deficiency-mediated metastasis in CTNNB1Cell biology and toxicology · 2026Article
- Loss of ErbB3 redirects Integrin β1 from early endosomal recycling to secretion in extracellular vesicles.The Journal of cell biology · 2026Article
- Cargo-selective regulation of clathrin-mediated endocytosis by AMP-activated protein kinase.iScience · 2025Article
- RET Inhibitor SPP86 Triggers Apoptosis and Activates the DNA Damage Response Through the Suppression of Autophagy and the PI3K/AKT Signaling Pathway in Melanoma Cells.Drug design, development and therapy · 2025Article
- Loss of tumor suppressor TMEM127 drives RET-mediated transformation through disrupted membrane dynamics.eLife · 2024Article
- Loss of Tumour Suppressor TMEM127 Drives RET-mediated Transformation Through Disrupted Membrane Dynamics.bioRxiv : the preprint server for biology · 2024Article
- Targeting the RET tyrosine kinase in neuroblastoma: A review and application of a novel selective drug design strategy.Biochemical pharmacology · 2023Review
- TMEM127 suppresses tumor development by promoting RET ubiquitination, positioning, and degradation.Cell reports · 2023Article
- Endocytic trafficking of GAS6-AXL complexes is associated with sustained AKT activation.Cellular and molecular life sciences : CMLS · 2022Article
- Discovery of N-Trisubstituted Pyrimidine Derivatives as Type I RET and RET Gatekeeper Mutant Inhibitors with a Novel Kinase Binding Pose.Journal of medicinal chemistry · 2022Article
- Stellettin B Isolated fromInternational journal of cell biology · 2022Article
- Oncolytic virus driven T-cell-based combination immunotherapy platform for colorectal cancer.Frontiers in immunology · 2022Article
- Evaluating Cell Membrane Localization and Intracellular Transport of Proteins by Biotinylation.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Reciprocal priming between receptor tyrosine kinases at recycling endosomes orchestrates cellular signalling outputs.The EMBO journal · 2021Article
- Review
- GDNF secreted by pre-osteoclasts induces migration of bone marrow mesenchymal stem cells and stimulates osteogenesis.BMB reports · 2020Article
- RET isoforms contribute differentially to invasive processes in pancreatic ductal adenocarcinoma.Oncogene · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The RET receptor tyrosine kinase plays important roles in regulating cellular proliferation, migration, and survival in the normal development of neural crest derived tissues. However, aberrant activation of RET, through oncogenic mutations or overexpression, can contribute to tumourigenesis, regional invasion, and metastasis of several human cancers. RET is expressed as two main isoforms with unique C-terminal sequences that differ in protein interactions and subcellular trafficking in response to RET activation, and which also have distinct oncogenic potentials. The long isoform, termed RET51, is internalized from the membrane in response to stimulation by its ligand, GDNF, but is known to recycle back to the surface via RAB11 endosomes. However, the mechanisms regulating this process and its cellular effects have not been defined. Here, we show that recycling of RET51 requires a multicomponent complex that includes the endosomal-sorting protein GGA3, which mediates GDNF-dependent slow recycling of RET51 receptors to the plasma membrane. Our data show that the GRB2 adapter associates with RET51 through interactions with its C-terminal sequences, facilitating recruitment of active ARF6 and GGA3 interaction, and that depletion of GGA3 or ARF6 reduced RET51 recycling. Further, GGA3 knockdown accelerated RET51 degradation and also attenuated RET-mediated AKT activation. Finally, we showed that recycling of RET51 to the cell surface through association with GGA3 and ARF6 contributes to RET51-dependent cell motility, migration, and invasion. Our data establish RET recycling as a mechanism coordinating location and duration of RET signals in order to direct cell movement and invasion.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.