ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Glial cell line-derived neurotrophic factor-dependent recruitment of Ret into lipid rafts enhances signaling by partitioning Ret from proteasome-dependent degradation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed.
- Review
- TDAG51 Mediates Negative Signaling Crosstalk Between NGF/p75Neurochemical research · 2025Article
- Proteolysis targeting chimera (PROTAC)-driven antibody internalization of oncogenic cell surface receptors.Communications biology · 2024Article
- 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
- Receptor Tyrosine Kinase Signaling and Targeting in Glioblastoma Multiforme.International journal of molecular sciences · 2021Review
- Growth Factors as Axon Guidance Molecules: Lessons FromFrontiers in neuroscience · 2021Review
- RET Receptor Tyrosine Kinase: Role in Neurodegeneration, Obesity, and Cancer.International journal of molecular sciences · 2020Review
- RET receptor expression and interaction with TRK receptors in neuroblastomas.Oncology reports · 2020Article
- FAT4 Fine-Tunes Kidney Development by Regulating RET Signaling.Developmental cell · 2019Article
- ATF4 destabilizes RET through nonclassical GRP78 inhibition to enhance chemosensitivity to bortezomib in human osteosarcoma.Theranostics · 2019Article
- GDNF, Neurturin, and Artemin Activate and Sensitize Bone Afferent Neurons and Contribute to Inflammatory Bone Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Ganglioside Metabolism and Parkinson's Disease.Frontiers in neuroscience · 2018Article
- Manganese-Mediated Decrease in Levels of c-RET and Tyrosine Hydroxylase Expression In Vitro.Neurotoxicity research · 2017Article
- Article
- Neuropilin-1 is a glial cell line-derived neurotrophic factor receptor in glioblastoma.Oncotarget · 2017Article
- Gene-environment interactions and the enteric nervous system: Neural plasticity and Hirschsprung disease prevention.Developmental biology · 2016Review
- Exon Skipping in the RET Gene Encodes Novel Isoforms That Differentially Regulate RET Protein Signal Transduction.The Journal of biological chemistry · 2016Article
- 7-dehydrocholesterol efficiently supports Ret signaling in a mouse model of Smith-Opitz-Lemli syndrome.Scientific reports · 2016Article
- Effects of Dipole Potential Modifiers on Heterogenic Lipid Bilayers.The Journal of membrane biology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The receptor tyrosine kinase (RTK) Ret is activated by the formation of a complex consisting of ligands such as glial cell line-derived neurotrophic factor (GDNF) and glycerophosphatidylinositol-anchored coreceptors termed GFRalphas. During activation, Ret translocates into lipid rafts, which is critical for functional responses to GDNF. We found that Ret was rapidly ubiquitinated and degraded in sympathetic neurons when activated with GDNF, but, unlike other RTKs that are trafficked to lysosomes for degradation, Ret was degraded predominantly by the proteasome. After GDNF stimulation, the majority of ubiquitinated Ret was located outside of lipid rafts and Ret was lost predominantly from nonraft membrane domains. Consistent with the predominance of Ret degradation outside of rafts, disruption of lipid rafts in neurons did not alter either the GDNF-dependent ubiquitination or degradation of Ret. GDNF-mediated survival of sympathetic neurons was inhibited by lipid raft depletion, and this inhibitory effect of raft disruption on GDNF-mediated survival was reversed if Ret degradation was blocked via proteasome inhibition. Therefore, lipid rafts sequester Ret away from the degradation machinery located in nonraft membrane domains, such as Cbl family E3 ligases, thereby sustaining Ret signaling.
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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.