ArticleCells2019
Extracellular Juxtamembrane Motif Critical for TrkB Preformed Dimer and Activation.
Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Discovery of a sulfotyrosine-motif in the human TrkB extracellular domain required for agonist activation.bioRxiv : the preprint server for biology · 2026Article
- Molecular determinants of signal transduction in tropomyosin receptor kinases.FEBS open bio · 2026Review
- Simulation of Neurotrophin Receptor Transmembrane Helix Interactions Reveals Active States and Distinct Signaling Mechanisms.JACS Au · 2025Article
- Combined Neurotoxic Effects of Commercial Formulations of Pyrethroid (Deltamethrin) and Neonicotinoid (Imidacloprid) Pesticides on Adult Zebrafish (Life (Basel, Switzerland) · 2025Article
- Phosphoproteome Microarray Analysis of Extracellular Particles as a Tool to Explore Novel Biomarker Candidates for Alzheimer's Disease.International journal of molecular sciences · 2024Article
- Legumain Functions as a Transient TrkB Sheddase.International journal of molecular sciences · 2023Article
- The role of the TrkB-T1 receptor in the neurotrophin-4/5 antagonism of brain-derived neurotrophic factor on corticostriatal synaptic transmission.Neural regeneration research · 2020Review
- Getting CD19 Into Shape: Expression of Natively Folded "Difficult-to- Express" CD19 for Staining and Stimulation of CAR-T Cells.Frontiers in bioengineering and biotechnology · 2020Article
- Exercise modulation of BDNF/TrkB signaling in Parkinson's disease: an evidence-calibrated review of neuroprotective mechanisms, biomarker limitations, and translational gaps.Frontiers in neurologyReview
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Receptor tyrosine kinases are believed to be activated through ligand-induced dimerization. We now demonstrate that in cultured neurons, a substantial amount of endogenous TrkB, the receptor for brain-derived neurotrophic factor (BDNF), exists as an inactive preformed dimer, and the application of BDNF activates the pre-existing dimer. Deletion of the extracellular juxtamembrane motif (EJM) of TrkB increased the amount of preformed dimer, suggesting an inhibitory role of EJM on dimer formation. Further, binding of an agonistic antibody (MM12) specific to human TrkB-EJM activated the full-length TrkB and unexpectedly also truncated TrkB lacking ECD (TrkBdelECD365), suggesting that TrkB is activated by attenuating the inhibitory effect of EJM through MM12 binding-induced conformational changes. Finally, in cells co-expressing rat and human TrkB, MM12 could only activate TrkB human-human dimer but not TrkB human-rat TrkB dimer, indicating that MM12 binding to two TrkB monomers is required for activation. Our results support a model that TrkB preforms as an inactive dimer and BDNF induces TrkB conformation changes leading to its activation.
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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.