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Zhe-Yu Chen

Researcher at Shandong University

Publications -  44
Citations -  5267

Zhe-Yu Chen is an academic researcher from Shandong University. The author has contributed to research in topics: Tropomyosin receptor kinase B & Brain-derived neurotrophic factor. The author has an hindex of 26, co-authored 43 publications receiving 4817 citations. Previous affiliations of Zhe-Yu Chen include Cornell University & Chinese Ministry of Education.

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Genetic variant BDNF (Val66Met) polymorphism alters anxiety-related behavior

TL;DR: A variant BDNF mouse (BDNFMet/Met) is generated that reproduces the phenotypic hallmarks in humans with the variant allele and may play a key role in genetic predispositions to anxiety and depressive disorders.
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ProBDNF Induces Neuronal Apoptosis via Activation of a Receptor Complex of p75NTR and Sortilin

TL;DR: In sympathetic neurons coexpressing sortilin and p75NTR, it is found that proBDNF is an apoptotic ligand that induces death at subnanomolar concentrations, suggesting that the neurotrophin family is capable of modulating diverse biological processes via differential processing of the proneurotrophins.
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Neuronal release of proBDNF

TL;DR: Using new tools to quantitate endogenous BDNF isoforms, it is found that mouse neurons secrete both proBDNF and mature BDNF, and BDNF actions are developmentally regulated by secretion ofPro–brain-derived neurotrophic factor or mature BD NF and by local expression of p75 and TrkB.
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Sortilin Controls Intracellular Sorting of Brain-Derived Neurotrophic Factor to the Regulated Secretory Pathway

TL;DR: A novel function for a Vps10p domain protein, sortilin, in controlling BDNF sorting to the regulated secretory pathway and a framework, based on divergent presynaptic regulation of sorting to secretory pathways, to explain how two ligands for tropomyosin-related kinase B, BDNF and NT-4, can mediate diverse biological responses are explained.
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Transactivation of Trk neurotrophin receptors by G-protein-coupled receptor ligands occurs on intracellular membranes.

TL;DR: The results indicate that there are alternative modes of activating Trk receptor tyrosine kinases in the absence of neurotrophin binding at the cell surface and that receptor signaling may occur and persist inside of neuronal cells.