title: Lysophosphatidylcholine potentiates BDNF-induced TrkB phosphorylation and downstream signals in cerebellar granule neurons.
abstract: We found that brain-derived neurotrophic factor (BDNF)-induced phosphorylation of mitogen-activated protein kinase (MAPK) and Akt in cerebellar granule neurons was specifically potentiated by LPC. LPC also augmented the BDNF-induced phosphorylation of TrkB, the receptor for BDNF. In TrkB-transfected CHO-K1 cells, LPC potentiated BDNF-induced MAPK phosphorylation. These results suggest that LPC plays a role in BDNF-TrkB signaling by regulating the activation of TrkB.
authors: Department of Biotechnology, The University of Tokyo.
authors: Wuhanqimuge
authors: Manabu
authors: M
authors: Arioka
mesh_terms: D000818:Animals; D019208:Brain-Derived Neurotrophic Factor / Q000494:pharmacology*; D016466:CHO Cells; D002531:Cerebellum / Q000166:cytology*; D006224:Cricetinae; D003412:Cricetulus; D006801:Humans; D008244:Lysophosphatidylcholines / Q000494:pharmacology*; D051379:Mice; D009474:Neurons / Q000166:cytology* / Q000187:drug effects*; D010766:Phosphorylation / Q000187:drug effects; D020813:Receptor, trkB / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D008244:Lysophosphatidylcholines; D020813:Receptor, trkB