ArticleThe EMBO journal1993
Tyrosine 785 is a major determinant of Trk--substrate interaction.
Article in The EMBO journal, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed.
- High-affinity TrkA and p75 neurotrophin receptor complexes: A twisted affair.The Journal of biological chemistry · 2022Review
- Photosensitive tyrosine analogues unravel site-dependent phosphorylation in TrkA initiated MAPK/ERK signaling.Communications biology · 2020Article
- Targeting BDNF/TrkB pathways for preventing or suppressing epilepsy.Neuropharmacology · 2020Review
- Muscle Contraction Regulates BDNF/TrkB Signaling to Modulate Synaptic Function through Presynaptic cPKCα and cPKCβI.Frontiers in molecular neuroscience · 2017Article
- A Comprehensive Functional Analysis of NTRK1 Missense Mutations Causing Hereditary Sensory and Autonomic Neuropathy Type IV (HSAN IV).Human mutation · 2017Article
- Hypofunctional TrkA Accounts for the Absence of Pain Sensitization in the African Naked Mole-Rat.Cell reports · 2016Article
- A Peptide Uncoupling BDNF Receptor TrkB from Phospholipase Cγ1 Prevents Epilepsy Induced by Status Epilepticus.Neuron · 2015Article
- Clostridium perfringens Alpha-Toxin Induces Gm1a Clustering and Trka Phosphorylation in the Host Cell Membrane.PloS one · 2015Article
- Biogenesis and function of the NGF/TrkA signaling endosome.International review of cell and molecular biology · 2015Review
- Regulation of neurotrophin receptor (Trk) signaling: suppressor of cytokine signaling 2 (SOCS2) is a new player.Frontiers in molecular neuroscience · 2014Review
- Slitrks as emerging candidate genes involved in neuropsychiatric disorders.Trends in neurosciences · 2011Review
- Trk retrograde signaling requires persistent, Pincher-directed endosomes.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Cardiovascular actions of neurotrophins.Physiological reviews · 2009Review
- Brain metastases in melanoma: roles of neurotrophins.Neuro-oncology · 2004Review
- Signalling pathways involved in the sensitisation of mouse nociceptive neurones by nerve growth factor.The Journal of physiology · 2003Article
- Brain-metastatic melanoma: a neurotrophic perspective.Pathology oncology research : POR · 2003Review
- Nerve growth factor signals via preexisting TrkA receptor oligomers.Biophysical journal · 2002Article
- A single autophosphorylation site on KDR/Flk-1 is essential for VEGF-A-dependent activation of PLC-gamma and DNA synthesis in vascular endothelial cells.The EMBO journal · 2001Article
- Regulated secretion of neurotrophins by metabotropic glutamate group I (mGluRI) and Trk receptor activation is mediated via phospholipase C signalling pathways.The EMBO journal · 2001Article
- BDNF-Induced potentiation of spontaneous twitching in innervated myocytes requires calcium release from intracellular stores.Journal of neurophysiology · 2000Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interaction of the nerve growth factor (NGF) receptor/Trk with cellular substrates was investigated by transient co-overexpression in human 293 fibroblasts using ET-R, a chimeric receptor consisting of the epidermal growth factor receptor (EGF-R) extracellular ligand binding domain and the Trk transmembrane and intracellular signal-generating sequences. The chimera was fully functional, and associated with and phosphorylated phospholipase C gamma (PLC gamma), ras GTPase-activating protein (GAP) and the non-catalytic subunit of phosphatidylinositol-3'-kinase, p85, in a ligand-dependent manner. Deletion of 15 C-terminal amino acids, including tyrosine 785 (Y-785) abrogated receptor and substrate phosphorylation activities. Mutation of Y-785 to phenylalanine somewhat impaired receptor phosphorylation activity, which was reflected in reduced GAP and p85 phosphorylation. In contrast, ET-YF phosphorylation of PLC gamma was significantly reduced, while the high affinity association potential with this substrate was abrogated by this point mutation in vitro and in intact cells. Furthermore, a tyrosine-phosphorylated synthetic C-terminal peptide competitively inhibited Trk cytoplasmic domain association with PLC gamma. Thus, the short C-terminal tail appears to be a crucial structural element of the Trk cytoplasmic domain, and phosphorylated Y-785 is a major and selective interaction site for PLC gamma.
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