ArticleJournal of neuroscience research2008
Mechanisms regulating ApTrkl, a Trk-like receptor in Aplysia sensory neurons.
Article in Journal of neuroscience research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Excitatory postsynaptic calcium transients atLearning & memory (Cold Spring Harbor, N.Y.) · 2021Article
- Contribution of PKC to the maintenance of 5-HT-induced short-term facilitation at sensorimotor synapses of Aplysia.Journal of neurophysiology · 2014Article
- The secret life of kinases: functions beyond catalysis.Cell communication and signaling : CCS · 2011Article
- The atypical protein kinase C in Aplysia can form a protein kinase M by cleavage.Journal of neurochemistry · 2009Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
An Aplysia Trk-like receptor (ApTrkl) was previously shown to be involved in cell wide long-term facilitation (LTF) and activation of ERK when serotonin (5-HT) is applied to the cell soma. The current study investigated the regulation of ApTrkl by overexpressing the receptor and several variants in Aplysia sensory neuron cultures. Kinase activity-dependent constitutive activation of ApTrkl was observed mainly on the plasma membrane. These studies revealed two modes of receptor internalization: (1) kinase activity-dependent internalization and (2) 5-HT-dependent, kinase activity-independent internalization. Both modes of internalization were ligand independent, and the action of 5-HT was mediated through G-protein-coupled receptors (GPCRs). On the other hand, methiothepin, an inverse agonist of 5-HT GPCRs activated endogenous ApTrkl to the same extent as 5-HT, suggesting a transactivation mechanism due to a novel coupling of GPCRs to receptor tyrosine kinase (RTK) activation that is also activated through inverse agonist binding. The neuropeptide sensorin could transiently activate ApTrkl but was not required for 5-HT-induced ApTrkl activation.
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Registered trials
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