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Endosomal GPCR signaling turned off by negative feedback actions of PKA and v-ATPase
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Endosomal GPCR signaling turned off by negative feedback actions of PKA and v-ATPase
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Journal Article
Endosomal GPCR signaling turned off by negative feedback actions of PKA and v-ATPase
2014
Overview
A GPCR, the parathyroid hormone receptor, can elicit a sustained signal from internal membranes after internalization. The signal was found to be terminated by a feedback mechanism where PKA activates the proton pump v-ATPase, which acidifies endosomes.
The PTH receptor is to our knowledge one of the first G protein–coupled receptor (GPCR) found to sustain cAMP signaling after internalization of the ligand–receptor complex in endosomes. This unexpected model is adding a new dimension on how we think about GPCR signaling, but its mechanism is incompletely understood. We report here that endosomal acidification mediated by the PKA action on the v-ATPase provides a negative feedback mechanism by which endosomal receptor signaling is turned off.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ 14/33
/ 38/35
/ 631/45
/ 82/83
/ 9/10
/ 96
/ Biochemistry, Molecular Biology
/ Biology
/ Cholera Toxin - pharmacology
/ Cyclic AMP-Dependent Protein Kinases - physiology
/ Fluorescence Resonance Energy Transfer
/ Humans
/ Ligands
/ Medicine
/ Receptor, Parathyroid Hormone, Type 1 - metabolism
/ Receptor, Parathyroid Hormone, Type 1 - physiology
/ Receptors, G-Protein-Coupled - physiology
