Endosomal GPCR signaling turned off by negative feedback actions of PKA and v-ATPase

The PTH receptor is one of the first 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 endosom...

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Detalles Bibliográficos
Autores principales: Gidon, Alexandre, Al-Bataineh, Mohammad M., Jean-Alphonse, Frederic G., Stevenson, Hilary, Watanabe, Tomoyuki, Louet, Claire, Khatri, Ashok, Calero, Guillermo, Pastor-Soler, Núria M., Gardella, Thomas J., Vilardaga, Jean-Pierre
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2014
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4138287/
https://www.ncbi.nlm.nih.gov/pubmed/25064832
http://dx.doi.org/10.1038/nchembio.1589
Descripción
Sumario:The PTH receptor is one of the first 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.

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