scholarly journals Role of G Protein-coupled Receptor Kinase 4 and β-Arrestin 1 in Agonist-stimulated Metabotropic Glutamate Receptor 1 Internalization and Activation of Mitogen-activated Protein Kinases

2003 ◽  
Vol 278 (14) ◽  
pp. 12433-12442 ◽  
Author(s):  
Luisa Iacovelli ◽  
Lorena Salvatore ◽  
Loredana Capobianco ◽  
Antonietta Picascia ◽  
Eliana Barletta ◽  
...  
2000 ◽  
Vol 275 (49) ◽  
pp. 38213-38220 ◽  
Author(s):  
Lianne B. Dale ◽  
Moshmi Bhattacharya ◽  
Pieter H. Anborgh ◽  
Barbara Murdoch ◽  
Mickie Bhatia ◽  
...  

2020 ◽  
Author(s):  
Maribel Donoso ◽  
Luisa Speranza ◽  
Magdalena Kalinowska ◽  
Catherine Castillo ◽  
Claudia De Sanctis ◽  
...  

AbstractAutophagy is an evolutionarily conserved, highly regulated catabolic process critical to neuronal homeostasis, function and survival throughout organismal lifespan. However, the external factors and signals that control autophagy in neurons are still poorly understood. Here we report that the G protein-coupled metabotropic glutamate receptor 1 (mGlu1) contributes to control basal autophagy in the brain. Autophagy is upregulated in the brain of adult mGlu1 knockout mice and genetic deletion or pharmacological inhibition of native mGlu1 receptors enhances autophagy flux in neurons. The evolutionarily conserved adaptor protein FEZ1, identified by a genome-wide screen as mGlu1 receptor interacting partner, was found to participate in the regulation of neuronal autophagy and to be required for repression of autophagy flux by the mGlu1 receptor. Furthermore, FEZ1 appears to enable association of mGlu1 with Ulk1, a core component of the autophagy pathway. Thus, we propose that the mGlu1 receptor contributes to restrain constitutive autophagy in neurons.


Sign in / Sign up

Export Citation Format

Share Document