scholarly journals Orphan GPCRs and Neuromodulation

Neuron ◽  
2012 ◽  
Vol 76 (1) ◽  
pp. 12-21 ◽  
Author(s):  
Olivier Civelli
Keyword(s):  
2015 ◽  
Vol 6 ◽  
Author(s):  
Derek M. Shore ◽  
Patricia H. Reggio

2018 ◽  
Vol 1 (1) ◽  
Author(s):  
Aliza T. Ehrlich ◽  
Grégoire Maroteaux ◽  
Anne Robe ◽  
Lydie Venteo ◽  
Md. Taufiq Nasseef ◽  
...  
Keyword(s):  

2008 ◽  
Vol 13 (1-2) ◽  
pp. 52-58 ◽  
Author(s):  
A LEVOYE

2015 ◽  
Vol 6 ◽  
Author(s):  
Jennifer A. Stockert ◽  
Lakshmi A. Devi
Keyword(s):  

2009 ◽  
Vol 89 (3-4) ◽  
pp. 131-134 ◽  
Author(s):  
Heather B. Bradshaw ◽  
Sung Ha Lee ◽  
Douglas McHugh

2013 ◽  
Vol 218 (2) ◽  
pp. B1-B8 ◽  
Author(s):  
Gina L C Yosten ◽  
Grant R Kolar ◽  
Lauren J Redlinger ◽  
Willis K Samson

Microvascular diseases, such as retinopathies, neuropathies, and nephropathies, are a devastating consequence of type 1 and type 2 diabetes. The etiology of diabetes-associated microvascular dysfunction is poorly understood, and, likewise, treatment modalities for these disorders are limited. Interestingly, proinsulin C-peptide has been shown to play a protective role against diabetes-associated complications in experimental animals and in diabetic humans and is thus an attractive therapeutic target. However, an important step in the development of C-peptide-based therapeutics is identification of the C-peptide receptor, which is likely a G protein-coupled receptor (GPCR). Using a unique Deductive Ligand-Receptor Matching Strategy, we sought to determine whether one of the known orphan GPCRs is essential for C-peptide signaling. Knockdown of GPR146, but not GPR107 or GPR160, blocked C-peptide-induced cFos expression in KATOIII cells. Furthermore, stimulation with C-peptide caused internalization of GPR146, and examples of punctate colocalization were observed between C-peptide and GPR146 on KATOIII cell membranes. These data indicate that GPR146 is likely a part of the C-peptide signaling complex and provide a platform for the elucidation of the C-peptide signalosome.


2019 ◽  
Vol 2019 (5) ◽  
Author(s):  
Stephen P.H. Alexander ◽  
Jim Battey ◽  
Helen E. Benson ◽  
Richard V. Benya ◽  
Tom I. Bonner ◽  
...  

Table 1 lists a number of putative GPCRs identified by NC-IUPHAR [194], for which preliminary evidence for an endogenous ligand has been published, or for which there exists a potential link to a disease, or disorder. These GPCRs have recently been reviewed in detail [150]. The GPCRs in Table 1 are all Class A, rhodopsin-like GPCRs. Class A orphan GPCRs not listed in Table 1 are putative GPCRs with as-yet unidentified endogenous ligands.Table 1: Class A orphan GPCRs with putative endogenous ligands GPR3GPR4GPR6GPR12GPR15GPR17GPR20 GPR22GPR26GPR31GPR34GPR35GPR37GPR39 GPR50GPR63GRP65GPR68GPR75GPR84GPR87 GPR88GPR132GPR149GPR161GPR183LGR4LGR5 LGR6MAS1MRGPRDMRGPRX1MRGPRX2P2RY10TAAR2 In addition the orphan receptors GPR18, GPR55 and GPR119 which are reported to respond to endogenous agents analogous to the endogenous cannabinoid ligands have been grouped together (GPR18, GPR55 and GPR119).


2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Daniel Eric Felsing ◽  
Sweta Raval ◽  
Manish Jain ◽  
Simon Xi ◽  
John A Allen

Sign in / Sign up

Export Citation Format

Share Document