scholarly journals Rate of Homologous Desensitization and Internalization of the GLP-1 Receptor

Molecules ◽  
2016 ◽  
Vol 22 (1) ◽  
pp. 22 ◽  
Author(s):  
Ghina Shaaban ◽  
Mabayoje Oriowo ◽  
Suleiman Al-Sabah
Keyword(s):  
Homologous Desensitization

scholarly journals GRKs as Modulators of Neurotransmitter Receptors

Cells ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 52
Author(s):  
Eugenia V. Gurevich ◽  
Vsevolod V. Gurevich
Keyword(s):  
G Protein ◽  
General Model ◽  
G Protein Coupled Receptors ◽  
Receptor Internalization ◽  
Neurotransmitter Receptors ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Receptor Kinase ◽  
G Protein Coupled ◽  
Homologous Desensitization

Many receptors for neurotransmitters, such as dopamine, norepinephrine, acetylcholine, and neuropeptides, belong to the superfamily of G protein-coupled receptors (GPCRs). A general model posits that GPCRs undergo two-step homologous desensitization: the active receptor is phosphorylated by kinases of the G protein-coupled receptor kinase (GRK) family, whereupon arrestin proteins specifically bind active phosphorylated receptors, shutting down G protein-mediated signaling, facilitating receptor internalization, and initiating distinct signaling pathways via arrestin-based scaffolding. Here, we review the mechanisms of GRK-dependent regulation of neurotransmitter receptors, focusing on the diverse modes of GRK-mediated phosphorylation of receptor subtypes. The immediate signaling consequences of GRK-mediated receptor phosphorylation, such as arrestin recruitment, desensitization, and internalization/resensitization, are equally diverse, depending not only on the receptor subtype but also on phosphorylation by GRKs of select receptor residues. We discuss the signaling outcome as well as the biological and behavioral consequences of the GRK-dependent phosphorylation of neurotransmitter receptors where known.

In vivo and in vitro homologous desensitization of rat glomerular bradykinin B2 receptors

1995 ◽  
Vol 294 (1) ◽  
pp. 173-182 ◽  
Author(s):  
Françoise Praddaude ◽  
Ivan Tack ◽  
Catherine Emond ◽  
Jean-Loup Bascands ◽  
Jean-Pierre Girolami ◽  
...  
Keyword(s):  
B2 Receptors ◽  
Homologous Desensitization

scholarly journals Insulin Reverses Growth Hormone-induced Homologous Desensitization

2006 ◽  
Vol 281 (31) ◽  
pp. 21594-21606 ◽  
Author(s):  
Jie Xu ◽  
Zhongyu Liu ◽  
Thomas L. Clemens ◽  
Joseph L. Messina
Keyword(s):  
Growth Hormone ◽  
Homologous Desensitization

scholarly journals Phosphorylation of the Prostacyclin Receptor during Homologous Desensitization

1998 ◽  
Vol 273 (36) ◽  
pp. 23258-23266 ◽  
Author(s):  
E. M. Smyth ◽  
W. Hong Li ◽  
G. A. FitzGerald
Keyword(s):  
Prostacyclin Receptor ◽  
Homologous Desensitization

Endothelin 1 increases cell calcium in mouse collecting tubule cells

1991 ◽  
Vol 261 (4) ◽  
pp. F720-F725 ◽  
Author(s):  
M. Naruse ◽  
S. Uchida ◽  
E. Ogata ◽  
K. Kurokawa
Keyword(s):  
Free Calcium ◽  
Second Phase ◽  
Endothelin 1 ◽  
Single Nephron ◽  
Heterologous Desensitization ◽  
Intracellular Free Calcium Concentration ◽  
Free Calcium Concentration ◽  
Collecting Tubules ◽  
Dose Dependent ◽  
Homologous Desensitization

Effects of endothelin 1 (ET-1) on intracellular free calcium concentration ([Ca2+]i) were examined in superfused single-nephron segments dissected from mouse kidney. ET-1, 10(-9) to 10(-6) M, caused a biphasic increase in [Ca2+]i consisting of an initial rapid rise followed by a second more sustained elevation in [Ca2+]i in cortical collecting tubules (CCT), outer medullary CT (OMCT), and inner medullary CT (IMCT). The magnitude of the response was dose dependent and was greater in CCT than in OMCT or IMCT. Additional studies using CCT revealed that Ca2+ removal from the superfusate resulted in attenuation of the second phase of [Ca2+]i with approximately 50% reduction in the height of the initial [Ca2+]i peak in response to 10(-6) M ET-1. Ca2+ channel blocker nicardipine had little effect on ET-1-evoked changes in [Ca2+]i. BAY K 8644 and high superfusate K+ also did not affect [Ca2+]i. Addition of ET-1 and arginine vasopressin (AVP), 10(-6) M each, showed the presence of homologous desensitization but the absence of heterologous desensitization in [Ca2+]i changes. There was no additive effect of ET-1 and AVP on [Ca2+]i when they were added together. These data show that ET-1 evokes a biphasic increase in [Ca2+]i of collecting tubules and suggest that the initial peak of the ET-1-evoked rise in [Ca2+]i is largely due to cell Ca2+ release and that the second sustained rise in [Ca2+]i is largely due to increased Ca2+ influx. Data also suggest that ET-1 and AVP may act in the collecting tubules through different receptors.

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