Introduction of GPR26
GPR26 is encoded by the GPR26 gene. It belongs to the G-protein-coupled receptor (GPCR) family which is increasingly discovered to be numerous therapies for many diseases. It is a central orphan GPCR whose endogenous ligand remains unclear. As to the amino acid sequence, GPR26 shares about 30% identify with serotonin receptor 5-HT5A and gastrin releasing hormone BB2 receptor, suggesting the possibility in regulating energy homeostasis.
|Basic Information of GPR26|
|Protein Name||G-protein coupled receptor 26|
|Organism||Homo sapiens (Human)|
Function of GPR26 Membrane Protein
GPR26 expresses in ventromedial hypothalamic nucleus and cortex abundantly. Using RNA interference method to knock down the expression of GPR26 in C. elegans results in the elevated body fat storage. Furthermore, the GPR26 deficiency mice show decreased energy expenditure and hyperphagia, which lead to the higher possibility of diet-induced obesity as well as propensity to metabolic complications. Consistent with the phenotype of the GPR26 deficiency mice, the level of phosphorylation of AMPK at ser172 increase significantly in GPR26 deficiency mice. The phosphorylation of AMPK activates the downstream relevant signaling pathway to regulate hyperphagia and onset of obesity. Although the detailed physiological function of GPR26 remains unclear, some studies have revealed the key role of GPR26 in energy homeostasis. Targeting GPR26 with monoclonal antibodies or chemical compounds may offer a new therapy for diet-induced obesity.
Fig.1 Structure of GPR26 membrane protein. (Stevens, 2013)
Application of GPR26 Membrane Protein in Literature
This article identifies GPR26 can modulate the hypothalamic AMPK activation and has hypothalamic AMPK activation, suggesting that the monoclonal antibodies or chemical compounds targeting GPR26 represent novel treatments for obesity.
This article analyzes the expression pattern of GPR26 and GPR39 in different tissues. The expression level of GPR26 decreases in the heart and aorta of metabolic syndrome mice model, suggesting that GPR26 and GPR39 may be involved in the development of the metabolic abnormalities.
This article identifies GPR26 to be a suppressor of primary glioblastoma development and targeting GPR26 may offer a new approach for primary glioblastoma treatment.
The authors in this article apply the immunohistochemical method to examine the expression pattern of GPR26 in patients’ brain tissue and reveal that GPR26 has a common role in the formation or degradation of intranuclear inclusions in several neurodegenerative diseases.
This article evaluates the phenotype of GPR26 knockout mice and indicates that GPR26 has an important role in the emotion regulation in mice by mediating the phosphorylation of CREB in the central amygdala.
GPR26 Preparation Options
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