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Zn(2+) acts as a agonist. Additionally we are shipping GPR39 Antibodies (114) and many more products for this protein.
Showing 6 out of 6 products:
Chronic administration of many antidepressants induces GPR39 up-regulation, which suggests that the Zn(2+)-sensing receptor may be considered as a new target for drug development in the field of depression.
Taken together, our results provided a novel regulatory mechanism for GPR39-1b in NTRS1 signaling.
ZnR/GPR39-dependent expression of tight junctional proteins, thereby leading to formation of a sealed intestinal epithelial barrier.
Data suggests alterations (down-regulation) of the GPR39 receptor and involvement of CREB (show CREB1 Proteins)-BDNF (show BDNF Proteins) pathway, possibly triggered by GPR39, as a new pathomechanism of depression
Zn(2+) -dependent activation of ZnR/GPR39 also enhances the expression of the Ca(2+) -binding protein (show PVALB Proteins) S100A4 (show S100A4 Proteins) that is linked to invasion of prostate cancer cells.
GPR39 was present in thyroid autoimmune disease, non-toxic nodular goiter and toxic nodular goiter at band p51(kDa).
ZnR/GPR39 is tuned to sense physiologically relevant changes in extracellular pH that regulate ZnR-dependent signaling and ion transport activity
GPR39 activation increased the expression of the anti-apoptotic protein clusterin in butyrate-treated cells. GPR39 mediates Zn2+-dependent cell growth.
GPR39 plays an important tumorigenic role in the development and progression of esophageal squamous cell carcinoma.
extracellular Zn(2+), either applied or released following injury, activates ZnR/GPR39 to promote signaling leading to epithelial repair
The resukts of this study suggested that mZnR/GPR39-dependent upregulation of KCC2 (show SLC12A5 Proteins) activity provides homeostatic adaptation to an excitotoxic stimulus by increasing inhibition.
The results indicate depressive-like behavior in GPR39 Knockout mice with an immune response similar to that observed in depressive disorder.
The results of this study indicated that neurons, mZnR/GPR39 activity and subsequent Zn2+-dependent Ca2+ rises, ERK1/2 phosphorylation and up-regulation of NHE activity are all abolished at acidic pHe.
Results indicate a possible role of the GPR39 receptor in monoaminergic and glutamatergic neurotransmission, which plays an important role in the pathophysiology of depression
GPR39 contributed positively to skin wound healing: its loss led to a delay in wound healing during the intermediate stage.
The results of this study indicate the involvement of the GPR39 Zn(2+)-sensing receptor in the pathophysiology of depression with component of anxiety.
the GPR39 Zn(2+)-sensing receptor may be responsible for lowering the BDNF (show BDNF Proteins) protein level and in consequence may be involved in the pathogenesis of depression.
GPR39 might modulate gut (show GUSB Proteins) motility via regulating TMEM16A (show ANO1 Proteins) function in fibroblast-like cells
Zn(2+) acts as a agonist. This receptor mediates its action by association with G proteins that activate a phosphatidylinositol-calcium second messenger system. Its effect is mediated mainly through G(q)-alpha and G(12)/G(13) proteins. Involved in regulation of body weight, gastrointestinal mobility, hormone secretion and cell death (By similarity).
G-protein coupled receptor 39
, G protein-coupled receptor 39
, G-protein coupled receptor 39-1
, G-protein coupled receptor 39-like
, orphan G-protein coupled receptor 39