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anti-Rat (Rattus) GPR39 Antibodies:
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Human Polyclonal GPR39 Primary Antibody for ICC, IF - ABIN270624
Besser, Chorin, Sekler, Silverman, Atkin, Russell, Hershfinkel: Synaptically released zinc triggers metabotropic signaling via a zinc-sensing receptor in the hippocampus. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2009
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Human Polyclonal GPR39 Primary Antibody for ICC, IF - ABIN270620
Zhao, Qiao, Zhang, Zhang, Lei, Wang, Deng, Ning, Cao, Guo, Liu, Duan: GPR39 marks specific cells within the sebaceous gland and contributes to skin wound healing. in Scientific reports 2015
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Human Polyclonal GPR39 Primary Antibody for WB - ABIN1537229
Kolodziejski, Pruszynska-Oszmalek, Sassek, Kaczmarek, Szczepankiewicz, Billert, Mackowiak, Strowski, Nowak: Changes in obestatin gene and GPR39 receptor expression in peripheral tissues of rat models of obesity, type 1 and type 2 diabetes. in Journal of diabetes 2017
data indicate that Zn(2+) acting via ZnR/GPR39 has a direct role in controlling Cl(-) absorption via upregulation of basolateral KCC1 in the colon. Moreover, colonocytic ZnR/GPR39 and KCC1 reduce water loss during diarrhea and may therefore serve as effective drug targets.
G protein-coupled receptor 39 (ZnR/GPR39) was shown to regulate the activity of ion transport mechanisms that are essential for the physiological function of epithelial and neuronal cells [Review].
Data suggest that expression of GPR39 undergoes Rho kinase-dependent desensitization following activation by zinc.
This study demonstrated that zinc upregulates PKCzeta by activating GPR39 to enhance the abundance of ZO-1, thereby improving epithelial integrity in S. typhimurium-infected Caco-2 cells.
obestatin/GPR39 system in the pathogenesis and/or clinical outcome of human gastric adenocarcinomas and highlight the potential usefulness of GPR39 as a prognostic marker in gastric cancer.
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-BDNF 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 S100A4 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
Data show that Phe-V:13 can serve as an aromatic lock for the proposed active conformation of the Trp-VI:13 rotameric switch, being involved in the global movement of TM-V and TM-VI in 7TM receptor activation.
ghrelin receptor, neurotensin receptor 2 and GPR39 display an unusually high degree of constitutive activity, determined by an aromatic cluster on the inner face of the extracellular ends of TMs VI and VII
GPR39 is probably not the obestatin receptor
could activate GPR39 by high concentrations of Zn(2+), demonstrating cell surface expression of a functional receptor that could elicit a Ca(2+) response.
GPR39 functions as a Gq-coupled Zn2+-sensing receptor
results suggest that zinc sensing by ZnR/Gpr39 affects the expression levels of zinc-dependent enzymes in osteoblasts and regulates collagen processing and deposition.
G protein-coupled receptor 39 exhibits an anti-inflammatory activity by enhancing IL-10 production from macrophages
Zac1/GPR39 system promotes the formation of type II muscle fibers by phosphorylation of CaMK-II. Cells lacking Zac1/GPR39 system tend to remain stemness and form type I muscle fibers after induced differentiation.
The zinc sensing receptor, ZnR/GPR39, triggers intracellular Ca(2+) signalling in colonocytes thereby inducing occludin expression. Moreover, ZnR/GPR39 is essential for epithelial barrier recovery in the dextran sodium sulfate (DSS) ulcerative colitis model.
This study used mice expressing a Gpr39 promoter-driven LacZ reporter system to detect Gpr39 expression in the reproductive system at different phases of the estrous cycle and found an interesting region-specific distribution of Gpr39 in the mouse oviduct epithelium, which was associated with zinc metabolism.
This study has demonstrated the presence of GPR39 and the insulinotropic actions of trace metals on BRIN-BD11 cells and pancreatic beta cells
The resukts of this study suggested that mZnR/GPR39-dependent upregulation of KCC2 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 protein level and in consequence may be involved in the pathogenesis of depression.
GPR39 might modulate gut motility via regulating TMEM16A function in fibroblast-like cells
These results suggest that SNARE proteins are necessary for the increased activity of KCC2 after Zn(2+) stimulation of mZnR/GPR39.
GPR39 also mediated Zn2+-sensing receptor -dependent upregulation of Na(+)/H(+) exchange activity as this activity was found in native colon tissue but not in tissue obtained from GPR39 knock-out mice.
GPR39 deficiency is associated with increased fat accumulation on a high-fat diet, conceivably due to decreased energy expenditure and adipocyte lipolytic activity.
It indicated that GPR39 was a transducer of Zn(2+), and enhanced proliferation and differentiation of porcine intramuscular preadipocytes through activation of the PI3K/Akt signaling pathway.
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