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this study establishes a role for GPR65 in inflammatory bowel disease susceptibility and identify lysosomal dysfunction as a potentially causative element in pathogenesis
TDAG8 expression is decreased by more than 50%.
GPR65 is a regulator upstream of MMP3, which is regulated by proton-sensing G-protein-coupled receptors
Acidosis promotes Bcl-2 (show BCL2 Proteins) family-mediated evasion of apoptosis: involvement of acid-sensing G protein-coupled receptor (show ADRA1A Proteins) Gpr65 signaling to Mek (show MAP2K1 Proteins)/Erk (show EPHB2 Proteins).
Data suggest that one physiological function of TDAG8 is negative regulation of inflammation by inhibiting production of pro-inflammatory cytokines in T-lymphocytes and macrophages.
These results support the hypothesis that TDAG8 enhances tumor development by promoting adaptation to the acidic environment to enhance cell survival/proliferation.
GPR4 (show GPR4 Proteins) and TDAG8 overexpression in human tumors plays a role in driving or maintaining tumor formation
TDAG8 is one of the proton-sensing GPCRs coupling to adenylyl cyclase and psychosine, and its related lysosphingolipids behave as if they were antagonists against protein-sensing receptors, including TDAG8, GPR4, and OGR1.
TDAG8 may play biological roles in immune response and cellular transformation under conditions accompanying tissue acidosis.
Expression of TDAG8 by immune cells may regulate responses in acidic microenvironments.
data identify TDAG8-dependent microglial acid sensing as a unique chemosensor for detecting and translating hypercapnia to fear-associated behavioral and physiological responses.
TDAG8 is a negative regulator for lung neutrophilic inflammation and injury, in part, through the inhibition of chemokine (show CCL1 Proteins) production.
TDAG8(-/-) mice showed significantly higher consumption of sucrose compared to wild type mice although sucrose preference was not significantly different between genotypes.
The results of this study indicated that the proton-sensing G protein-coupled receptor (show GPR34 Proteins) GPR65 may be involved in a mechanism that supports survival of photoreceptors in the degenerating retina.
This study demonstrates differential regulation of eosinophils and mast cells in inflammatory tissue, with mast cell viability and accumulation being independent of GPR65.
IL-1beta (show IL1B Proteins) mRNA and protein were attenuated in microglia from TDAG8-deficient mice. TDAG8/PKA signaling inhibits LPS (show TLR4 Proteins)-induced ERK (show EPHB2 Proteins) and JNK (show MAPK8 Proteins). This inhibits IL-1beta (show IL1B Proteins) production. TDAG8 may mediate the proton-induced inhibition of LPS (show TLR4 Proteins)-induced cytokine production.
Results suggest that the enhancement of TDAG8 function represents a new strategy for preventing bone resorption diseases, such as osteoporosis.
Acidosis promotes Bcl-2 (show BCL2 Proteins) family-mediated evasion of apoptosis: involvement of acid-sensing G protein-coupled receptor (show GPR34 Proteins) Gpr65 signaling to Mek (show MDK Proteins)/Erk (show EPHB2 Proteins).
Data suggest that one physiological function of TDAG8 is negative regulation of inflammation by inhibiting production of pro-inflammatory cytokines in T-lymphocytes, macrophages, and splenocytes.
TDAG8 is involved in the GC-induced anti-inflammatory actions in macrophages.
Receptor for the glycosphingolipid psychosine (PSY) and several related glycosphingolipids. May have a role in activation- induced cell death or differentiation of T-cells.
G protein-coupled receptor 65
, psychosine receptor
, G-protein coupled receptor 65
, T-cell death-associated gene 8 protein
, G-protein coupled receptor 25
, T cell death associated protein 8