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Gene Review:

GPR65 - G protein-coupled receptor 65

Homo sapiens

Synonyms: G-protein coupled receptor 65, Psychosine receptor, T-cell death-associated gene 8 protein, TDAG8, hTDAG8

Kyaw, H. et al., Ishii, S. et al., Wang, J.Q. et al., Sin, W.C. et al., Duong, C.Q. et al., et al.

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Disease relevance of GPR65

These results suggest that TDAG8 may play biological roles in immune response and cellular transformation under conditions accompanying tissue acidosis [1].
Fluorescent in situ hybridization (FISH) revealed that hTDAG8 maps to human chromosome 14q31-32.1, a region in which abnormalities associated with human T-cell lymphoma or leukemia are found [2].

High impact information on GPR65

Here we document that an orphan G protein-coupled receptor, T cell death-associated gene 8, is a specific psychosine receptor [3].
As a signaling pathway downstream of TDAG8, accumulation of cyclic AMP was observed in response to solutions with a pH value lower than 7 [1].
Upon acid stimulation, stably expressed TDAG8 was internalized from the plasma membrane [1].
T cell death-associated gene 8 (TDAG8) has been reported to be a receptor for psychosine [4].
TDAG8 is a proton-sensing and psychosine-sensitive G-protein-coupled receptor [4].

Biological context of GPR65

Overexpression of GPR4 or TDAG8 in HEK293 cells led to transcriptional activation from SRE- and CRE-driven promoters, independent of exogenously added ligand [5].
An expressed sequence tag (EST) corresponding to hTDAG8 was identified from a human thyroid cDNA library and subsequently used to isolate a full-length genomic clone [2].

Anatomical context of GPR65

Immunoblots revealed that S1P(1), S1P(2), S1P(4), LPA(1), LPA(2) and GPR65 are expressed in monocytes and macrophages, while S1P(5) and LPA(3) have not been detected [6].
Here we show that GPR4 also malignantly transforms NIH3T3 cells and that TDAG8 malignantly transforms the normal mammary epithelial cell line NMuMG [5].
Taken together, these data implicate the hTDAG8 gene in T-cell-associated diseases in humans, but its actual physiological and pathological role in the human immune system needs further investigation [2].
Stably transfected mammalian CHO cells were generated, and heterologous expression of hTDAG8 was confirmed by Northern blot analysis [2].
Northern blot analysis revealed that the hTDAG8 gene is expressed predominantly in lymphoid tissues, including peripheral blood leukocytes, spleen, lymph nodes, and thymus [2].

Associations of GPR65 with chemical compounds

5. The pH effect was inhibited by copper ions and was reduced or lost in cells expressing mutated TDAG8 in which histidine residues were changed to phenylalanine [4].

Other interactions of GPR65

T cell death-associated gene 8 (TDAG8) is a G-protein-coupled receptor mainly expressed in lymphoid organs and cancer tissues [1].

References

Identification of T cell death-associated gene 8 (TDAG8) as a novel acid sensing G-protein-coupled receptor. Ishii, S., Kihara, Y., Shimizu, T. J. Biol. Chem. (2005) [Pubmed]
Cloning, characterization, and mapping of human homolog of mouse T-cell death-associated gene. Kyaw, H., Zeng, Z., Su, K., Fan, P., Shell, B.K., Carter, K.C., Li, Y. DNA Cell Biol. (1998) [Pubmed]
Identification of a molecular target of psychosine and its role in globoid cell formation. Im, D.S., Heise, C.E., Nguyen, T., O'Dowd, B.F., Lynch, K.R. J. Cell Biol. (2001) [Pubmed]
TDAG8 is a proton-sensing and psychosine-sensitive G-protein-coupled receptor. Wang, J.Q., Kon, J., Mogi, C., Tobo, M., Damirin, A., Sato, K., Komachi, M., Malchinkhuu, E., Murata, N., Kimura, T., Kuwabara, A., Wakamatsu, K., Koizumi, H., Uede, T., Tsujimoto, G., Kurose, H., Sato, T., Harada, A., Misawa, N., Tomura, H., Okajima, F. J. Biol. Chem. (2004) [Pubmed]
G protein-coupled receptors GPR4 and TDAG8 are oncogenic and overexpressed in human cancers. Sin, W.C., Zhang, Y., Zhong, W., Adhikarakunnathu, S., Powers, S., Hoey, T., An, S., Yang, J. Oncogene (2004) [Pubmed]
Expression of the lysophospholipid receptor family and investigation of lysophospholipid-mediated responses in human macrophages. Duong, C.Q., Bared, S.M., Abu-Khader, A., Buechler, C., Schmitz, A., Schmitz, G. Biochim. Biophys. Acta (2004) [Pubmed]

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