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What is the GPR55 receptor?

Jeremy Anderson

What is the GPR55 receptor?

GPR55 is a G-protein-coupled receptor (GPCR) that has been identified as a new cannabinoid receptor. Given the wide localization of GPR55 in brain and peripheral tissues, this receptor has emerged as a regulator of multiple biological actions.

What is alphascreen GPR55?

A Functional Assay for GPR55: Envision Protocol AlphaScreen(®) SureFire(®) assay is a novel technology that combines luminescent oxygen channeling technology, nano-beads, and monocloncal antibodies to detect the level of a selected protein in a volume lower than 5 μl. This method is more sensitive compared with the traditional enzyme-linked immun …

Could GPR55 become a new drug target for treating Type 2 diabetes?

The potential of GPR55 to become a new pharmaceutical target to treat obesity and type 2 diabetes, as well as the foreseeing difficulties are also discussed. Keywords: GPR55; adipose tissue; cannabinoids; diabetes II.

Does GPR55 mediate the effects of cannabinoids?

Although antagonists of GPR55 have been described [45,46], they have not yet been widely applied, so the physiological significance of GPR55 as a potential mediator of effects of cannabinoids is not yet defined. A third cannabinoid receptor-like GPCR is GPR119.

Is LPI the ligand for GPR55 in endothelial cells?

In human endothelial cells, LPI activates GPR55 and elicits Ca2+transients (Waldeck-Weiermair et al., 2008). Thus, these studies support the contention that LPI is the ligand for GPR55.

Does the lpi/gpr55 axis enhance human breast cancer cell migration?

The LPI/GPR55 axis enhances human breast cancer cell migration via HBXIP and p-MLC signaling The G protein-coupled receptor 55 (GPR55) is expressed in multiple tissues, and has been implicated in cancer pathogenesis, but little is known about its role in the migratory behavior of cancer cells, particularly breast cancer cells.

Which GPR55 is expressed in rat mesenteric artery?

GPR55 is expressed in rat mesenteric artery. LPI caused biphasic elevations of endothelial cell intracellular Ca2+. Pretreatment with thapsigargin or 2-aminoethoxydiphenyl borate abolished both phases.