Disease relevance of GPR92

• The increased intracellular Ca(2+) by GPR93 activation was observed without the addition of a promiscuous Galpha protein and was pertussis toxin sensitive, which suggests Galpha(q)- and Galpha(i)-mediated pathways [1].

High impact information on GPR92

• Here we report an interim result of one screen to identify receptors that produced LPA-dependent changes in cell shape: the orphan receptor GPR92 has properties of a new LPA receptor [2].
• Sequence analyses of human GPR92 and its mouse homolog have approximately 35% amino acid identity with LPA4/GPR23 [2].
• GPR92 as a new G(12/13)- and G(q)-coupled lysophosphatidic acid receptor that increases cAMP, LPA5 [2].
• Specific [3H]LPA binding was detected in cell membranes heterologously expressing GPR92 but not control membranes [2].
• In the present study, for the first time, we identified GPR93 expression in enterocytes and demonstrated its activation in these cells by protein hydrolysate with EC(50) of 10.6 mg/ml as determined by the induction of intracellular free Ca(2+) [1].

Biological context of GPR92

• These data suggest that, physiologically, the composition of stimuli might determine GPR93 activity or its sensitivity toward a given activator and suggest a new mechanism of the regulation of mucosal cell proliferation and differentiation and hormonal secretion by dietary products in the lumen [1].
• Activated GPR93 also induced pertussis toxin-sensitive ERK1/2 phosphorylation [1].

Anatomical context of GPR92

• The GPR93 sequence retrieved an identical, human EST sequence from human primary tonsil B-cells and an EST partially encoding mouse GPR93 from small intestinal tissue [3].
• Both nuclear factor of activated T cells and 12-O-tetradecanoylphorbol 13-acetate responsive elements reporter activities were induced by protein hydrolysate in cells exogenously expressing GPR93 [1].

Associations of GPR92 with chemical compounds

• The peptidomimetic cefaclor by itself did not activate GPR93 but potentiated the protein hydrolysate response and further amplified the synergistic enhancement of GPR93 activation by protein hydrolysate and LPA [1].

References