Disease relevance of Gprc5a

• Using a differential substractive hybridization cloning procedure we have recently identified Stra6 as a novel retinoic acid-induced gene in murine P19 embryonal carcinoma cells [1].
• Protein kinase C-activating phorbol esters and okadaic acid, both of which were without effect on the enzyme induction by themselves, enhanced the retinoic acid-induced gene expression, which was in turn inhibited partially by pertussis toxin and totally by inhibitors of protein kinase C in either the presence or absence of phorbol esters [2].

High impact information on Gprc5a

• Within their expression domains in the spinal cord and brain, RAR-alpha was ubiquitously expressed, whereas RAR-beta transcripts showed very specific patterns of expression, suggesting that this receptor is involved in mediating retinoic acid-induced gene expression in relation to the development of specific neural structures or pathways [3].
• An analysis of retinoic acid-induced gene expression and metabolism in AB1 embryonic stem cells [4].
• Our studies suggest that the modulation of intracellular cyclic AMP levels may have pronounced effects on retinoic acid-induced gene expression in myeloid cells [5].
• T cell activation and increases in protein kinase C activity enhance retinoic acid-induced gene transcription [6].
• Analysis of other family members demonstrated some overlapping embryonic expression of RAIG3 mRNA that could have led to functional redundancy in the single RAIG1 null mutant mouse [7].

Chemical compound and disease context of Gprc5a

• It is likely that certain autocrine factor(s) liberated during culture of macrophages may afford conditions favorable for retinoic acid-induced gene expression, presumably via pertussis toxin-sensitive G protein-mediated phosphoinositide metabolism leading to activation of protein kinase C [2].

Biological context of Gprc5a

• To elucidate the mechanisms that mediate its regulation, we isolated and characterized the mouse gene (Rai3) and promoter region [8].
• Rai3 spans about 18 kb containing four exons separated by three introns and maps to mouse chromosome 6 near D6mit25 [8].
• The results from these studies show that COUP-TFI is a potent regulator of retinoic acid-induced gene expression in Xenopus embryonic cells, and that misexpression of COUP-TFI causes deficiencies in anterior neural structures and head development in Xenopus embryos with a concomitant change in anterior neural gene expression [9].

Anatomical context of Gprc5a

• Given its abundant lung-specific expression and role in retinoic acid signaling, we hypothesized that RAIG1 plays a role in epithelial cell differentiation during lung development [7].
• Cloning of a retinoic acid-induced gene, GT1, in the embryonal carcinoma cell line P19: neuron-specific expression in the mouse brain [10].
• Retinoic acid-induced gene expression of tissue transglutaminase via protein kinase C-dependent pathway in mouse peritoneal macrophages [2].

Associations of Gprc5a with chemical compounds

• Inhibition of retinoic-acid-induced gene expression by 2,3,7,8-tetrachlorodibenzo-p-dioxin [11].

Other interactions of Gprc5a

• RAIG1, 2, and 3 and GPCR5d represent a new subfamily of orphan G protein-coupled receptors [7].

References