Disease relevance of GPRC5A

• The constitutive RAIG1 mRNA levels, which were low in three of five head and neck and four of six lung cancer cell lines, increased after ATRA treatment in most cell lines [1].
• Using differential display, we identified the cDNA of a novel gene, designated retinoic acid-inducible gene 1 (RAIG1), which was induced by ATRA in the squamous carcinoma cell line UMSCC-22B [1].
• A novel, retinoic acid-induced gene, GRP1-associated scaffold protein (GRASP), was isolated from P19 embryonal carcinoma cells using a subtractive screening strategy [2].
• Identification of RAI3 as a therapeutic target for breast cancer [3].
• All-trans retinoic acid induced gene expression and growth inhibition in head and neck cancer cell lines [4].

High impact information on GPRC5A

• Retinoic acid-induced gene expression in normal and leukemic myeloid cells [5].
• Follow-up studies on one gene, RAI3, suggested that p53 interacts with the promoter of RAI3 and repressed its expression at the onset of apoptosis [6].
• Taken together, these data suggest a role for RAI3 in tumor growth and demonstrate the predictive power of integrative genomics [6].
• Downstream of retinoic acid production, we identified hoxc8 as a retinoic acid-induced gene that, when ectopically expressed, rescued phenotypes of APC- and zRDHB-deficient zebrafish [7].
• We cloned the coding region of a retinoic acid-induced gene from a human thymus library, which was the mRNA encoding the 666-amino acid human homologue of mouse proline-rich protein 76 [8].

Biological context of GPRC5A

• Conversely, cell number was increased by GPRC5A overexpression [9].
• We first report the novel negative feedback model of cAMP signaling through GPRC5A gene expression [9].
• This evidence explains one of the mechanisms of the GPRC5A-regulated cell growth in some cancer cell lines [9].
• Although recent studies reported that this gene was highly expressed in the cancer cell lines and that GPRC5A might positively regulate cell proliferation, its mechanism remains unknown [9].
• RAIG1 was mapped to chromosome 12p12 [1].

Anatomical context of GPRC5A

• Granulocyte macrophage colony-stimulating factor enhances retinoic acid-induced gene expression [10].

Associations of GPRC5A with chemical compounds

• In addition, expression of RAIG-2 and RAIG-3 mRNA was increased following treatment with all-trans-retinoic acid in a manner similar to that previously described for RAIG-1 [11].
• Heterodimerization of retinoic acid receptors (RARs) with 9-cis-retinoic receptors (RXRs) is a prerequisite for binding of RXR.RAR dimers to DNA and for retinoic acid-induced gene regulation [12].
• Interaction of GRASP, a protein encoded by a novel retinoic acid-induced gene, with members of the cytohesin family of guanine nucleotide exchange factors [2].

Regulatory relationships of GPRC5A

• Integrative genomics revealed RAI3 is a cell growth-promoting gene and a novel P53 transcriptional target [6].

Other interactions of GPRC5A

• GPRC5A is a member of G-protein-coupled receptors, which was originally identified as an all-trans-retinoic acid-induced gene [9].
• The expression of retinoic acid-induced gene 1 (RIG1), a class II tumor suppressor gene, is induced in cells treated with retinoids [13].
• Purification and functional characterization of a novel protein encoded by a retinoic acid-induced gene, RA28 [14].

Analytical, diagnostic and therapeutic context of GPRC5A

• Using quantitative reverse transcription-PCR (RT-PCR), we documented increased expression of RAI3 in 19 of 25 primary breast cancers and in 6 of 11 breast-cancer cell lines examined, by comparison with normal mammary-gland tissue [3].

References