The directly repeated RG(G/T)TCA motifs of the rat and mouse cellular retinol-binding protein II genes are promiscuous binding sites for RAR, RXR, HNF-4, and ARP-1 homo- and heterodimers.

摘要: We show here that the element which was previously characterized as a retinoid X receptor (RXR)-specific response (RXRE) in rat cellular retinol-binding protein II (CRBPII) gene is not conserved mouse gene. However, two cis-acting elements (RE2 and RE3) located promoter region of CRBPII genes mediate transactivation by retinoic acid receptors (RARs) RXRs transfected Cos-1, CV-1, HeLa cells. The RE3 major (RA) also binds transcription factors HNF-4 ARP-1. constitutively activates promoter, whereas ARP-1 represses activation mediated RARs, RXRs, HNF-4. In contrast, RA has no effect on activity human colon carcinoma cell line CaCo-2 expresses RAR alpha, gamma, RXR HNF-4, ARP-1, under conditions where beta 2 readily induced RA. Our results suggest may be RA-inducible tissues expressing inducibility observed transfection experiments reflects promiscuous binding RARs/RXRs to elements.