| First Author | Fujita A | Year | 1999 |
| Journal | Biochem Biophys Res Commun | Volume | 255 |
| Issue | 3 | Pages | 625-30 |
| PubMed ID | 10049761 | Mgi Jnum | J:53270 |
| Mgi Id | MGI:1331590 | Doi | 10.1006/bbrc.1999.0243 |
| Citation | Fujita A, et al. (1999) Differential regulation of ligand-dependent and ligand-independent functions of the mouse retinoid X receptor beta by alternative splicing. Biochem Biophys Res Commun 255(3):625-30 |
| abstractText | RXR is involved in two distinct signal transduction pathways. RXR activates transcription ligand-dependently on RXRE and behaves as a positive heterodimer partner with permissive receptors; while it behaves as a ligand-independent silent partner with nonpermissive receptors. We studied the functions of a unique isoform of mouse RXRbeta2 (mRXRbeta2E) which has an in-frame four-amino-acid insertion in the ligand binding domain. mRXRbeta2E did not bind 9-cis RA with high affinity and did not activate transcription on RXRE. However, mRXRbeta2E formed heterodimers with TR, VDR, RAR, and LXR, and enhanced transcriptional activity of the nonpermissive VDR to the same extent as mRXRbeta2. With the permissive LXR, mRXRbeta2E did not show 9-cis RA-dependent transactivation and inhibited mRXRbeta2 activity. Thus, although mRXRbeta2E can perform ligand-independent functions of RXR, it cannot mediate the ligand-dependent functions of RXR, indicating that alternative splicing plays an important role in the differential regulation of these two important functions of RXR. Copyright 1999 Academic Press. |
