| First Author | Okumura K | Year | 2004 |
| Journal | Biochem Biophys Res Commun | Volume | 320 |
| Issue | 2 | Pages | 487-92 |
| PubMed ID | 15219855 | Mgi Jnum | J:90951 |
| Mgi Id | MGI:3045557 | Doi | 10.1016/j.bbrc.2004.05.191 |
| Citation | Okumura K, et al. (2004) c-Jun and Sp1 family are critical for retinoic acid induction of the lamin A/C retinoic acid-responsive element. Biochem Biophys Res Commun 320(2):487-92 |
| abstractText | The expression of A-type lamins, subdivided into lamin A and C, is developmentally regulated. Retinoic acid (RA)-induced differentiation of P19 embryonic carcinoma cells, in which A-type lamins are absent, increases the expression of lamin A/C. We previously showed, using P19 cells as a model system, that the lamin A/C promoter has a retinoic acid-responsive element (L-RARE), and that Sp1 and Sp3 bind the CACCC box of the L-RARE. In this study, we report that Sp1, Sp3, and c-Jun increase transactivation of the L-RARE during RA treatment. Sp1 and Sp3 regulate the lamin A/C promoter in Sp1-deficient SL2 cells and contribute to RA-dependent activation in GAL4-based transcriptional assays. Overexpression of c-Jun causes transactivation of a chimeric promoter consisting of four tandem L-RARE repeats fused with the luciferase gene in P19 cells. c-Jun also transactivates a reporter construct with five tandem GAL4-binding sites, only when co-expressed with either GAL4-Sp1 or Sp3 fusion proteins. Furthermore, we detect a physiological interaction between c-Jun with Sp1/Sp3 in RA-treated cells. Our data suggest that Sp1, Sp3, and c-Jun play an important role in gene expression through the L-RARE during RA treatment. |
