| First Author | Knutson DC | Year | 2008 |
| Journal | Arch Biochem Biophys | Volume | 477 |
| Issue | 1 | Pages | 163-74 |
| PubMed ID | 18585997 | Mgi Jnum | J:141908 |
| Mgi Id | MGI:3820014 | Doi | 10.1016/j.abb.2008.06.005 |
| Citation | Knutson DC, et al. (2008) atRA Regulation of NEDD9, a gene involved in neurite outgrowth and cell adhesion. Arch Biochem Biophys 477(1):163-74 |
| abstractText | We previously identified NEDD9 (RAINB2/HEF1/Cas-L) as a new downstream target of all-trans retinoic acid (atRA) and its receptors in the human neuroblastoma cell line, SH-SY5Y [R.A. Merrill, A.W.-M. See, M.L. Wertheim, M. Clagett-Dame, Dev. Dyn. 231 (2004) 564-575; R.A. Merrill, J.M. Ahrens, M.E. Kaiser, K.S. Federhart, V.Y. Poon, M. Clagett-Dame, Biol. Chem. 385 (2004) 605-614]. We now provide functional evidence that NEDD9 is directly regulated by atRA through a complex retinoic acid response element (RARE) located in the NEDD9 proximal promoter and consisting of four conserved half-sites separated by 1, 5, and 1 intervening base pairs. We show that a region of the human NEDD9 promoter from -1670 to +15 is sufficient to confer atRA-responsiveness and that a complex RARE located from -475 to -445 is necessary for this effect. While mutation of any one half-site does not eliminate complex formation in electrophoretic mobility shift assays (EMSA); these same mutations, when tested in transient transfection assays, markedly decrease atRA-responsiveness. Finally, chromatin immunoprecipitation (ChIP) assays demonstrate that RAR and RXR are bound to the RARE in cells. |
