| First Author | Zhu J | Year | 2007 |
| Journal | Cancer Cell | Volume | 12 |
| Issue | 1 | Pages | 23-35 |
| PubMed ID | 17613434 | Mgi Jnum | J:122822 |
| Mgi Id | MGI:3715569 | Doi | 10.1016/j.ccr.2007.06.004 |
| Citation | Zhu J, et al. (2007) RXR Is an Essential Component of the Oncogenic PML/RARA Complex In Vivo. Cancer Cell 12(1):23-35 |
| abstractText | Although PML-enforced RARA homodimerization allows PML/RARA to bind DNA independently of its coreceptor RXR, the latter was identified within the PML/RARA complex. We demonstrate that a PML/RARA mutant defective for RXR binding fails to trigger APL development in transgenic mice, although it still transforms primary hematopoietic progenitors ex vivo. RXR enhances PML/RARA binding to DNA and is required for rexinoid-induced APL differentiation. In RA-treated PML/RARA-transformed cells, the absence of RXR binding results in monocytic, rather than granulocytic, differentiation. PML/RARA enhances posttranslational modifications of RXRA, including its sumoylation, suggesting that PML-bound sumoylation enzymes target RXRA and possibly other PML/RARA-bound chromatin proteins, further contributing to deregulated transcription. Thus, unexpectedly, RXR contributes to several critical aspects of in vivo transformation. |
