| First Author | Moreno-Miralles I | Year | 2005 |
| Journal | J Biol Chem | Volume | 280 |
| Issue | 48 | Pages | 40097-103 |
| PubMed ID | 16199529 | Mgi Jnum | J:132783 |
| Mgi Id | MGI:3776951 | Doi | 10.1074/jbc.M506855200 |
| Citation | Moreno-Miralles I, et al. (2005) The inv(16) cooperates with ARF haploinsufficiency to induce acute myeloid leukemia. J Biol Chem 280(48):40097-103 |
| abstractText | The inv(16) is one of the most frequent chromosomal translocations associated with acute myeloid leukemia (AML) and creates a chimeric fusion protein consisting of most of the runt-related X1 co-factor, core binding factor beta fused to the smooth muscle myosin heavy chain MYH11. Expression of the ARF tumor suppressor is regulated by runt-related X1, suggesting that the inv(16) fusion protein (IFP) may repress ARF expression. We established a murine bone marrow transplant model of the inv(16) in which wild type, Arf+/-, and Arf-/- bone marrow were engineered to express the IFP. IFP expression was sufficient to induce a myelomonocytic AML even when expressed in wild type bone marrow, yet removal of only a single allele of Arf greatly accelerated the disease, indicating that Arf is haploinsufficient for the induction of AML in the presence of the inv(16). |
