| Nup98 functions as a potential tumor suppressor and regulates posttranscriptional expression of select p53 target genes. | None |
| the recurrent NUP98-CCDC28A is an oncogene that induces a rapid and transplantable myeloid neoplasm in recipient mice. They also provide additional evidence for an alternative leukemogenic mechanism for NUP98 oncogenes. | neoplasm, |
| Data indicate that loss of cyclin-dependent kinase inhibitor p15 (p15Ink4b) collaborates with oncogene fusion protein Nup98-HoxD13 transgene in the development of predominantly myeloid neoplasms. | neoplasm, |
| Oncogenic interaction between BCR-ABL and NUP98-HOXA9 demonstrated by the use of an in vitro purging culture system. | None |
| The oncogene Nup98-HOXA9 induces gene transcription in myeloid cells. | None |
| Dissection of the transformation of primary human hematopoietic cells by the oncogene NUP98-HOXA9. | None |
| Effects of the NUP98-DDX10 oncogene on primary human CD34+ cells: role of a conserved helicase motif. | None |
| Amino-terminal enhancer of split (AES) interacts with the oncoprotein NUP98-HOXA9 and enhances its transforming ability. | None |
| Functional analysis of the NUP98-CCDC28A fusion protein. | None |
| Molecular basis for the anchoring of proto-oncoprotein Nup98 to the cytoplasmic face of the nuclear pore complex. | None |
| Homeobox partners create more potent NUP98 fusion oncogenes than do non-homeobox partners. | None |
| NUP98 oncoproteins predispose myeloid cells to oncogenic transformation or malignant progression by promoting whole chromosome instability. | None |
| AF10 regulates progressive H3K79 methylation and HOX gene expression in diverse AML subtypes. | None |
| Results provide evidence that transformation driven by MLL fusions as well as the recurrent AML-associated NUP98-NSD1 fusion oncogene is critically dependent on the ability of AF10 to stimulate DOT1L activity. | None |