期刊
CELL REPORTS
卷 3, 期 1, 页码 116-127出版社
CELL PRESS
DOI: 10.1016/j.celrep.2012.12.016
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资金
- Medical Research Council (MRC) UK
- LLS SCOR [7132-08]
- STARR Cancer Consortium
- Burroughs Welcome Foundation
- Chemotherapy Foundation
- Wellcome Trust [090532/Z/09/Z]
- MRC Hub grant [G0900747 91070]
- Medical Research Council [MC_UU_12009/6, 1145012, G1000801h, 1148235, MC_UU_12009/2] Funding Source: researchfish
- MRC [MC_UU_12009/2, MC_UU_12009/6] Funding Source: UKRI
The Mixed Lineage Leukemia (MLL) protein is an important epigenetic regulator required for the maintenance of gene activation during development. MLL chromosomal translocations produce novel fusion proteins that cause aggressive leukemias in humans. Individual MLL fusion proteins have distinct leukemic phenotypes even when expressed in the same cell type, but how this distinction is delineated on a molecular level is poorly understood. Here, we highlight a unique molecular mechanism whereby the RUNX1 gene is directly activated by MLL-AF4 and the RUNX1 protein interacts with the product of the reciprocal AF4-MLL translocation. These results support a mechanism of transformation whereby two oncogenic fusion proteins cooperate by activating a target gene and then modulating the function of its downstream product.
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