The MOZ gene was initially isolated as a consequence of two variant translocations that were identified in a distinct subtype of acute myeloid leukemias and resulted in the formation of MOZ fusion proteins. These fusions involve the HAT domain of MOZ with the activation domain of either transcriptional co-activator protein TIF2/GRIP1 or CBP, and lead to enhanced transcriptional activation by a mechanism involving aberrant histone acetylation. Additional MOZ-related proteins, including MORF (MOZrelated factor) and TIP60 (TAT-interacting proteins 60), share significant similarities with MOZ including the putuative HAT domain. TIP60 was originally identified as a co-activator for the HIV TAT protein and also functions as a nuclear hormone receptor co-activator that enhances ligand dependent steroid receptor-mediated transactivation involving the androgen, estrogen and progesterone receptors.
