The histone acetyl transferase activity of monocytic leukemia zinc finger is critical for the proliferation of hematopoietic precursors

Crosstalk between leukemia-associated proteins MOZ and MLL regulates HOX gene expression in human cord blood CD34+ cells

“…This domain remains intact in fusion proteins from chromosome translocations in related leukemia (Yang and Ullah, 2007), suggesting that MLL may also interact with the leukemic fusion proteins. In addition, depletion of MOZ as well as depletion of MLL affect CD34 þ cells commitment to myeloid progenitors, suggesting a role of each of these proteins in myelopoiesis and thus corroborating the observations made with Moz knockout mice (Katsumoto et al, 2006;Thomas et al, 2006;Perez-Campo et al, 2009). Additional studies will be needed to determine whether the cooperation between MOZ and MLL may explain the partially common leukemogenic pathway observed in MOZ-and MLL-rearranged leukemias (Camos et al, 2006).…”

“…Additional studies will be needed to determine whether the cooperation between MOZ and MLL may explain the partially common leukemogenic pathway observed in MOZ-and MLL-rearranged leukemias (Camos et al, 2006). This pathway may possibly involve altered Hox genes expression and the associated deficiencies observed in hematopoietic stem cells from Mll or Moz knockout cells (Katsumoto et al, 2006;Terranova et al, 2006;Thomas et al, 2006;Jude et al, 2007;McMahon et al, 2007;Perez-Campo et al, 2009).…”

“…MOZ is a coactivator of various transcription factors particularly with hematopoietic specificity, such as RUNX1 (AML1) or Spi-1/ PU.1 (Kitabayashi et al, 2001;Katsumoto et al, 2006). Analysis of Moz knockout mice suggested its important role in the maintenance of hematopoietic stem cells and differentiation of myeloid cells (Katsumoto et al, 2006;Thomas et al, 2006;Perez-Campo et al, 2009).…”

Epigenetic regulation of aging stem cells

“…Members of the MYST family of HATs have likewise been implicated in tissuespecific stem cell function. For example, MYST3/MOZ is necessary for self-renewal of embryonic HSCs, as shown by decreased numbers of stem and early progenitors and decreased long-term repopulating capacity of HSCs in Moz mutants (Katsumoto et al, 2006;Thomas et al, 2006;Perez-Campo et al, 2009). The role of MOZ in adult HSCs has not yet been determined due to embryonic lethality of Moz-deficient mouse mutants, but MOZ is likely to play a similar role in adult HSC self-renewal.…”

MOZ-TIF2 Fusion Protein Binds to Histone Chaperon Proteins CAF-1A and ASF1B Through Its MOZ Portion

“…MOZ -/-mice died at embryonic day 15 and exhibited a significant decrease of mature erythrocytes (Katsumoto et al, 2006). The histone acetyltransferase activity of MOZ is required to maintain normal functions of hematopoietic stem cells (HSC) (Perez-Campo et al, 2009). Mice with mutation at HAT or MYST domain (G657E) showed a decreased population of HSC in fetal liver.…”