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HDAC1 — KIT
Text-mined interactions from Literome
Liu et al., Cancer Cell 2010
(Leukemia, Myeloid) :
Our results provide evidence that the mechanisms of
Sp1/NFkappaB/HDAC/miR-29b dependent
KIT overexpression contribute to leukemia growth and can be successfully targeted by pharmacological disruption of the Sp1/NFkappaB/HDAC complex or synthetic miR-29b treatment in KIT-driven AML
Iordache et al., International journal of molecular sciences 2012
:
Furthermore, flow cytometry analysis illustrated that
HDAC inhibitors selectively
reduce the expression of VEGFR(2),
CD117 , VE-cadherin, and ICAM-1, whereas the expression of CD34 and CD45 remained unchanged, demonstrating that HDAC is involved in endothelial differentiation of progenitor cells