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KIT — RBBP7

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