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KIT — MYLIP

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
Lee et al., Blood 2011 (Mastocytosis, Systemic) : We found that miR-539 and miR-381 are down-regulated by KIT signaling and they repressed MITF expression through conserved miRNA binding sites in the MITF 3'-untranslated region
Gao et al., Zhongguo Shi Yan Xue Ye Xue Za Zhi 2011 : The aim of this study was to investigate the effect of microRNA-193b (miR-193b) on C-KIT protein expression and biological behaviors in K562 cells ... Compared with the negative control group, overexpression of miR-193b in K562 cells significantly inhibited the levels of C-KIT and phosphorylated C-KIT protein ... It is concluded that miR-193b can reduce C-KIT expression and inhibit cell growth in K562 cells
Li et al., Blood 2013 (Leukemia, Myeloid, Acute) : Suppression of miR-193a expands the oncogenic activity of the fusion protein AML-ETO, because miR-193a represses the expression of multiple target genes, such as AML1/ETO, DNMT3a, HDAC3, KIT , CCND1, and MDM2 directly, and increases PTEN indirectly