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. Author manuscript; available in PMC: 2016 Jan 1.

Published in final edited form as: Exp Cell Res. 2014 Oct 16;330(1):199–211. doi: 10.1016/j.yexcr.2014.10.003

Fig. 5 — AML cells were transfected with silencing oligonucleotides to M-CSFR before addition of 1,25D and ERK5 inhibitor XMD8-92. (A) siM-CSFR abrogated the XMD+1,25D-induced increase in M-CSFR protein levels in HL60 and U937 cells. The protein levels of a loading control, Crk-L, were not significantly altered. (B) The knock down of M-CSFR markedly diminished the effect of XMD8-92 on increasing CD11b expression and inhibition of CD14 expression in both HL60 and U937 cells. Asterisks (*) show a significant (p<0.05) decrease in cells subjected to M-CSFR knockdown, while # denotes a significant (p<0.05) increase.

Fig. 5 — AML cells were transfected with silencing oligonucleotides to M-CSFR before addition of 1,25D and ERK5 inhibitor XMD8-92. (A) siM-CSFR abrogated the XMD+1,25D-induced increase in M-CSFR protein levels in HL60 and U937 cells. The protein levels of a loading control, Crk-L, were not significantly altered. (B) The knock down of M-CSFR markedly diminished the effect of XMD8-92 on increasing CD11b expression and inhibition of CD14 expression in both HL60 and U937 cells. Asterisks (*) show a significant (p<0.05) decrease in cells subjected to M-CSFR knockdown, while # denotes a significant (p<0.05) increase.