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. 2019 Dec 9;10(12):936. doi: 10.1038/s41419-019-2177-x

Fig. 4. The LCN2-RPS3 complex inhibited P65 phosphorylation.

Fig. 4

a Immunoblot analysis of the effects of vitamin D and cisplatin treatment on NF-κB (P65) activation (p-p65); b After the inhibition of LCN2 expression, cisplatin and TNF-α stimulation had a weak effect on the expression of P-P65, whereas the expression of P-P65 in the control group was significantly increased. The treatment had little effect on the expression of RPS3; c After the upregulation of LCN2, vitamin D and NF-κB inhibitors (BAY-11-7085, P65-I in this legend) exhibited a decreased ability to inhibit P-P65 expression, and this treatment had little effect on RPS3 expression; d After the SFB tag was fused to LCN2, IP experiments were performed using an SFB tag, which revealed weak binding between LCN2 and the NF-κB pathway; e Endogenous RPS3-IP experiment: interaction between RPS3 and LCN2 and P65; f Endogenous NF-κB IP assay: NF-κB binds directly to RPS3 but not LCN2; g The RPS3-IP experiment was performed in LCN2 stable cell lines: the binding between RPS3 and P65 was decreased after LCN2 inhibition; the binding ability between RPS3 and P65 was enhanced after LCN2 expression was up-regulated. Med, culture medium; Cis, cisplatin; P65-I, p65 inhibitor.