Fig. 5: ERdj5 deficiency causes ER stress and inflammation mediated by NF-κB activation. | Experimental & Molecular Medicine

Fig. 5: ERdj5 deficiency causes ER stress and inflammation mediated by NF-κB activation.

From: ERdj5 protects goblet cells from endoplasmic reticulum stress-mediated apoptosis under inflammatory conditions

Fig. 5: ERdj5 deficiency causes ER stress and inflammation mediated by NF-κB activation.

a Expression profile of ER stress-related proteins in the colons of WT or ERdj5-KO mice treated with DSS (n = 6 per group). b Relative band intensities are expressed as the mean ± SEM. c ER stress proteins in ERdj5-KO MODE-K cells altered by the CRISPR/Cas9 system. d The level of CXCL1 in ERdj5-KO MODE-K cells after Pam3CSK4 treatment (100, 200, 500, and 1000 ng/ml) for 6 h (n = 3 per group). e The protein expression of NF-κB pathway factors in MODE-K cells treated with Pam3CSK4 (1 µg/ml) for 0, 5, 15, 30, 60, 180, and 360 min. f Nuclear translocation of NF-κB/p65 in ERdj5-KO MODE-K cells at the indicated time points after Pam3CSK4 treatment (1 µg/ml). f Immunofluorescence image (×200, scale bar 10 µm). g The mean fluorescence intensity of NF-κB/p65 (green) is shown (n = 9~27 per group). The data are representative of three independent experiments, and the values are expressed as the mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001; Student’s t test.

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