Skip to main content
. 2018 Oct 23;38(11):1787–1801. doi: 10.1038/s41388-018-0551-2

Fig. 4.

Fig. 4

Stat6 regulates IEC death and alkylating-inducing DNA damage al. ac Immunohistochemical staining and index of cleaved CASPASE 3 expression in unchallenged (d0) and AOM-treated (8 h) WT and Stat6−/− IEC (WT d0 n = 6; Stat6−/− d0 n = 3; WT 8 h AOM n = 8; Stat6−/− 8 h AOM n = 6); df Immunohistochemical staining and index of cleaved CASPASE 3 expression in IEC on day 8 (d 8) of the CAC model (n = 5/genotype); g, h Immunohistochemical staining and index of p-H2AX in AOM-treated (4 h) WT and Stat6−/− IEC (WT 4 h AOM n = 7; Stat6−/− 4 h AOM n = 6); i Immunoblot analysis of H2AX phosphorylation and STAT6 in WT (Stat6+/+) and Stat6−/− colonic organoids treated 2.5 h with 25 μM MNNG or 0.03% DMSO in PBS (sham). β-actin as loading control; j Immunoblot analysis of p-ATM, p-CHK2, IRE1-a, p-EIF2A, p-PERK, CHOP, BCL-XL, BCL-2, BAX, and STAT6 performed with IEC lysates from unchallenged (d0) or AOM-treated (4 h) mice. β-actin as loading control; k, l Immunohistochemical staining and index of p-P53 S15 expression in unchallenged (d0) and AOM-treated (8 h) WT and Stat6−/− IEC (WT d0 n = 6; Stat6−/− d0 n = 3; WT 8 h AOM n = 9; Stat6−/− 8 h AOM n = 6). Data are mean ± SEM