Fig. 1

ΔNp63α knockdown experiments with HMECs. (a) Domain structure of human p53 and p63 isotypes. TAp63 and ΔNp63, highlighting the transactivation (TA), DNA-binding, oligomerization, and SAM domains. (b) mRNA expression concordant with positions (1)-(4) shown in Fig. 1a. hiPSCs were used as a negative control for p63. (c) Time-dependent variation in ΔNp63α and cytokeratin 14 (CK14) protein expression in p63 siRNA (sip63)- or scramble siRNA (scr)-treated HMECs. The arrow indicates the ΔNp63α protein band. (d) Representative immunofluorescence (IF) images of HMECs treated with sip63 and stained with ΔNp63 and CK14 antibodies. Red and green indicate ΔNp63 and CK14, respectively. Scale bar, 10 μm. (e, f) Time-dependent variations in ΔNp63 mRNA (e) and ΔNp63α protein (f) contained in whole-cell extracts of HMECs treated with sip63 for 24 h after irradiation. (g) Measurement of DNA damage response (DDR)-marker mRNA expression in sip63-treated HMECs. (h) Western blotting analyses of BAX and p21 proteins. (i) Comparison of EdU-positive frequencies in sip63- and scr-treated cells, which was evaluated by flow cytometry (FCM). (j) Frequencies of apoptotic cells detected by FCM in sip63- or scr-treated HMECs. All values in mRNA expression data were scaled to the expression level of GAPDH as an internal control. Data represent the means and SEs of at least three independent assays. *P < 0.05, **P < 0.01 by Student’s t test