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. 2018 Jun 26;9(49):29146–29161. doi: 10.18632/oncotarget.25635

Figure 7. Model of how either TP63 or Δ133TP53 may regulate expression of IFN-γ signalling genes in different breast cancer subsets.

Figure 7

(A) In the absence of ER signalling and wtTP53, TAp63 can bind the promoter of genes involved in IFN-γ signalling. (B) In the absence of ER signalling and presence of mTP53, TAp63 is blocked by mp53 and hence cannot bind gene promoters. (C) In the presence of ER signalling and wtTP53, TAp63 transcriptional activity is blocked by binding Δ133p53. (D) In the presence of ER signalling and mTP53, mp53 can bind and inhibit TAp63. Mp53 however can no longer bind to gene promoters, thus allowing Δ133p53 to access the promoter and turn on the expression of these genes.