Fig. 7
From: TAZ maintains telomere length in TNBC cells by mediating Rad51C expression
Working model of TAZ regulating telomere length in TNBC cells. In TAZ-knocked down TNBC cells, the binding of TAZ-TEADs to the promoter of Rad51C was decreased, and the transcription of Rad51C was further impaired. Lack of Rad51C causes the telomere shortening and impaired telomere functions. The protein levels of shelterin components is decreased, along with increased telomere-induced DNA damage foci (TIF) and DDR activation. Moreover, the increased levels of TERRAs in TAZ-deficient cells may also contribute to the observed telomere loss phenotype