Fig. 7: TAp63α accumulation is regulated at the initiating step before activation through CHK2 and CK1.
From: Oocyte death is triggered by the stabilization of TAp63α dimers in response to cisplatin
A–C Quantification of primordial follicles in ovaries treated with 20 µM ATM inhibitor (KU-55933), 20 µM CHK2 inhibitor (CK2II), and 20 µM ATR inhibitor (BEZ235) in response to 20 µM CDDP or 0.45 Gy irradiation. D Immunoblot analysis of TAp63α and GAPDH in ovaries cultured with 20 µM BEZ235 or 20 µM CK2II for 6 h. E Quantification of TAp63α and GAPDH in immunoblots. F, G Immunofluorescence assay of p-ATR and TAp63α, along with TAp63α intensity at 6 h post-treatment. H, I Histological analysis and quantification of primordial follicles in the ovaries 24 h post-exposure to 0.45 Gy irradiation, 0.45 Gy irradiation+25 µM PF-670462, 20 µM CDDP, or 20 µM CDDP + 25 µM PF-670462. Intact primordial follicles and apoptotic ones are indicated by green and blue arrowheads, respectively. J Graphic summary of TAp63α turnover in intact oocytes and the stabilization and activation cascade of TAp63α following DNA damage detection. Statistical significance: n.s. not significant; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.
