西亚试剂：Axin determines cell fate by controlling the p53 activation

Axin determines cell fate by controlling the p53 activation threshold after DNA damage

Qinxi Li1,2, Shuyong Lin1,2, Xuan Wang1,2, Guili Lian1, Zailian Lu1, Huiling Guo1, Ka Ruan1, Yanhai Wang1, Zhiyun Ye1, Jiahuai Han1 & Sheng-Cai Lin1

Cells can undergo either cell-cycle arrest or apoptosis after genotoxic stress, based on p53 activity1, 2, 3, 4, 5, 6. Here we show that cellular fate commitment depends on Axin forming distinct complexes with Pirh2, Tip60, HIPK2 and p53. In cells treated with sublethal doses of ultra-violet (UV) radiation or doxorubicin (Dox), Pirh2 abrogates Axin-induced p53 phosphorylation at Ser 46 catalysed by HIPK2, by competing with HIPK2 for binding to Axin. However, on lethal treatment, Tip60 interacts with Axin and abrogates Pirh2–Axin binding, forming an Axin–Tip60–HIPK2–p53 complex that allows maximal p53 activation to trigger apoptosis. We also provide evidence that the ATM/ATR pathway mediates the Axin–Tip60 complex assembly. An axin mutation promotes carcinogenesis in AxinFu/+ (Axin-Fused) mice, consistent with a dominant-negative role for AxinFu in p53 activation. Thus, Axin is a critical determinant in p53-dependent tumour suppression in which Pirh2 and Tip60 have different roles in triggering cell-cycle arrest or apoptosis depending on the severity of genotoxic stress.

1 Key Laboratory for Cell Biology and Tumor Cell Engineering of the Ministry of Education, School of Life Sciences, Xiamen University, Fujian 361005, China.
2 These authors contributed equally to this work.

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