作者: H. You , K. Yamamoto , T. W. Mak
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摘要: The tumor suppressor p53 can trigger cell death independently of its transcriptional activity through subcellular translocation and activation proapoptotic Bcl-2 family members. regulation such endogenous in response to stress remains largely unknown. Here we show that nuclear, activated FOXO3a could impair activity. However, either on serum starvation or by expressing a constitutively active form induce p53-dependent apoptosis, even cells bearing transcriptionally inactive p53. Furthermore, promote cytoplasmic accumulation increasing association with nuclear exporting machinery. Our data also suggest PUMA Bax are required for apoptosis manner is independent