学术报告

报告题目：p53 isoforms ∆133p53/∆113p53 are p53-target genes that antagonize p53 apoptotic activity via Bcl2 activation
报 告 人：Chen Jun 博士
报告时间：2008年4月2日下午3：00
报告地点：生物二馆122会议室

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p53 isoforms ∆133p53/∆113p53 are p53-target genes that antagonize p53 apoptotic activity via Bcl2 activation

p53 is a well-known tumor suppressor and is also involved in processes of organismal aging and developmental control. A recent exciting development in the p53 field is the discovery of various p53 isoforms. One p53 isoform is human ∆133p53 and its zebrafish counterpart ∆113p53. These N-terminal truncated p53 isoforms are initiated from an alternative p53 promoter but their expression regulation and physiological significance are not well understood. We show here that both zebrafish ∆113p53 and human ∆133p53 are p53-dependent genes and are directly induced by full length p53 in response to DNA-damaging signals. More importantly, we show that knock-down of the ∆113p53 in zebrafish or ∆133p53 in human cells modulate gene expression enhancing p53-mediated apoptosis under stress conditions. Finally, we show that ∆113p53 and ∆133p53 antagonize p53-induced apoptosis via activating the Bcl2 gene. Thus, the p53 genetic locus contains a new p53-response gene that negatively regulates p53-induced apoptosis via selectively activating an anti-apoptotic pathway. Our results suggest that modulation of p53 pathway by p53 isoforms might have an impact on p53 tumor suppressor activity.

Chen Jun 博士 CV