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Prof Andreas Strasser 生物论坛讲座5月28日4:30pm生物新馆143



下周一(05/28/2012)下午430pm (生物新馆NBB, Rm143)我们邀请了Prof Andreas Strasser (Walter and Eliza Hall Institute, Australia) 来为我们的生物论坛作报告。

Prof Strasser 在细胞凋亡及肿瘤发生方面做了非常具有开创性的工作,在这个领域也具有很高的地位。他也是澳大利亚科学院的院士。





How does p53, the most important gene in human cancer, suppress tumour development?




The tumour suppressor p53, called the guardian of the genome, is mutated in ~50% of human cancers. p53 functions as a transcription factor. It can be activated by diverse stress stimuli, most notably DNA damage, hypoxia and deregulated activation of certain oncogenes (e.g. c-myc). Once activated, p53 can transcriptionally induce a range of  several effector processes, such as cell cycle arrest, apoptotic cell death, cellular senescence and coordination of DNA repair. For several of these effector processes it is not clear which p53 target genes are essential for their initiation and, perhaps even more importantly, it is still not known which

p53 effector processes are critical for its ability to suppress tumour development.

We have discovered that Puma and (to a lesser extent) Noxa, two pro-apoptotic BH3-only members of the Bcl-2 protein family, are essential and sufficient for the apoptosis inducing action of p53. We also found that other p53 target genes that were reported to be critical for its ability to trigger apoptosis, are dispensable for this process. In addition we found that Puma and Noxa are also essential for the ability of p63, a close relative of p53, to trigger apoptosis in primordial follicle oocytes, the cells that maintain female fertility. Remarkably, female mice lacking Puma (or both Puma and Noxa) that had been exposed to a sterilising dose of g-irradiation, could produce normal numbers of healthy (phenotypically normal) offspring. Finally, using mouse models of tumour development, we revealed that induction of apoptosis by p53 is not critical for its ability to suppress cancer development. We are currently using several genetic screens to identify the processes activated by p53 that are essential for its ability to suppress tumour development.

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