Fuchs S Y, Adler V, Buschmann T, Wu X, Ronai Z
Ruttenberg Cancer Center, Mount Sinai School of Medicine, New York, NY 10029, USA.
Oncogene. 1998 Nov 12;17(19):2543-7. doi: 10.1038/sj.onc.1202200.
Key to p53 ability to mediate its multiple cellular functions lies in its stability. In the present study we have elucidated the mechanism by which Mdm2 regulates p53 degradation. Using in vitro and in vivo ubiquitination assays we demonstrate that Mdm2 association with p53 targets p53 ubiquitination. Exposure of cells to UV-irradiation inhibits this targeting. Mdm2 which is deficient in p53 binding failed to target p53 ubiquitination, suggesting that the association is essential for Mdm2 targeting ability. While mdm2-p53 complex is found in non-stressed cells, the amount of p53-bound mdm2 is decreased after UV-irradiation, further pointing to the relationship between mdm2 binding and p53 level. Similar to Swiss 3T3 cells, the dissociation of mdm2-p53 complex was also found in UV-treated Scid cells, lacking functional DNA-PK, suggesting that DNA-PK is not sufficient for dissociating mdm2 from p53. Together our studies point to the role of Mdm2, as one of p53-associated proteins, in targeting p53 ubiquitination.
p53介导其多种细胞功能的关键在于其稳定性。在本研究中,我们阐明了Mdm2调节p53降解的机制。通过体外和体内泛素化试验,我们证明Mdm2与p53的结合靶向p53的泛素化。将细胞暴露于紫外线照射下会抑制这种靶向作用。缺乏p53结合能力的Mdm2无法靶向p53的泛素化,这表明这种结合对于Mdm2的靶向能力至关重要。虽然在未受应激的细胞中发现了mdm2-p53复合物,但紫外线照射后与p53结合的mdm2量减少,这进一步表明了mdm2结合与p53水平之间的关系。与瑞士3T3细胞类似,在缺乏功能性DNA-PK的紫外线处理的Scid细胞中也发现了mdm2-p53复合物的解离,这表明DNA-PK不足以使mdm2与p53解离。我们的研究共同表明,作为与p53相关的蛋白质之一,Mdm2在靶向p53泛素化方面发挥着作用。