Accumulation of p53 in a mutant cell line defective in the ubiquitin pathway.
Accumulation of p53 in a mutant cell line defective in the ubiquitin pathway.
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p53 在泛素途径缺陷的突变细胞系中积累。
DOI：
10.1128/mcb.14.3.1997-2003.1994
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发表时间：
1994
影响因子：
5.3
通讯作者：
Ozer,HL
中科院分区：
文献类型：
--
作者：
Chowdary,DR;Dermody,JJ;Jha,KK;Ozer,HL
野生型p53基因产物在控制细胞增殖、分化和存活中起着重要作用。功能改变通常与p53稳定性的改变有关。我们利用来自小鼠细胞系BALB/c 3T3的温度敏感突变体ts20，研究了泛素化途径在p53降解中的作用。我们发现野生型p53显著积累，因为当细胞转移到限制温度时，分解减少。引入编码人类泛素激活酶El的序列，纠正了温度敏感性缺陷ints20，并防止了p53的积累。因此，这些数据强烈表明野生型p53通过泛素介导的蛋白水解途径在细胞内降解。
The wild-type p53 gene product plays an important role in the control of cell proliferation, differentiation, and survival. Altered function is frequently associated with changes in p53 stability. We have studied the role of the ubiquitination pathway in the degradation of p53, utilizing a temperature-sensitive mutant,ts20, derived from the mouse cell line BALB/c 3T3. We found that wild-type p53 accumulates markedly because of decreased breakdown when cells are shifted to the restrictive temperature. Introduction of sequences encoding the human ubiquitin-activating enzyme El corrects the temperature sensitivity defect ints20and prevents accumulation of p53. The data therefore strongly indicate that wild-type p53 is degraded intracellularly by the ubiquitin-mediated proteolytic pathway.