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首页> 外文期刊>Cell cycle >Depletion of ribosomal protein L37 occurs in response to DNA damage and activates p53 through the L11/MDM2 pathway.
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Depletion of ribosomal protein L37 occurs in response to DNA damage and activates p53 through the L11/MDM2 pathway.

机译：核糖体蛋白L37的耗竭是对DNA损伤的响应，并通过L11 / MDM2途径激活p53。

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Perturbation of ribosomal biogenesis has recently emerged as a relevant p53-activating pathway. This pathway can be initiated by depletion of certain ribosomal proteins, which is followed by the binding and inhibition of MDM2 by a different subset of ribosomal proteins that includes L11. Here, we report that depletion of L37 leads to cell cycle arrest in a L11- and p53-dependent manner. DNA damage can initiate ribosomal stress, although little is known about the mechanisms involved. We have found that some genotoxic insults, namely, UV light and cisplatin, lead to proteasomal degradation of L37 in the nucleoplasm and to the ensuing L11-dependent stabilization of p53. Moreover, ectopic L37 overexpression can attenuate the DNA damage response mediated by p53. These results support the concept that DNA damage-induced proteasomal degradation of L37 constitutes a mechanistic link between DNA damage and the ribosomal stress pathway, and is a relevant contributing signaling pathway for the activation of p53 in response to DNA damage.
机译：核糖体生物发生的扰动最近已作为相关的p53激活途径出现。该途径可以通过消耗某些核糖体蛋白来启动，然后通过包括L11在内的另一种核糖体蛋白子集对MDM2的结合和抑制。在这里，我们报告说，L37的耗竭以L11和p53依赖的方式导致细胞周期停滞。 DNA损伤可引发核糖体应激，尽管有关机制尚不清楚。我们发现，某些遗传毒性损伤，即紫外线和顺铂，会导致核仁中L37的蛋白酶体降解，并导致随后的p53依赖L11的稳定。此外，异位L37的过表达可以减弱p53介导的DNA损伤反应。这些结果支持了这样的概念，即L37的DNA损伤诱导的蛋白酶体降解构成了DNA损伤与核糖体应激途径之间的机械联系，并且是响应于DNA损伤而激活p53的相关促成信号途径。

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