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首页> 外文期刊>Cell cycle >Downregulation of DeltaNp63alpha in keratinocytes by p14ARF-mediated SUMO-conjugation and degradation.
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Downregulation of DeltaNp63alpha in keratinocytes by p14ARF-mediated SUMO-conjugation and degradation.

机译：通过p14ARF介导的SUMO偶联和降解，在角质形成细胞中下调DeltaNp63alpha。

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The tumor suppressor p14(ARF) inhibits cell growth in response to oncogenic stress in a p53-dependent and independent manner. However, new physiologic roles for ARF activation have been proposed. We have previously demonstrated that ARF interacts with p63, influencing its transcriptional activity. p63 is a member of the p53 family involved in skin and limb development, as well as in the homeostasis of mature epidermis. Here, we show that, in human keratinocytes, as well as in tumor-derived cell lines, ARF targets DeltaNp63alpha, the most abundantly expressed p63 isoform, to proteasomal degradation by stimulating its sumoylation. Interestingly, we have observed an increase of ARF expression in differentiating keratinocytes, that is concomitant to the already described upregulation of SUMO2/3. Remarkably, we found that DeltaNp63alpha is preferentially sumoylated by SUMO2, instead of SUMO1, and p14(ARF) increases the efficiency of this process.
机译：肿瘤抑制因子p14（ARF）以依赖p53的方式独立于致癌应激而抑制细胞生长。然而，已经提出了ARF激活的新的生理作用。先前我们已经证明ARF与p63相互作用，影响其转录活性。 p63是p53家族的成员，参与皮肤和四肢的发育以及成熟表皮的稳态。在这里，我们显示，在人类角质形成细胞以及肿瘤来源的细胞系中，ARF通过刺激其sumoylation将ΔNp63alpha（表达最丰富的p63亚型）靶向到蛋白酶体降解。有趣的是，我们已经观察到分化角质形成细胞中ARF表达的增加，这与已经描述的SUMO2 / 3上调相关。值得注意的是，我们发现DeltaNp63alpha优先被SUMO2取代，而不是SUMO1，而p14（ARF）提高了此过程的效率。

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