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首页> 外文期刊>Molecular and Cellular Biology >The MYC-Associated Protein CDCA7 Is Phosphorylated by AKT To Regulate MYC-Dependent Apoptosis and Transformation
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The MYC-Associated Protein CDCA7 Is Phosphorylated by AKT To Regulate MYC-Dependent Apoptosis and Transformation

机译：AKT将MYC相关蛋白CDCA7磷酸化，以调节MYC依赖性细胞凋亡和转化。

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Cell division control protein A7 (CDCA7) is a recently identified target of MYC-dependent transcriptional regulation. We have discovered that CDCA7 associates with MYC and that this association is modulated in a phosphorylation-dependent manner. The prosurvival kinase AKT phosphorylates CDCA7 at threonine 163, promoting binding to 14-3-3, dissociation from MYC, and sequestration to the cytoplasm. Upon serum withdrawal, induction of CDCA7 expression in the presence of MYC sensitized cells to apoptosis, whereas CDCA7 knockdown reduced MYC-dependent apoptosis. The transformation of fibroblasts by MYC was reduced by coexpression of CDCA7, while the non-MYC-interacting protein Δ(156–187)-CDCA7 largely inhibited MYC-induced transformation. These studies provide insight into a new mechanism by which AKT signaling to CDCA7 could alter MYC-dependent growth and transformation, contributing to tumorigenesis.
机译：细胞分裂控制蛋白A7（CDCA7）是最近确定的MYC依赖转录调控的目标。我们发现CDCA7与MYC关联，并且该关联以磷酸化依赖性方式被调节。生存前激酶AKT在苏氨酸163处使CDCA7磷酸化，从而促进与14-3-3的结合，与MYC的解离以及对细胞质的隔离。血清停药后，在存在MYC的情况下诱导CDCA7表达可使细胞对细胞凋亡敏感，而CDCA7抑制可减少MYC依赖性细胞凋亡。 CDCA7的共表达减少了MYC对成纤维细胞的转化，而非MYC相互作用蛋白Δ（156–187）-CDCA7在很大程度上抑制了MYC诱导的转化。这些研究提供了一种新机制的洞察力，AKT信号转导至CDCA7可以改变MYC依赖性生长和转化，从而促进肿瘤发生。

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