Cell regulation by the Apc protein.: Apc as master regulator of epithelia
Cell regulation by the Apc protein.: Apc as master regulator of epithelia
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DOI：
10.1016/j.ceb.2008.02.001
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发表时间：
2008-04-01
影响因子：
7.5
通讯作者：
Nathke, Inke S.
中科院分区：
文献类型：
--
作者：
McCartney, Brooke M.;Nathke, Inke S.
腺瘤性大肠息肉病（Apc）蛋白参与了许多控制上皮组织的基本细胞过程：Apc直接参与调节β -连环蛋白的可用性，用于Tcf/ LEF转录因子的转录抑制，它有助于间期和有丝分裂微管的稳定性，并影响f -肌动蛋白的动力学。因此，Apc直接或间接地参与细胞的增殖、分化、迁移和凋亡。这种特殊的多功能性可以解释为什么Apc的破坏对肠道上皮尤其有害，因为Apc突变在大多数癌症中都很常见。我们总结了最近的数据，阐明了参与Apc不同功能的分子机制。
The adenomatous polyposis coli (Apc) protein participates in many of the fundamental cellular processes that govern epithelial tissues: Apc is directly involved in regulating the availability of beta-catenin for transcriptional cle-repression of Tcf/ LEF transcription factors, it contributes to the stability of microtubules in interphase and mitosis, and has an impact on the dynamics of F-actin. Thus Apc contributes directly and/or indirectly to proliferation, differentiation, migration, and apoptosis. This particular multifunctionality can explain why disruption of Apc is especially detrimental for the epithelium of the gut, where Apc mutations are common in most cancers. We summarise recent data that shed light on the molecular mechanisms involved in the different functions of Apc.