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THE EPITHELIAL CELL DEFAULT-PHENOTYPE HYPOTHESIS AND ITS IMPLICATIONS FOR CANCER [Review]

机译:上皮细胞默认表型假说及其对癌症的意义[综述]

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The expression of epithelial cell adhesion and cytoskeletal genes is orchestrated by an apparently unique set of rules. No tissue-specific transactivator proteins have been found to drive them; only ubiquitous factors are utilized. In nonepithelial cells, they are actively repressed. Moreover, it was recently found that a single protein (adenovirus E1a) coordinately represses non-epithelial genes while inducing epithelial genes. A simple model is offered to explain how epithelial gene expression is coordinated. Under this model, the epithelial cell gene expression program is a transcriptional 'default'; that is, it occurs in the absence of tissue-specific transactivation. Conversion to tt-iis default requires only that mesenchymal transactivators are not expressed, or that central 'integrator' proteins are inactive. In their absence, mesenchymal gene expression cannot occur. Moreover, because the repressors cease to be expressed, the epithelial genes are induced. Oncogenes generally cause the breakdown of the epithelial phenotype - generating carcinomas - so genes such as Ela that cause epithelial conversion may prove useful for both understanding and controlling cancer. [References: 37]
机译:上皮细胞粘附和细胞骨架基因的表达是通过一组明显独特的规则来协调的。没有发现组织特异性反式激活蛋白驱动它们。仅利用普遍存在的因素。在非上皮细胞中,它们被积极抑制。此外,最近发现,单个蛋白(腺病毒E1a)在诱导上皮基因的同时协同抑制非上皮基因。提供了一个简单的模型来解释上皮基因表达是如何协调的。在这种模型下,上皮细胞基因表达程序是转录的“默认值”。也就是说,它在没有组织特异性反式激活的情况下发生。转换为tt-iis默认值仅要求间质反式激活子不表达,或中枢“整合子”蛋白无活性。如果没有它们,就不会发生间充质基因表达。此外,因为阻遏物不再表达,所以诱导了上皮基因。癌基因通常会导致上皮表型的分解-产生癌症-因此,引起上皮转化的基因(例如Ela)可能对理解和控制癌症均有用。 [参考:37]

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