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致癌物诱导胚胎蛋白合成的理论机制。II. 翻译后核蛋白修饰的扰动

Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins. II. Perturbations of post-translational nuclear protein modification.

作者信息

Hancock R L

出版信息

Med Hypotheses. 1978 May-Jun;4(3):290-301. doi: 10.1016/0306-9877(78)90010-5.

Abstract

An hypothesis of carcinogenesis is derived which suggests that carcinogens initially induce derepressions of structional genes of post-translational modifying enzymes. Although the resulting cascade of changes in genic activity would be measureable because of the large number of differentiated cells present in a tissue, only stem cells are vulnerable to the neoplastic array of genic expression by virtue of their repressors being more vulnerable to conformational modification. Furthermore it is derived that there are at least three major classes of repressors and the repressors that are synthesized during embryogenesis are particularly susceptible to derepression mechanisms.

摘要

由此得出一种致癌作用假说,该假说认为致癌物最初会诱导翻译后修饰酶结构基因的去抑制。尽管由于组织中存在大量分化细胞,由此产生的基因活性变化级联是可测量的,但只有干细胞容易受到肿瘤性基因表达阵列的影响,因为它们的阻遏物更容易受到构象修饰的影响。此外,还得出至少有三大类阻遏物,并且在胚胎发育过程中合成的阻遏物特别容易受到去抑制机制的影响。

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