蛋白质折叠、细胞压力和癌症。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
Armando Aranda-Anzaldo, Myrna A.R. Dent, Edith Segura-Anaya, Alejandro Martínez-Gómez
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引用次数: 0

摘要

蛋白质被认为是基因型的表型表现,因为蛋白质编码基因携带着构成蛋白质的氨基酸串的信息。人们普遍认为,蛋白质的功能取决于细胞内实现的相应 "原生 "结构或折叠,而原生蛋白质折叠对应于特定蛋白质的最低自由能最小值。然而,蛋白质在细胞内的折叠是一个非确定的耗散过程,相同的输入可能产生不同的结果,因此折叠蛋白质的构象异质性是常规而非例外。细胞内环境的局部变化会促进蛋白质折叠的变化。因此,蛋白质折叠需要大量伴侣和辅助伴侣的 "监督",它们帮助客户蛋白质根据当地环境实现最稳定的折叠。在细胞应激反应(CSRs)的帮助下,这种环境对蛋白质折叠的影响不断传递,这可能会导致蛋白质之间的接触规则发生变化,因此相应的蛋白质相互作用组可能会被环境所改变,从而导致另一种细胞表型。这使得表型具有可塑性,有助于在细胞水平上适应突变和/或短暂的环境变化。从这个角度出发,我们在下文中提出这样一个论点:持续的细胞压力加上高效的 CSR,可能会导致细胞蛋白质组(以及相应的相互作用组)适应这种压力条件,从而选择一种异常表型,这可能是导致癌症的常见表观遗传学途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Protein folding, cellular stress and cancer

Proteins are acknowledged as the phenotypical manifestation of the genotype, because protein-coding genes carry the information for the strings of amino acids that constitute the proteins. It is widely accepted that protein function depends on the corresponding “native” structure or folding achieved within the cell, and that native protein folding corresponds to the lowest free energy minimum for a given protein. However, protein folding within the cell is a non-deterministic dissipative process that from the same input may produce different outcomes, thus conformational heterogeneity of folded proteins is the rule and not the exception. Local changes in the intracellular environment promote variation in protein folding. Hence protein folding requires “supervision” by a host of chaperones and co-chaperones that help their client proteins to achieve the folding that is most stable according to the local environment. Such environmental influence on protein folding is continuously transduced with the help of the cellular stress responses (CSRs) and this may lead to changes in the rules of engagement between proteins, so that the corresponding protein interactome could be modified by the environment leading to an alternative cellular phenotype. This allows for a phenotypic plasticity useful for adapting to sudden and/or transient environmental changes at the cellular level. Starting from this perspective, hereunder we develop the argument that the presence of sustained cellular stress coupled to efficient CSRs may lead to the selection of an aberrant phenotype as the resulting adaptation of the cellular proteome (and the corresponding interactome) to such stressful conditions, and this can be a common epigenetic pathway to cancer.

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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
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