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细胞成熟和消亡:Proteostasis崩溃

短剑聚酯薄膜^1*

¹编辑部、生物化学:一个印度日报,印度

*通信:

短剑聚酯薄膜、编辑部、生物化学:一个印度日报》电子邮件::chemicalinformatics@chemjournals.org

文摘

我们展示的结果更缓慢的解释和聚合氧化伤害,proteostasis,或崩溃,护送,随着年龄的增长和保护蛋白质的工作发生内爆。随着时间的推移,不可逆转损害蛋白质积聚,崩溃的监护人转移固体蛋白质细胞所需要的。每当替换难以置信的蛋白质的步伐永远不会再次保持意识到错误折叠所带来的疲惫的步伐,聚集,伤害,有机实体踢了踢水桶。生活术语缩写与扩展非线性温度或添加氧化剂固定在线虫线虫,而生命长度扩张与更多的陪伴或水解酶怪胎,表示的模型。它代表了龚帕兹像提升死亡率预测扩张在不同动物和人的细胞随着年龄的氧化伤害。总的来说,模型显示了蛋白质颤抖意味着伤害聚集的速度随着年龄的增长,干扰细胞的正常proteostasis平衡。细胞在高等生物衰老和死亡,因为正常的周期。考虑到原子组件是大多数细胞大分子由成熟的影响,证明很难隔离导致的结果。

评论:

我们展示的结果更缓慢的解释和聚合氧化伤害,proteostasis,或崩溃,护送,随着年龄的增长和保护蛋白质的工作发生内爆。随着时间的推移,不可逆转损害蛋白质积聚,崩溃的监护人转移固体蛋白质细胞所需要的。每当替换难以置信的蛋白质的步伐永远不会再次保持意识到错误折叠所带来的疲惫的步伐,聚集,伤害,有机实体踢了踢水桶。生活术语缩写与扩展非线性温度或添加氧化剂固定在线虫线虫,而生命长度扩张与更多的陪伴或水解酶怪胎,表示的模型。它代表了龚帕兹像提升死亡率预测扩张在不同动物和人的细胞随着年龄的氧化伤害。总的来说,模型显示了蛋白质颤抖意味着伤害聚集的速度随着年龄的增长,干扰细胞的正常proteostasis平衡。细胞在高等生物衰老和死亡,因为正常的周期。考虑到原子组件是大多数细胞大分子由成熟的影响,证明很难隔离导致的结果。氧化伤害的工作无疑是已知的。相当多的我们所熟悉的细胞成熟来自“基地”考试,这将困扰的品质一次淘汰赛,重击ins,或点变化,或者使用继承对比质量与质量信息基地。成熟的“分层”问题组件,我们接受框架是一个更广泛的失望的电话,是我们特定的担心。一个孤独的质量不能阻止成熟系统或拓宽一个人的寿命。不管什么类型的细胞内生物分子或其空间情况,氧化损害是不可预测和模糊。我们接受成熟和预期寿命带来的深远和随机删除而不是一个单独的活动。有各种各样的假设细胞成熟。质量驱动的一些理论,强调收集的影响伤害转换DNA从长远来看。转换和一致的缩短的端粒是这种变化的实例。 Different thoughts center around how changes to DNA and DNA-restricting proteins modify how qualities are perused, for example, epigenetics. DNA methylation, histone adjustment, and chromosomal association misfortune are altogether instances of these changes. Besides, modifications in histone stoichiometry and serious exhaustion of histone levels could influence record factor restricting. Such changes could be to be faulted for the maturing related loss of proper courier RNA and protein stoichiometry. One more hypothesis is that maturing is brought about by weakening of protein quality-control frameworks associated with protein combination, corruption, and escorting, which are answerable for safeguarding the proteins in the phone's proteome. The decrease in protein quality control, which is integral to proteostasis, has been connected to in excess of 50 infections described by strange protein testimony (proteinopathies), the principle hazard factor for which is propelling age, "likely on the grounds that cell guideline and protein creation and removal become progressively compromised with age. "Proteostasis is a characteristic reason for maturing since it is the principal line of guard against pressure and in light of the fact that proteins are the phone's essential repairers and maintainers." All known gerontogenes give pressure opposition," as indicated by the specialists. Protein oxidation is a preferred indicator of radiation endurance over DNA harm, so protein harm is a vital proportion of such obstruction. Protein harm can bring about a deficiency of security and capacity, as well as challenges with protein blend and corruption. Protein harm is just one of many changes that influence the proteome as individuals progress in years, however it is a huge element. We're keen on the cell-wide biophysics of how proteins overlap, the impacts of temperature and oxidation, and how proteostasis decays with age, rather than the hereditary qualities and organic chemistry of a specific quality or protein. Proteostasis models in the past have commonly centered around the component of hotness shock initiation or the instruments through which chaperone frameworks advance collapsing. Others have looked for more extensive rules that decide collapsing yield or how collapsing and corruption are divided. While these examinations have added to a superior comprehension of protein properties upstream of harm, their downstream properties and impacts have gotten less consideration. Our recreations check out the effect of protein conformity on oxidizability, as well as the job of harmed proteins in redirecting scant chaperone assets from their whole partners' collapsing. In the worm C. elegans, we show how proteostasis lessens with age. The idea clarifies two exceptional trial perceptions, in particular, that when worms are raised in heat or with an extra oxidant, their life expectancy lessens by two significant degrees. Most significantly, the模型澄清如何走出protein-collapsing显著的依赖能源和氧化剂的外来蛋白质放行。因此,最突出的地区之一成熟的非线性扩张死亡率随着年龄的增长有一个系统,称为龚珀兹法。依靠增加多少不可逆转损害蛋白质作为个人变得更成熟,将陪伴崩溃的声音,细胞需要的蛋白质。每当替换的蛋白质的速度在这一点上没有准备好待知道不幸的步伐,因为伤害和收集,有机实体踢了踢水桶。相比之下的无情的爆炸伤害,增加成熟的蛋白质组被认为是一个直接后果更慢的蛋白质融合和营业额