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mTOR对衰老的调控

Senescence regulation by mTOR.

作者信息

Dulic Vjekoslav

机构信息

Institut de Génétique Moléculaire, Montpellier, France.

出版信息

Methods Mol Biol. 2013;965:15-35. doi: 10.1007/978-1-62703-239-1_2.

DOI:10.1007/978-1-62703-239-1_2
PMID:23296649
Abstract

The senescence program is activated in response to diverse stress stimuli potentially compromising genetic stability and leads to an irreversible cell cycle arrest. The mTOR pathway plays a crucial role in the regulation of cell metabolism and cellular growth. The goal of this chapter is to present evidence linking these two processes, which have one common regulator-the tumor suppressor p53. While the role of mTOR in senescence is still controversial, recent papers have shed new light onto this issue. This review, far from being exhaustive given the complexity of the field, will hopefully stimulate further research in this domain, whose relevance for ageing is becoming increasingly documented.

摘要

衰老程序会因各种可能损害基因稳定性的应激刺激而被激活,并导致不可逆的细胞周期停滞。mTOR通路在细胞代谢和细胞生长的调节中起着关键作用。本章的目的是提供证据,将这两个过程联系起来,它们有一个共同的调节因子——肿瘤抑制因子p53。虽然mTOR在衰老中的作用仍存在争议,但最近的论文为这个问题提供了新的线索。鉴于该领域的复杂性,本综述远非详尽无遗,希望能激发该领域的进一步研究,其与衰老的相关性正越来越多地得到文献记载。

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1
Senescence regulation by mTOR.mTOR对衰老的调控
Methods Mol Biol. 2013;965:15-35. doi: 10.1007/978-1-62703-239-1_2.
2
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The cell fate: senescence or quiescence.细胞命运:衰老还是静止。
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Weak p53 permits senescence during cell cycle arrest.弱 p53 允许细胞周期停滞时衰老。
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The p53 inducing drug dosage may determine quiescence or senescence.诱导p53的药物剂量可能决定细胞静止或衰老。
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The activation of the p53 pathway by the AMP mimetic AICAR is reduced by inhibitors of the ATM or mTOR kinases.AMP 模拟物 AICAR 通过 ATM 或 mTOR 激酶抑制剂激活 p53 通路的作用降低。
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Cell cycle arrest is not yet senescence, which is not just cell cycle arrest: terminology for TOR-driven aging.细胞周期停滞并非衰老,衰老不仅仅是细胞周期停滞:关于TOR驱动衰老的术语。
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mTOR Activity and Autophagy in Senescent Cells, a Complex Partnership.
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Cellular senescence and its role in white adipose tissue.细胞衰老及其在白色脂肪组织中的作用。
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Linking ABCC6 Deficiency in Primary Human Dermal Fibroblasts of PXE Patients to p21-Mediated Premature Cellular Senescence and the Development of a Proinflammatory Secretory Phenotype.将原发性进行性皮肤弹力纤维溶解症(PXE)患者的原代表皮成纤维细胞中的ABCC6缺陷与p21介导的细胞早衰及促炎分泌表型的发展联系起来。
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BMAL1 knockdown triggers different colon carcinoma cell fates by altering the delicate equilibrium between AKT/mTOR and P53/P21 pathways.BMAL1 敲低通过改变 AKT/mTOR 和 P53/P21 通路之间的微妙平衡来触发不同的结肠癌细胞命运。
Aging (Albany NY). 2020 May 10;12(9):8067-8083. doi: 10.18632/aging.103124.
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