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Mammalian longevity under the protection of PARP-1's multi-facets.
Ageing Research Reviews ( IF 13.1 ) Pub Date : 2003-02-28 , DOI: 10.1016/s1568-1637(02)00062-4
Marie-Laure Muiras 1
Affiliation  

Given the presence of continuous endogenous and exogenous sources of stress, mammalian species have evolved complex systems of protection, detoxification and repair, in order to maintain homeostasis during development and until reproductive maturity for the sake of the species. However, since no system is perfect, complete prevention of damage is unlikely to occur. Accumulation of macromolecular damage, including damage to DNA and genomic instability, is considered a driving force for the ageing process and age-related diseases. One of the immediate eukaryotic cellular responses to DNA breakage is the covalent post-translational modification of nuclear proteins with poly(ADP-ribose) from NAD+ as precursor, mostly catalysed by poly(ADP-ribose) polymerase-1 (PARP-1). Poly(ADP-ribosyl)ation is involved in DNA base-excision repair (BER), DNA-damage signalling and regulation of genomic stability. In recent years, many groups have become involved in PARP field, shedding light on new partners for PARP-1, new members of the PARP family and new physiological and pathophysiological properties for the founding member of the poly(ADP-ribose) polymerase super family. The present review focuses on PARP-1 and its role in the maintenance of genome stability and in mammalian longevity.

中文翻译:

哺乳动物的寿命受PARP-1多方面保护。

鉴于存在持续的内源性和外源性应激源,哺乳动物物种已经进化出了复杂的保护,解毒和修复系统,以便在该物种的发育过程中保持稳态,直至繁殖成熟。但是,由于没有完美的系统,因此不可能完全防止损坏。大分子损伤的积累,包括对DNA的损伤和基因组的不稳定性,被认为是衰老过程和与年龄有关的疾病的驱动力。对DNA断裂的直接的真核细胞反应之一是核蛋白的共价翻译后修饰,其中NAD +的聚ADP-核糖为前体,主要由聚ADP-核糖聚合酶-1(PARP-1)催化。聚(ADP-核糖基)参与DNA碱基切除修复(BER),DNA损伤信号传导和基因组稳定性调节。近年来,许多小组都参与了PARP领域,阐明了PARP-1的新伙伴,PARP家族的新成员以及poly(ADP-核糖)聚合酶超家族的创始成员的新生理和病理生理特性。 。目前的审查集中在PARP-1及其在维持基因组稳定性和哺乳动物寿命中的作用。
更新日期:2019-11-01
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