The p53 network: cellular and systemic DNA damage responses in aging and cancer.
The p53 network: cellular and systemic DNA damage responses in aging and cancer.
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DOI：
10.1016/j.tig.2011.12.002
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发表时间：
2012-03
影响因子：
11.4
通讯作者：
Schumacher, Bjoern
中科院分区：
文献类型：
--
作者：
Reinhardt, H. Christian;Schumacher, Bjoern
基因组的不稳定性有助于癌症的发展，并加速与年龄相关的病理，由基因组维持机制缺陷引起的各种先天性癌症易感性和孕激素综合征就是明证。通过抑癌基因P53介导的DNA损伤反应通路在细胞对基因组不稳定的内在反应中发挥着重要作用，包括短暂的细胞周期停滞、衰老和凋亡。衰老和凋亡都是强大的肿瘤抑制途径，可以防止转化细胞的失控增殖。然而，这两种途径都有可能耗尽干细胞库和祖细胞库，从而促进组织退化和器官衰竭，这两个都是衰老的标志。P53信号还参与介导与天然免疫系统的非细胞自主相互作用，并参与衰老过程中的系统调节。因此，P53靶基因网络在癌症预防和衰老生理方面起着重要的调节作用。
Genome instability contributes to cancer development and accelerates age-related pathologies as evidenced by a variety of congenital cancer susceptibility and progeroid syndromes that are caused by defects in genome maintenance mechanisms. DNA damage response pathways that are mediated through the tumor suppressor p53 play an important role in the cell intrinsic responses to genome instability, including a transient cell cycle arrest, senescence and apoptosis. Both senescence and apoptosis are powerful tumor suppressive pathways preventing the uncontrolled proliferation of transformed cells. However, both pathways can potentially deplete stem and progenitor cell pools, thus promoting tissue degeneration and organ failure, which are both hallmarks of aging. p53 signaling is also involved in mediating non-cell autonomous interactions with the innate immune system and in the systemic adjustments during the aging process. The network of p53 target genes thus functions as an important regulator of cancer prevention and the physiology of aging.
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影响因子：
11.2
作者：
Bavik, C;Coleman, I;Nelson, PS
通讯作者：
Nelson, PS
影响因子：
64.8
作者：
Bartkova, J;Horejsi, Z;Bartek, J
通讯作者：
Bartek, J
影响因子：
64.8
作者：
Bartkova, Jirina;Rezaei, Nousin;Gorgoulis, Vassilis G.
通讯作者：
Gorgoulis, Vassilis G.
影响因子：
64.8
作者：
Di Micco, Raffaella;Fumagalli, Marzia;di Fagagna, Fabrizio d'Adda
通讯作者：
di Fagagna, Fabrizio d'Adda
影响因子：
3.7
作者：
Coppé JP;Patil CK;Rodier F;Krtolica A;Beauséjour CM;Parrinello S;Hodgson JG;Chin K;Desprez PY;Campisi J
通讯作者：
Campisi J