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2
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3
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本文引用的文献

1
Nucleolar proteins suppress Caenorhabditis elegans innate immunity by inhibiting p53/CEP-1.核仁蛋白通过抑制 p53/CEP-1 来抑制秀丽隐杆线虫的先天免疫。
PLoS Genet. 2009 Sep;5(9):e1000657. doi: 10.1371/journal.pgen.1000657. Epub 2009 Sep 18.
2
The F-box protein FBXO45 promotes the proteasome-dependent degradation of p73.F-box蛋白FBXO45促进p73的蛋白酶体依赖性降解。
Oncogene. 2009 Sep 3;28(35):3157-66. doi: 10.1038/onc.2009.177. Epub 2009 Jul 6.
3
Caenorhabditis elegans protein arginine methyltransferase PRMT-5 negatively regulates DNA damage-induced apoptosis.秀丽隐杆线虫蛋白精氨酸甲基转移酶PRMT-5负向调控DNA损伤诱导的细胞凋亡。
PLoS Genet. 2009 Jun;5(6):e1000514. doi: 10.1371/journal.pgen.1000514. Epub 2009 Jun 12.
4
p53/CEP-1 increases or decreases lifespan, depending on level of mitochondrial bioenergetic stress.p53/CEP-1会根据线粒体生物能量应激水平的高低来延长或缩短寿命。
Aging Cell. 2009 Aug;8(4):380-93. doi: 10.1111/j.1474-9726.2009.00482.x. Epub 2009 Apr 22.
5
Expression of the apoptosis inducer gene head involution defective in primordial germ cells of the Drosophila embryo requires eiger, p53, and loki function.果蝇胚胎原始生殖细胞中凋亡诱导基因头部内卷缺陷的表达需要埃iger、p53和洛基蛋白的功能。
Dev Growth Differ. 2009 May;51(4):453-61. doi: 10.1111/j.1440-169X.2009.01108.x.
6
Functional dissection of Caenorhabditis elegans CLK-2/TEL2 cell cycle defects during embryogenesis and germline development.秀丽隐杆线虫CLK-2/TEL2在胚胎发生和生殖系发育过程中细胞周期缺陷的功能剖析。
PLoS Genet. 2009 Apr;5(4):e1000451. doi: 10.1371/journal.pgen.1000451. Epub 2009 Apr 10.
7
Endocycling cells do not apoptose in response to DNA rereplication genotoxic stress.内循环细胞不会因DNA再复制基因毒性应激而凋亡。
Genes Dev. 2008 Nov 15;22(22):3158-71. doi: 10.1101/gad.1710208.
8
The Caenorhabditis elegans ing-3 gene regulates ionizing radiation-induced germ-cell apoptosis in a p53-associated pathway.秀丽隐杆线虫的ing-3基因在一条与p53相关的信号通路中调控电离辐射诱导的生殖细胞凋亡。
Genetics. 2009 Feb;181(2):473-82. doi: 10.1534/genetics.107.080515. Epub 2008 Nov 17.
9
C. elegans SIR-2.1 translocation is linked to a proapoptotic pathway parallel to cep-1/p53 during DNA damage-induced apoptosis.秀丽隐杆线虫SIR-2.1易位与DNA损伤诱导的凋亡过程中平行于cep-1/p53的促凋亡途径相关联。
Genes Dev. 2008 Oct 15;22(20):2831-42. doi: 10.1101/gad.482608.
10
Telomere loss provokes multiple pathways to apoptosis and produces genomic instability in Drosophila melanogaster.端粒缺失引发多种细胞凋亡途径,并在黑腹果蝇中产生基因组不稳定。
Genetics. 2008 Dec;180(4):1821-32. doi: 10.1534/genetics.108.093625. Epub 2008 Oct 9.

无脊椎动物 p53 超家族的系统发生和功能。

Phylogeny and function of the invertebrate p53 superfamily.

机构信息

Wellcome Trust Centre for Gene Regulation and Expression, College of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland, United Kingdom.

出版信息

Cold Spring Harb Perspect Biol. 2010 Jul;2(7):a001131. doi: 10.1101/cshperspect.a001131. Epub 2010 May 5.

DOI:10.1101/cshperspect.a001131
PMID:20595397
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2890203/
Abstract

The origin of the p53 superfamily predates animal evolution and first appears in unicellular Flagellates. Invertebrate p53 superfamily members appear to have a p63-like domain structure, which seems to be evolutionarily ancient. The radiation into p53, p63, and p73 proteins is a vertebrate invention. In invertebrate models amenable to genetic analysis p53 superfamily members mainly act in apoptosis regulation in response to genotoxic agents and do not have overt developmental functions. We summarize the literature on cnidarian and mollusc p53 superfamily members and focus on the function and regulation of Drosophila melanogaster and Caenorhabditis elegans p53 superfamily members in triggering apoptosis. Furthermore, we examine the emerging evidence showing that invertebrate p53 superfamily proteins also have functions unrelated to apoptosis, such as DNA repair, cell cycle checkpoint responses, compensatory proliferation, aging, autophagy, and innate immunity.

摘要

p53 超家族的起源早于动物进化,最早出现在单细胞鞭毛生物中。无脊椎动物 p53 超家族成员似乎具有 p63 样的结构域结构,这似乎是古老的进化特征。p53、p63 和 p73 蛋白的辐射是脊椎动物的发明。在可进行遗传分析的无脊椎动物模型中,p53 超家族成员主要在响应遗传毒性物质的细胞凋亡调节中发挥作用,而没有明显的发育功能。我们总结了有关刺胞动物和软体动物 p53 超家族成员的文献,并重点介绍了果蝇和秀丽隐杆线虫 p53 超家族成员在触发细胞凋亡方面的功能和调节。此外,我们还研究了新出现的证据,表明无脊椎动物 p53 超家族蛋白也具有与细胞凋亡无关的功能,例如 DNA 修复、细胞周期检查点反应、代偿性增殖、衰老、自噬和先天免疫。