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1
Mdm2 regulates p53 independently of p19(ARF) in homeostatic tissues.在稳态组织中，Mdm2独立于p19(ARF)对p53进行调控。
Mol Cell Biol. 2004 Jan;24(1):186-91. doi: 10.1128/MCB.24.1.186-191.2004.
2
p19(ARF) is dispensable for oncogenic stress-induced p53-mediated apoptosis and tumor suppression in vivo.p19（ARF）在体内致癌应激诱导的p53介导的细胞凋亡和肿瘤抑制过程中并非必需。
Mol Cell Biol. 2002 Jan;22(1):370-7. doi: 10.1128/MCB.22.1.370-377.2002.
3
Sumoylation induced by the Arf tumor suppressor: a p53-independent function.由Arf肿瘤抑制因子诱导的类泛素化修饰：一种不依赖p53的功能
Proc Natl Acad Sci U S A. 2005 May 24;102(21):7689-94. doi: 10.1073/pnas.0502978102. Epub 2005 May 16.
4
p53-independent apoptosis is induced by the p19ARF tumor suppressor.p19ARF肿瘤抑制因子可诱导不依赖p53的细胞凋亡。
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P19(ARF) stabilizes p53 by blocking nucleo-cytoplasmic shuttling of Mdm2.P19（急性肾衰竭）通过阻断Mdm2的核质穿梭来稳定p53。
Proc Natl Acad Sci U S A. 1999 Jun 8;96(12):6937-41. doi: 10.1073/pnas.96.12.6937.
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Functional and physical interactions of the ARF tumor suppressor with p53 and Mdm2.ARF肿瘤抑制因子与p53和Mdm2的功能及物理相互作用。
Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8292-7. doi: 10.1073/pnas.95.14.8292.
7
Nucleolar Arf tumor suppressor inhibits ribosomal RNA processing.核仁Arf肿瘤抑制因子抑制核糖体RNA加工。
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Oncogenic ras activates the ARF-p53 pathway to suppress epithelial cell transformation.致癌性Ras激活ARF-p53通路以抑制上皮细胞转化。
Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5025-30. doi: 10.1073/pnas.091100298. Epub 2001 Apr 17.
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Disruption of the ARF-Mdm2-p53 tumor suppressor pathway in Myc-induced lymphomagenesis.在Myc诱导的淋巴瘤发生过程中ARF-Mdm2-p53肿瘤抑制通路的破坏。
Genes Dev. 1999 Oct 15;13(20):2658-69. doi: 10.1101/gad.13.20.2658.

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Celecoxib prevents tumor necrosis factor-α (TNF-α)-induced cellular senescence in human chondrocytes.塞来昔布可预防肿瘤坏死因子-α（TNF-α）诱导的人软骨细胞衰老。
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Peptide, Peptidomimetic, and Small-molecule Antagonists of the p53-HDM2 Protein-Protein Interaction.p53-HDM2 蛋白质-蛋白质相互作用的肽、拟肽和小分子拮抗剂
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Distinct E2F-mediated transcriptional program regulates p14ARF gene expression.独特的E2F介导的转录程序调控p14ARF基因表达。
EMBO J. 2005 Nov 2;24(21):3724-36. doi: 10.1038/sj.emboj.7600836. Epub 2005 Oct 6.
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Nucleophosmin (B23) targets ARF to nucleoli and inhibits its function.核磷蛋白（B23）将ARF靶向核仁并抑制其功能。
Mol Cell Biol. 2005 Feb;25(4):1258-71. doi: 10.1128/MCB.25.4.1258-1271.2005.

本文引用的文献

1
Mdm2 haplo-insufficiency profoundly inhibits Myc-induced lymphomagenesis.Mdm2单倍体不足显著抑制Myc诱导的淋巴瘤发生。
EMBO J. 2003 Mar 17;22(6):1442-50. doi: 10.1093/emboj/cdg133.
2
Oligomerization of the human ARF tumor suppressor and its response to oxidative stress.人类ARF肿瘤抑制因子的寡聚化及其对氧化应激的反应。
J Biol Chem. 2003 May 23;278(21):18720-9. doi: 10.1074/jbc.M211007200. Epub 2003 Feb 11.
3
mdm2 Is critical for inhibition of p53 during lymphopoiesis and the response to ionizing irradiation.MDM2在淋巴细胞生成过程中对p53的抑制以及对电离辐射的反应中起着关键作用。
Mol Cell Biol. 2003 Jan;23(2):462-72. doi: 10.1128/MCB.23.2.462-473.2003.
4
INK4a-ARF alterations and p53 mutations in primary and consecutive squamous cell carcinoma of the head and neck.头颈部原发性及连续性鳞状细胞癌中的INK4a-ARF改变与p53突变
Virchows Arch. 2002 Aug;441(2):133-42. doi: 10.1007/s00428-002-0637-6. Epub 2002 Apr 4.
5
Loss of p19ARF enhances the defects of Mdm2 overexpression in the mammary gland.p19ARF的缺失会加剧Mdm2在乳腺中过表达所导致的缺陷。
Oncogene. 2002 May 16;21(22):3525-31. doi: 10.1038/sj.onc.1205441.
6
ARF differentially modulates apoptosis induced by E2F1 and Myc.急性肾衰竭对由E2F1和Myc诱导的细胞凋亡有不同的调节作用。
Mol Cell Biol. 2002 Mar;22(5):1360-8. doi: 10.1128/MCB.22.5.1360-1368.2002.
7
p19(ARF) is dispensable for oncogenic stress-induced p53-mediated apoptosis and tumor suppression in vivo.p19（ARF）在体内致癌应激诱导的p53介导的细胞凋亡和肿瘤抑制过程中并非必需。
Mol Cell Biol. 2002 Jan;22(1):370-7. doi: 10.1128/MCB.22.1.370-377.2002.
8
Differential requirement for p19ARF in the p53-dependent arrest induced by DNA damage, microtubule disruption, and ribonucleotide depletion.DNA 损伤、微管破坏和核糖核苷酸耗竭诱导的 p53 依赖性细胞停滞中对 p19ARF 的不同需求。
Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3266-71. doi: 10.1073/pnas.97.7.3266.
9
The p53 tumor suppressor protein does not regulate expression of its own inhibitor, MDM2, except under conditions of stress.p53肿瘤抑制蛋白不会调节其自身抑制剂MDM2的表达，除非在应激条件下。
Mol Cell Biol. 2000 Mar;20(6):2023-30. doi: 10.1128/MCB.20.6.2023-2030.2000.
10
INK4a/ARF mutations accelerate lymphomagenesis and promote chemoresistance by disabling p53.INK4a/ARF 突变通过使 p53 失活加速淋巴瘤发生并促进化疗耐药。
Genes Dev. 1999 Oct 15;13(20):2670-7. doi: 10.1101/gad.13.20.2670.

在稳态组织中，Mdm2独立于p19(ARF)对p53进行调控。

Mdm2 regulates p53 independently of p19(ARF) in homeostatic tissues.

作者信息

O'Leary Kathleen A, Mendrysa Susan M, Vaccaro Abram, Perry Mary Ellen

机构信息

Department of Oncology, University of Wisconsin, Madison, Wisconsin 53706, USA.

出版信息

Mol Cell Biol. 2004 Jan;24(1):186-91. doi: 10.1128/MCB.24.1.186-191.2004.

DOI:10.1128/MCB.24.1.186-191.2004
PMID:14673154
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC303350/
Abstract

Tumor suppressor proteins must be exquisitely regulated since they can induce cell death while preventing cancer. For example, the p19(ARF) tumor suppressor (p14(ARF) in humans) appears to stimulate the apoptotic function of the p53 tumor suppressor to prevent lymphomagenesis and carcinogenesis induced by oncogene overexpression. Here we present a genetic approach to defining the role of p19(ARF) in regulating the apoptotic function of p53 in highly proliferating, homeostatic tissues. In contrast to our expectation, p19(ARF) did not activate the apoptotic function of p53 in lymphocytes or epithelial cells. These results demonstrate that the mechanisms that control p53 function during homeostasis differ from those that are critical for tumor suppression. Moreover, the Mdm2/p53/p19(ARF) pathway appears to exist only under very restricted conditions.

摘要

肿瘤抑制蛋白必须受到精确调控，因为它们既能诱导细胞死亡又能预防癌症。例如，p19(ARF)肿瘤抑制蛋白（人类中的p14(ARF)）似乎能刺激p53肿瘤抑制蛋白的凋亡功能，以防止因癌基因过表达诱导的淋巴瘤发生和癌变。在此，我们提出一种遗传学方法，用于确定p19(ARF)在高度增殖的稳态组织中调节p53凋亡功能的作用。与我们的预期相反，p19(ARF)并未激活淋巴细胞或上皮细胞中p53的凋亡功能。这些结果表明，在稳态过程中控制p53功能的机制与对肿瘤抑制至关重要的机制不同。此外，Mdm2/p53/p19(ARF)通路似乎仅在非常有限的条件下存在。