A20对泛素和自身免疫模式进行编辑。 - Suppr

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超能文献

A20 edits ubiquitin and autoimmune paradigms.

作者信息

Martin Flavius, Dixit Vishva M

出版信息

Nat Genet. 2011 Aug 29;43(9):822-3. doi: 10.1038/ng.916.

DOI:10.1038/ng.916

PMID:21874034

Abstract

摘要

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A20 edits ubiquitin and autoimmune paradigms.A20对泛素和自身免疫模式进行编辑。

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A20 (TNFAIP3) deficiency in myeloid cells triggers erosive polyarthritis resembling rheumatoid arthritis.髓样细胞中 A20（TNFAIP3）的缺失可引发类似于类风湿关节炎的侵蚀性多关节炎。

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Phosphorylation and linear ubiquitin direct A20 inhibition of inflammation.磷酸化和线性泛素化直接调控 A20 抑制炎症。

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B cells lacking the tumor suppressor TNFAIP3/A20 display impaired differentiation and hyperactivation and cause inflammation and autoimmunity in aged mice.肿瘤抑制因子 TNFAIP3/A20 缺失的 B 细胞表现出分化障碍和过度激活，并导致老年小鼠发生炎症和自身免疫。

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The ubiquitin editing enzyme A20 (TNFAIP3) is upregulated during permanent middle cerebral artery occlusion but does not influence disease outcome.泛素编辑酶A20（TNFAIP3）在大脑中动脉永久性闭塞期间上调，但不影响疾病转归。

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The seventh zinc finger motif of A20 is required for the suppression of TNF-α-induced apoptosis.A20的第七个锌指基序是抑制肿瘤坏死因子-α诱导的细胞凋亡所必需的。

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A20 deficiency sensitizes pancreatic beta cells to cytokine-induced apoptosis in vitro but does not influence type 1 diabetes development in vivo.A20缺陷在体外使胰腺β细胞对细胞因子诱导的凋亡敏感，但在体内不影响1型糖尿病的发展。

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Keratinocyte-specific ablation of the NF-κB regulatory protein A20 (TNFAIP3) reveals a role in the control of epidermal homeostasis.角质形成细胞特异性敲除 NF-κB 调节蛋白 A20（TNFAIP3）揭示了其在控制表皮稳态中的作用。

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O-glycosylation regulates ubiquitination and degradation of the anti-inflammatory protein A20 to accelerate atherosclerosis in diabetic ApoE-null mice.O-糖基化调节抗炎蛋白 A20 的泛素化和降解，从而加速糖尿病 ApoE 基因敲除小鼠的动脉粥样硬化。

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Repression of transcription by the glucocorticoid receptor: A parsimonious model for the genomics era.糖皮质激素受体对转录的抑制：基因组时代的简约模型。

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The Ubiquitin-Proteasome System in Immune Cells.免疫细胞中的泛素-蛋白酶体系统。

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The Footprints of Poly-Autoimmunity: Evidence for Common Biological Factors Involved in Multiple Sclerosis and Hashimoto's Thyroiditis.自身免疫性疾病的足迹：多发性硬化症和桥本甲状腺炎中涉及的共同生物学因素的证据。

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NF-κB Pathway in Autoinflammatory Diseases: Dysregulation of Protein Modifications by Ubiquitin Defines a New Category of Autoinflammatory Diseases.自身炎症性疾病中的NF-κB信号通路：泛素介导的蛋白质修饰失调定义了一类新的自身炎症性疾病。

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Lessons from characterization and treatment of the autoinflammatory syndromes.自身炎症性综合征的特征与治疗经验

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Advantages of Extracellular Ubiquitin in Modulation of Immune Responses.细胞外泛素在调节免疫反应中的优势。

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Loss-of-function mutations in TNFAIP3 leading to A20 haploinsufficiency cause an early-onset autoinflammatory disease.TNFAIP3功能丧失性突变导致A20单倍体不足，引发早发性自身炎症性疾病。

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In Vivo Silencing of A20 via TLR9-Mediated Targeted SiRNA Delivery Potentiates Antitumor Immune Response.通过TLR9介导的靶向小干扰RNA递送在体内沉默A20可增强抗肿瘤免疫反应。

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TNFAIP3 promotes survival of CD4 T cells by restricting MTOR and promoting autophagy.TNFAIP3通过限制MTOR并促进自噬来促进CD4 T细胞的存活。

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本文引用的文献

Nat Genet. 2011 Aug 14;43(9):908-12. doi: 10.1038/ng.874.

Cell Death Differ. 2011 Dec;18(12):1845-53. doi: 10.1038/cdd.2011.55. Epub 2011 May 13.

A20 deficiency in B cells enhances B-cell proliferation and results in the development of autoantibodies.B 细胞中 A20 的缺乏会增强 B 细胞的增殖，导致自身抗体的产生。

Eur J Immunol. 2011 Mar;41(3):595-601. doi: 10.1002/eji.201041313. Epub 2011 Feb 10.

Blood. 2011 Feb 17;117(7):2227-36. doi: 10.1182/blood-2010-09-306019. Epub 2010 Nov 18.

The ubiquitin modifying enzyme A20 restricts B cell survival and prevents autoimmunity.泛素修饰酶 A20 限制 B 细胞存活并防止自身免疫。

Immunity. 2010 Aug 27;33(2):181-91. doi: 10.1016/j.immuni.2010.07.017. Epub 2010 Aug 12.

Enterocyte-specific A20 deficiency sensitizes to tumor necrosis factor-induced toxicity and experimental colitis.肠上皮细胞特异性 A20 缺乏使细胞对肿瘤坏死因子诱导的毒性和实验性结肠炎敏感。

J Exp Med. 2010 Jul 5;207(7):1513-23. doi: 10.1084/jem.20092474. Epub 2010 Jun 7.

Targeting lymphocyte co-stimulation: from bench to bedside.靶向淋巴细胞共刺激：从基础到临床。

Autoimmunity. 2010 Nov;43(7):514-25. doi: 10.3109/08916931003674741.

A20: from ubiquitin editing to tumour suppression.A20：从泛素编辑到肿瘤抑制。

Nat Rev Cancer. 2010 May;10(5):332-41. doi: 10.1038/nrc2775. Epub 2010 Apr 12.

The ubiquitin-editing enzyme A20 (TNFAIP3) is a central regulator of immunopathology.泛素编辑酶A20（TNFAIP3）是免疫病理学的核心调节因子。

Trends Immunol. 2009 Aug;30(8):383-91. doi: 10.1016/j.it.2009.05.007. Epub 2009 Jul 28.

A20: central gatekeeper in inflammation and immunity.A20：炎症与免疫的核心把关者

J Biol Chem. 2009 Mar 27;284(13):8217-21. doi: 10.1074/jbc.R800032200. Epub 2008 Nov 13.

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