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本文引用的文献

1
The RNA-binding protein TTP is a global post-transcriptional regulator of feedback control in inflammation.RNA结合蛋白TTP是炎症中反馈控制的全局转录后调节因子。
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A Retrospective Cohort Study Comparing Utilization and Costs of Biologic Therapies and JAK Inhibitor Therapy Across Four Common Inflammatory Indications in Adult US Managed Care Patients.一项回顾性队列研究:比较美国成年管理式医疗患者四种常见炎症指征下生物疗法和JAK抑制剂疗法的使用情况及成本
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High Elmo1 expression aggravates and low Elmo1 expression prevents diabetic nephropathy.高Elmo1表达加重糖尿病肾病,而低Elmo1表达则预防糖尿病肾病。
Proc Natl Acad Sci U S A. 2016 Feb 23;113(8):2218-22. doi: 10.1073/pnas.1600511113. Epub 2016 Feb 8.
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Enhanced stability of tristetraprolin mRNA protects mice against immune-mediated inflammatory pathologies.三氧化四脯氨酸信使核糖核酸(Tristetraprolin mRNA)稳定性的增强可保护小鼠免受免疫介导的炎症性疾病侵害。
Proc Natl Acad Sci U S A. 2016 Feb 16;113(7):1865-70. doi: 10.1073/pnas.1519906113. Epub 2016 Feb 1.
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TNF biology, pathogenic mechanisms and emerging therapeutic strategies.肿瘤坏死因子的生物学特性、致病机制及新出现的治疗策略。
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Functional equivalence of an evolutionarily conserved RNA binding module.一个进化上保守的RNA结合模块的功能等效性。
J Biol Chem. 2015 Oct 2;290(40):24413-23. doi: 10.1074/jbc.M115.673012. Epub 2015 Aug 19.
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A Genome-wide CRISPR Screen in Primary Immune Cells to Dissect Regulatory Networks.在原代免疫细胞中进行全基因组CRISPR筛选以剖析调控网络
Cell. 2015 Jul 30;162(3):675-86. doi: 10.1016/j.cell.2015.06.059. Epub 2015 Jul 16.
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Chemically modified guide RNAs enhance CRISPR-Cas genome editing in human primary cells.化学修饰的引导RNA增强了人类原代细胞中的CRISPR-Cas基因组编辑。
Nat Biotechnol. 2015 Sep;33(9):985-989. doi: 10.1038/nbt.3290. Epub 2015 Jun 29.
9
Dominant Suppression of Inflammation via Targeted Mutation of the mRNA Destabilizing Protein Tristetraprolin.通过对mRNA去稳定蛋白Tristetraprolin进行靶向突变对炎症进行显性抑制。
J Immunol. 2015 Jul 1;195(1):265-76. doi: 10.4049/jimmunol.1402826. Epub 2015 May 22.
10
Tristetraprolin (TTP) coordinately regulates primary and secondary cellular responses to proinflammatory stimuli.锌指蛋白36(TTP)协同调节细胞对促炎刺激的初级和次级反应。
J Leukoc Biol. 2015 Apr;97(4):723-36. doi: 10.1189/jlb.3A0214-106R. Epub 2015 Feb 5.

锌指蛋白36作为炎症性疾病的治疗靶点

Tristetraprolin as a Therapeutic Target in Inflammatory Disease.

作者信息

Patial Sonika, Blackshear Perry J

机构信息

Signal Transduction Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA; Current address: Louisiana Animal Disease Diagnostic Laboratory (LADDL), School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803, USA.

Signal Transduction Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA; Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA; Department of Biochemistry, Duke University Medical Center, Durham, NC 27710, USA.

出版信息

Trends Pharmacol Sci. 2016 Oct;37(10):811-821. doi: 10.1016/j.tips.2016.07.002. Epub 2016 Aug 5.

DOI:10.1016/j.tips.2016.07.002
PMID:27503556
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5030171/
Abstract

Members of the tristetraprolin (TTP) family of RNA-binding proteins are found in all major eukaryotic groups. TTP family members, from plants through humans, can bind adenosine-uridine rich elements in target mRNAs with high affinity. In mammalian cells, these proteins then promote deadenylation and decay of target transcripts. Four such proteins are found in mice, of which the best studied is TTP. When the gene encoding TTP is disrupted in mice, the animals develop a severe syndrome of arthritis, autoimmunity, cachexia, dermatitis, and myeloid hyperplasia. Conversely, recent overexpression studies have demonstrated protection against several experimental models of immune inflammatory disease. This endogenous anti-inflammatory protein could serve as the basis for novel approaches to therapy of similar conditions in humans.

摘要

RNA结合蛋白三磷酸腺苷结合盒转运体(TTP)家族成员存在于所有主要的真核生物类群中。从植物到人类,TTP家族成员能够以高亲和力结合靶mRNA中富含腺苷-尿苷的元件。在哺乳动物细胞中,这些蛋白质随后促进靶转录本的去腺苷酸化和降解。小鼠体内发现了四种这样的蛋白质,其中研究得最深入的是TTP。当编码TTP的基因在小鼠体内被破坏时,动物会出现严重的关节炎、自身免疫、恶病质、皮炎和髓样增生综合征。相反,最近的过表达研究表明,它对几种免疫炎症性疾病的实验模型具有保护作用。这种内源性抗炎蛋白可以作为治疗人类类似疾病新方法的基础。