• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

相似文献

1
PolyIC Induces Retinoic Acid-inducible Gene-I and Melanoma Differentiation-associated Gene 5 and Modulates Inflammation in Podocytes.多聚肌苷酸诱导维甲酸诱导基因-I 和黑色素瘤分化相关基因 5,并调节足细胞中的炎症。
In Vivo. 2021 Jan-Feb;35(1):147-153. doi: 10.21873/invivo.12242.
2
TLR4 signaling induces retinoic acid-inducible gene-I and melanoma differentiation-associated gene 5 in mesangial cells.Toll样受体4信号通路可诱导系膜细胞中的视黄酸诱导基因I和黑色素瘤分化相关基因5。
J Nephrol. 2013 Sep-Oct;26(5):886-93. doi: 10.5301/jn.5000254. Epub 2013 Apr 5.
3
Melanoma differentiation-associated gene 5 regulates the expression of a chemokine CXCL10 in human mesangial cells: implications for chronic inflammatory renal diseases.黑色素瘤分化相关基因 5 调节人肾小球系膜细胞趋化因子 CXCL10 的表达:对慢性炎症性肾脏疾病的影响。
Tohoku J Exp Med. 2012 Sep;228(1):17-26. doi: 10.1620/tjem.228.17.
4
Interaction between interferon-stimulated gene 56 and melanoma differentiation-associated gene 5 in Toll-like receptor 3 signaling in normal human mesangial cells.干扰素刺激基因 56 与黑色素瘤分化相关基因 5 在正常人类肾小球系膜细胞 Toll 样受体 3 信号转导中的相互作用。
Am J Nephrol. 2013;37(2):118-25. doi: 10.1159/000346415. Epub 2013 Jan 29.
5
Retinoic acid inducible gene-I and melanoma differentiation-associated gene 5 are induced but not essential for dengue virus induced type I interferon response.维甲酸诱导基因-I 和黑色素瘤分化相关基因 5 被诱导,但对于登革病毒诱导的 I 型干扰素反应不是必需的。
Mol Biol Rep. 2011 Aug;38(6):3867-73. doi: 10.1007/s11033-010-0502-7. Epub 2010 Nov 27.
6
Toll-like receptor 3 and RIG-I-like receptor activation induces innate antiviral responses in mouse ovarian granulosa cells.Toll 样受体 3 和 RIG-I 样受体激活诱导小鼠卵巢颗粒细胞中的先天抗病毒反应。
Mol Cell Endocrinol. 2013 Jun 15;372(1-2):73-85. doi: 10.1016/j.mce.2013.03.027. Epub 2013 Apr 6.
7
Cytosolic Sensors of Viral RNA Are Involved in the Production of Interleukin-6 via Toll-Like Receptor 3 Signaling in Human Glomerular Endothelial Cells.病毒RNA的胞质传感器通过人肾小球内皮细胞中的Toll样受体3信号通路参与白细胞介素-6的产生。
Kidney Blood Press Res. 2019;44(1):62-71. doi: 10.1159/000498837. Epub 2019 Feb 22.
8
Both RIG-I and MDA5 RNA helicases contribute to the induction of alpha/beta interferon in measles virus-infected human cells.RIG-I 和 MDA5 RNA 解旋酶均有助于麻疹病毒感染的人细胞中诱导产生α/β干扰素。
J Virol. 2010 Jan;84(1):372-9. doi: 10.1128/JVI.01690-09.
9
Molecular characterization and immune responsive expression of feline MDA5 gene.猫MDA5基因的分子特征及免疫反应性表达
J Vet Med Sci. 2018 Aug 22;80(8):1266-1270. doi: 10.1292/jvms.17-0278. Epub 2018 Jul 3.
10
Negative regulation of melanoma differentiation-associated gene 5 (MDA5)-dependent antiviral innate immune responses by Arf-like protein 5B.Arf样蛋白5B对黑色素瘤分化相关基因5(MDA5)依赖性抗病毒天然免疫反应的负调控
J Biol Chem. 2015 Jan 9;290(2):1269-80. doi: 10.1074/jbc.M114.611053. Epub 2014 Dec 1.

引用本文的文献

1
TLR3 activation mediates partial epithelial-to-mesenchymal transition in human keratinocytes.TLR3 激活介导人角质形成细胞的部分上皮间质转化。
Life Sci Alliance. 2024 Sep 30;7(12). doi: 10.26508/lsa.202402777. Print 2024 Dec.
2
Damage-Associated Molecular Patterns and Pattern Recognition Receptors in the Podocyte.足细胞中的损伤相关分子模式与模式识别受体
J Am Soc Nephrol. 2025 Jan 1;36(1):136-143. doi: 10.1681/ASN.0000000531. Epub 2024 Sep 27.
3
Role of the Innate Immune Response in Glomerular Disease Pathogenesis: Focus on Podocytes.固有免疫反应在肾小球疾病发病机制中的作用:聚焦于足细胞。
Cells. 2024 Jul 6;13(13):1157. doi: 10.3390/cells13131157.

本文引用的文献

1
Comparative Structure and Function Analysis of the RIG-I-Like Receptors: RIG-I and MDA5.RIG-I 样受体:RIG-I 和 MDA5 的比较结构与功能分析。
Front Immunol. 2019 Jul 17;10:1586. doi: 10.3389/fimmu.2019.01586. eCollection 2019.
2
Toll-like receptor 3 (TLR-3), TLR-4 and CD80 expression in peripheral blood mononuclear cells and urinary CD80 levels in children with idiopathic nephrotic syndrome.特发性肾病综合征患儿外周血单个核细胞中Toll样受体3(TLR-3)、TLR-4及CD80的表达以及尿CD80水平
Pediatr Nephrol. 2017 Aug;32(8):1355-1361. doi: 10.1007/s00467-017-3613-8. Epub 2017 Feb 16.
3
TLR4 signaling induces retinoic acid-inducible gene-I and melanoma differentiation-associated gene 5 in mesangial cells.Toll样受体4信号通路可诱导系膜细胞中的视黄酸诱导基因I和黑色素瘤分化相关基因5。
J Nephrol. 2013 Sep-Oct;26(5):886-93. doi: 10.5301/jn.5000254. Epub 2013 Apr 5.
4
Toll-like receptor 3 ligand, polyIC, induces proteinuria and glomerular CD80, and increases urinary CD80 in mice.Toll 样受体 3 配体聚肌苷酸诱导蛋白尿和肾小球 CD80,并增加小鼠尿液中 CD80 的含量。
Nephrol Dial Transplant. 2013 Jun;28(6):1439-46. doi: 10.1093/ndt/gfs543. Epub 2012 Dec 21.
5
Toll-like receptor 3 ligands induce CD80 expression in human podocytes via an NF-κB-dependent pathway.Toll 样受体 3 配体通过 NF-κB 依赖途径诱导人足细胞 CD80 的表达。
Nephrol Dial Transplant. 2012 Jan;27(1):81-9. doi: 10.1093/ndt/gfr271. Epub 2011 May 26.
6
Toll-like receptors and their crosstalk with other innate receptors in infection and immunity. toll 样受体及其在感染和免疫中与其他先天受体的相互作用。
Immunity. 2011 May 27;34(5):637-50. doi: 10.1016/j.immuni.2011.05.006.
7
Retinoic acid-inducible gene-I is induced by double-stranded RNA and regulates the expression of CC chemokine ligand (CCL) 5 in human mesangial cells.维甲酸诱导基因-I 由双链 RNA 诱导,并调节人肾小球系膜细胞中 CC 趋化因子配体(CCL)5 的表达。
Nephrol Dial Transplant. 2010 Nov;25(11):3534-9. doi: 10.1093/ndt/gfq270. Epub 2010 May 19.
8
Pattern recognition receptors and inflammation.模式识别受体与炎症。
Cell. 2010 Mar 19;140(6):805-20. doi: 10.1016/j.cell.2010.01.022.
9
Proteinuria: an enzymatic disease of the podocyte?蛋白尿:足细胞的酶性疾病?
Kidney Int. 2010 Apr;77(7):571-80. doi: 10.1038/ki.2009.424. Epub 2009 Nov 18.
10
Viral RNA induces type I interferon-dependent cytokine release and cell death in mesangial cells via melanoma-differentiation-associated gene-5: Implications for viral infection-associated glomerulonephritis.病毒 RNA 通过黑色素瘤分化相关基因-5 诱导系膜细胞中 I 型干扰素依赖性细胞因子释放和细胞死亡:与病毒感染相关的肾小球肾炎的意义。
Am J Pathol. 2009 Nov;175(5):2014-22. doi: 10.2353/ajpath.2009.080585. Epub 2009 Oct 22.

多聚肌苷酸诱导维甲酸诱导基因-I 和黑色素瘤分化相关基因 5,并调节足细胞中的炎症。

PolyIC Induces Retinoic Acid-inducible Gene-I and Melanoma Differentiation-associated Gene 5 and Modulates Inflammation in Podocytes.

机构信息

Department of Cardiology and Nephrology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.

Department of Cardiology and Nephrology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan;

出版信息

In Vivo. 2021 Jan-Feb;35(1):147-153. doi: 10.21873/invivo.12242.

DOI:10.21873/invivo.12242
PMID:33402460
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7880774/
Abstract

BACKGROUND/AIM: Viral infection often exacerbates proteinuria, which has been suggested to be due to antiviral responses of podocytes. We examined the effect of polyinosinic-polycytidylic acid (polyIC) on the expression of retinoic acid-inducible gene-I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5) in differentiated human podocytes in culture.

MATERIALS AND METHODS

The podocytes were treated with 2 ng/ml to 500 μg/ml of polyIC for 3 to 36 h, and also transfected with siRNA against RIG-I and MDA5. F-actin staining was performed to assess actin reorganization.

RESULTS

PolyIC induced the expression of RIG-I and MDA5 in dose- and time-dependent manner, accompanied with interferon-β (IFN-β) and interleukin-6 (IL-6) up-regulation and actin reorganization. Temporal knockdown of RIG-I by siRNA decreased IFN-β expression, while MDA5 siRNA inhibited IFN-β and IL-6 expression. Actin reorganization was attenuated by RIG-I and MDA5 knockdown.

CONCLUSION

RIG-I and MDA5 may play a role in the antiviral responses of podocytes.

摘要

背景/目的:病毒感染常使蛋白尿加重,这被认为是由于足细胞的抗病毒反应。我们研究了多聚肌苷酸-多聚胞苷酸(polyIC)对培养分化的人足细胞中视黄酸诱导基因-I(RIG-I)和黑色素瘤分化相关基因 5(MDA5)表达的影响。

材料和方法

将足细胞用 2ng/ml 至 500μg/ml 的 polyIC 处理 3 至 36 小时,并用 RIG-I 和 MDA5 的 siRNA 转染。通过 F-肌动蛋白染色评估肌动蛋白重排。

结果

polyIC 以剂量和时间依赖的方式诱导 RIG-I 和 MDA5 的表达,伴随干扰素-β(IFN-β)和白细胞介素-6(IL-6)的上调和肌动蛋白重排。通过 siRNA 瞬时敲低 RIG-I 可降低 IFN-β 的表达,而 MDA5 siRNA 抑制 IFN-β 和 IL-6 的表达。RIG-I 和 MDA5 的敲低可减轻肌动蛋白重排。

结论

RIG-I 和 MDA5 可能在足细胞的抗病毒反应中发挥作用。