• 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

一种用于TWEAK-Fn14信号通路的生物信息学资源。

A Bioinformatics Resource for TWEAK-Fn14 Signaling Pathway.

作者信息

Bhattacharjee Mitali, Raju Rajesh, Radhakrishnan Aneesha, Nanjappa Vishalakshi, Muthusamy Babylakshmi, Singh Kamlendra, Kuppusamy Dheebika, Lingala Bhavya Teja, Pan Archana, Mathur Premendu Prakash, Harsha H C, Prasad T S Keshava, Atkins Gerald J, Pandey Akhilesh, Chatterjee Aditi

机构信息

Institute of Bioinformatics, International Tech Park, Bangalore 560066, India.

出版信息

J Signal Transduct. 2012;2012:376470. doi: 10.1155/2012/376470. Epub 2012 May 9.

DOI:10.1155/2012/376470
PMID:22649723
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3357548/
Abstract

TNF-related weak inducer of apoptosis (TWEAK) is a new member of the TNF superfamily. It signals through TNFRSF12A, commonly known as Fn14. The TWEAK-Fn14 interaction regulates cellular activities including proliferation, migration, differentiation, apoptosis, angiogenesis, tissue remodeling and inflammation. Although TWEAK has been reported to be associated with autoimmune diseases, cancers, stroke, and kidney-related disorders, the downstream molecular events of TWEAK-Fn14 signaling are yet not available in any signaling pathway repository. In this paper, we manually compiled from the literature, in particular those reported in human systems, the downstream reactions stimulated by TWEAK-Fn14 interactions. Our manual amassment of the TWEAK-Fn14 pathway has resulted in cataloging of 46 proteins involved in various biochemical reactions and TWEAK-Fn14 induced expression of 28 genes. We have enabled the availability of data in various standard exchange formats from NetPath, a repository for signaling pathways. We believe that this composite molecular interaction pathway will enable identification of new signaling components in TWEAK signaling pathway. This in turn may lead to the identification of potential therapeutic targets in TWEAK-associated disorders.

摘要

肿瘤坏死因子相关凋亡弱诱导因子(TWEAK)是肿瘤坏死因子超家族的新成员。它通过通常被称为Fn14的肿瘤坏死因子受体超家族成员12A(TNFRSF12A)进行信号传导。TWEAK与Fn14的相互作用调节细胞活动,包括增殖、迁移、分化、凋亡、血管生成、组织重塑和炎症。尽管已有报道称TWEAK与自身免疫性疾病、癌症、中风及肾脏相关疾病有关,但在任何信号通路知识库中都没有TWEAK-Fn14信号传导的下游分子事件。在本文中,我们从文献中,特别是在人体系统中报道的文献中,手动汇编了由TWEAK-Fn14相互作用刺激的下游反应。我们对TWEAK-Fn14通路的手动收集已导致对参与各种生化反应的46种蛋白质进行编目,以及TWEAK-Fn14诱导的28个基因的表达。我们已使来自信号通路知识库NetPath的各种标准交换格式的数据可供使用。我们相信,这种复合分子相互作用通路将有助于识别TWEAK信号通路中的新信号成分。这反过来可能会导致识别TWEAK相关疾病中的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e02/3357548/5c0fa6addad5/JST2012-376470.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e02/3357548/a35da7f39bad/JST2012-376470.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e02/3357548/248e814d7717/JST2012-376470.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e02/3357548/5c0fa6addad5/JST2012-376470.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e02/3357548/a35da7f39bad/JST2012-376470.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e02/3357548/248e814d7717/JST2012-376470.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e02/3357548/5c0fa6addad5/JST2012-376470.003.jpg

相似文献

1
A Bioinformatics Resource for TWEAK-Fn14 Signaling Pathway.一种用于TWEAK-Fn14信号通路的生物信息学资源。
J Signal Transduct. 2012;2012:376470. doi: 10.1155/2012/376470. Epub 2012 May 9.
2
Role of the TWEAK/Fn14 pathway in autoimmune diseases.TWEAK/Fn14信号通路在自身免疫性疾病中的作用。
Immunol Res. 2016 Feb;64(1):44-50. doi: 10.1007/s12026-015-8761-y.
3
TWEAK Progress in Dermatology: A Review.TWEAK在皮肤病学领域的进展:综述
Indian J Dermatol. 2023 Jul-Aug;68(4):425-429. doi: 10.4103/ijd.ijd_885_22.
4
TWEAK/Fn14 signaling in tumors.肿瘤中的TWEAK/Fn14信号传导
Tumour Biol. 2017 Jun;39(6):1010428317714624. doi: 10.1177/1010428317714624.
5
TWEAK/Fn14 Axis: A Promising Target for the Treatment of Cardiovascular Diseases.肿瘤坏死因子样弱凋亡诱导因子/成纤维细胞生长因子诱导14轴:心血管疾病治疗的一个有前景的靶点。
Front Immunol. 2014 Jan 20;5:3. doi: 10.3389/fimmu.2014.00003. eCollection 2014.
6
Therapeutic potential of the TWEAK/Fn14 pathway in intractable gastrointestinal cancer.TWEAK/Fn14信号通路在难治性胃肠道癌中的治疗潜力
Exp Ther Med. 2011 Jan;2(1):103-108. doi: 10.3892/etm.2010.181. Epub 2010 Dec 2.
7
TWEAK/Fn14 Axis-Targeted Therapeutics: Moving Basic Science Discoveries to the Clinic.TWEAK/Fn14 轴靶向治疗:将基础科学发现推向临床。
Front Immunol. 2013 Dec 23;4:473. doi: 10.3389/fimmu.2013.00473.
8
Tumor Necrosis Factor-Like Weak Inducer of Apoptosis (TWEAK)/Fibroblast Growth Factor-Inducible 14 (Fn14) Axis in Cardiovascular Diseases: Progress and Challenges.肿瘤坏死因子样弱凋亡诱导因子(TWEAK)/成纤维细胞生长因子诱导 14 (Fn14)轴在心血管疾病中的作用:进展与挑战。
Cells. 2020 Feb 11;9(2):405. doi: 10.3390/cells9020405.
9
The TNF-like weak inducer of the apoptosis/fibroblast growth factor-inducible molecule 14 axis mediates histamine and platelet-activating factor-induced subcutaneous vascular leakage and anaphylactic shock.肿瘤坏死因子样凋亡/成纤维细胞生长因子诱导分子 14 轴的弱诱导剂介导组胺和血小板激活因子诱导的皮下血管渗漏和过敏休克。
J Allergy Clin Immunol. 2020 Feb;145(2):583-596.e6. doi: 10.1016/j.jaci.2019.09.019. Epub 2019 Oct 31.
10
TWEAK/FN14 promotes profibrogenic pathway activation in Prominin-1-expressing hepatic progenitor cells in biliary atresia.TWEAK/FN14促进胆道闭锁中表达Prominin-1的肝祖细胞中的促纤维化途径激活。
Hepatology. 2023 May 1;77(5):1639-1653. doi: 10.1097/HEP.0000000000000026. Epub 2023 Jan 3.

引用本文的文献

1
Synovial Fluid Markers and Extracellular Vesicles in Rheumatoid Arthritis.类风湿关节炎中的滑液标志物与细胞外囊泡
Medicina (Kaunas). 2024 Nov 26;60(12):1945. doi: 10.3390/medicina60121945.
2
TWEAK and TNFα, Both TNF Ligand Family Members and Multiple Sclerosis-Related Cytokines, Induce Distinct Gene Response in Human Brain Microvascular Endothelial Cells.TWEAK 和 TNFα 均为 TNF 配体家族成员和与多发性硬化症相关的细胞因子,可诱导人脑血管内皮细胞产生不同的基因反应。
Genes (Basel). 2022 Sep 24;13(10):1714. doi: 10.3390/genes13101714.
3
Lower Expression of TWEAK is Associated with Poor Survival and Dysregulate TIICs in Lung Adenocarcinoma.

本文引用的文献

1
A comprehensive curated resource for follicle stimulating hormone signaling.一个全面整理的促卵泡激素信号传导资源。
BMC Res Notes. 2011 Oct 13;4:408. doi: 10.1186/1756-0500-4-408.
2
NetSlim: high-confidence curated signaling maps.NetSlim:高可信度精心策划的信号转导图谱。
Database (Oxford). 2011 Sep 29;2011:bar032. doi: 10.1093/database/bar032. Print 2011.
3
Interleukin-13 damages intestinal mucosa via TWEAK and Fn14 in mice-a pathway associated with ulcerative colitis.白细胞介素-13 通过 TWEAK 和 Fn14 损伤肠道黏膜-与溃疡性结肠炎相关的通路。
低表达 TWEAK 与肺腺癌不良预后相关,并可调节 TIICs。
Dis Markers. 2022 Jun 6;2022:8661423. doi: 10.1155/2022/8661423. eCollection 2022.
4
Road to Metastasis: The TWEAK Pathway as a Discriminant between Metastasizing and Non-Metastasizing Thick Melanomas.转移之路:TWEAK 通路作为转移性和非转移性厚黑色素瘤的鉴别指标。
Int J Mol Sci. 2021 Sep 29;22(19):10568. doi: 10.3390/ijms221910568.
5
The TWEAK/Fn14/CD163 axis-implications for metabolic disease.TWEAK/Fn14/CD163 轴与代谢性疾病的关系。
Rev Endocr Metab Disord. 2022 Jun;23(3):449-462. doi: 10.1007/s11154-021-09688-4. Epub 2021 Sep 20.
6
E-type prostanoid receptor 4 drives resolution of intestinal inflammation by blocking epithelial necroptosis.E 型前列腺素受体 4 通过阻断上皮细胞坏死性凋亡来驱动肠道炎症的消退。
Nat Cell Biol. 2021 Jul;23(7):796-807. doi: 10.1038/s41556-021-00708-8. Epub 2021 Jul 8.
7
Potential Molecular Mechanism of TNF Superfamily-Related Genes in Glioblastoma Multiforme Based on Transcriptome and Epigenome.基于转录组和表观基因组的多形性胶质母细胞瘤中肿瘤坏死因子超家族相关基因的潜在分子机制
Front Neurol. 2021 Feb 11;12:576382. doi: 10.3389/fneur.2021.576382. eCollection 2021.
8
Evaluation of Computationally Designed Peptides against TWEAK, a Cytokine of the Tumour Necrosis Factor Ligand Family.针对肿瘤坏死因子配体家族细胞因子 TWEAK 的计算设计肽的评估。
Int J Mol Sci. 2021 Jan 21;22(3):1066. doi: 10.3390/ijms22031066.
9
Human Eosinophils Express a Distinct Gene Expression Program in Response to IL-3 Compared with Common β-Chain Cytokines IL-5 and GM-CSF.人类嗜酸性粒细胞在响应 IL-3 时表达与常见的β-链细胞因子 IL-5 和 GM-CSF 不同的基因表达谱。
J Immunol. 2019 Jul 15;203(2):329-337. doi: 10.4049/jimmunol.1801668. Epub 2019 Jun 7.
10
TRAF3IP2 mediates TWEAK/TWEAKR-induced pro-fibrotic responses in cultured cardiac fibroblasts and the heart.TRAF3IP2 在培养的心肌成纤维细胞和心脏中介导 TWEAK/TWEAKR 诱导的促纤维化反应。
J Mol Cell Cardiol. 2018 Aug;121:107-123. doi: 10.1016/j.yjmcc.2018.07.003. Epub 2018 Jul 5.
Gastroenterology. 2011 Dec;141(6):2119-2129.e8. doi: 10.1053/j.gastro.2011.08.040. Epub 2011 Sep 3.
4
A comprehensive manually curated reaction map of RANKL/RANK-signaling pathway.RANKL/RANK 信号通路的综合人工 curated 反应图谱。
Database (Oxford). 2011 Jul 8;2011:bar021. doi: 10.1093/database/bar021. Print 2011.
5
Vascular proteomics and the discovery process of clinical biomarkers: The case of TWEAK.血管蛋白质组学与临床生物标志物的发现过程:以 TWEAK 为例。
Proteomics Clin Appl. 2011 Jun;5(5-6):281-8. doi: 10.1002/prca.201000102. Epub 2011 Apr 28.
6
TWEAK induces apoptosis through a death-signaling complex comprising receptor-interacting protein 1 (RIP1), Fas-associated death domain (FADD), and caspase-8.TWEAK 通过包含受体相互作用蛋白 1(RIP1)、Fas 相关死亡结构域(FADD)和半胱天冬酶-8 的死亡信号复合物诱导细胞凋亡。
J Biol Chem. 2011 Jun 17;286(24):21546-54. doi: 10.1074/jbc.M110.203745. Epub 2011 Apr 27.
7
Detection of the TNFSF members BAFF, APRIL, TWEAK and their receptors in normal kidney and renal cell carcinomas.检测正常肾脏组织和肾细胞癌中 TNFSF 成员 BAFF、APRIL、TWEAK 及其受体。
Anal Cell Pathol (Amst). 2011;34(1-2):49-60. doi: 10.3233/ACP-2011-0001.
8
Soluble TWEAK predicts hemodynamic impairment and functional capacity in patients with pulmonary arterial hypertension.可溶性 TWEAK 可预测肺动脉高压患者的血液动力学损伤和功能能力。
Clin Res Cardiol. 2011 Oct;100(10):879-85. doi: 10.1007/s00392-011-0318-z. Epub 2011 Apr 11.
9
TWEAK and Fn14 expression in the pathogenesis of joint inflammation and bone erosion in rheumatoid arthritis.TWEAK 和 Fn14 在类风湿关节炎关节炎症和骨侵蚀发病机制中的表达。
Arthritis Res Ther. 2011 Mar 24;13(2):R51. doi: 10.1186/ar3294.
10
New pre-conception immune biomarkers for clinical practice: interleukin-18, interleukin-15 and TWEAK on the endometrial side, G-CSF on the follicular side.新的孕前免疫生物标志物用于临床实践:子宫内膜侧的白细胞介素-18、白细胞介素-15 和 TWEAK,卵泡侧的粒细胞集落刺激因子。
J Reprod Immunol. 2011 Mar;88(2):118-23. doi: 10.1016/j.jri.2011.01.007. Epub 2011 Feb 18.