TWEAK-Fn14信号通路的生物信息学资源。

Journal of signal transduction Pub Date : 2012-01-01 Epub Date: 2012-05-09 DOI:10.1155/2012/376470
Mitali Bhattacharjee, Rajesh Raju, Aneesha Radhakrishnan, Vishalakshi Nanjappa, Babylakshmi Muthusamy, Kamlendra Singh, Dheebika Kuppusamy, Bhavya Teja Lingala, Archana Pan, Premendu Prakash Mathur, H C Harsha, T S Keshava Prasad, Gerald J Atkins, Akhilesh Pandey, Aditi Chatterjee
{"title":"TWEAK-Fn14信号通路的生物信息学资源。","authors":"Mitali Bhattacharjee,&nbsp;Rajesh Raju,&nbsp;Aneesha Radhakrishnan,&nbsp;Vishalakshi Nanjappa,&nbsp;Babylakshmi Muthusamy,&nbsp;Kamlendra Singh,&nbsp;Dheebika Kuppusamy,&nbsp;Bhavya Teja Lingala,&nbsp;Archana Pan,&nbsp;Premendu Prakash Mathur,&nbsp;H C Harsha,&nbsp;T S Keshava Prasad,&nbsp;Gerald J Atkins,&nbsp;Akhilesh Pandey,&nbsp;Aditi Chatterjee","doi":"10.1155/2012/376470","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":89176,"journal":{"name":"Journal of signal transduction","volume":"2012 ","pages":"376470"},"PeriodicalIF":0.0000,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/376470","citationCount":"31","resultStr":"{\"title\":\"A Bioinformatics Resource for TWEAK-Fn14 Signaling Pathway.\",\"authors\":\"Mitali Bhattacharjee,&nbsp;Rajesh Raju,&nbsp;Aneesha Radhakrishnan,&nbsp;Vishalakshi Nanjappa,&nbsp;Babylakshmi Muthusamy,&nbsp;Kamlendra Singh,&nbsp;Dheebika Kuppusamy,&nbsp;Bhavya Teja Lingala,&nbsp;Archana Pan,&nbsp;Premendu Prakash Mathur,&nbsp;H C Harsha,&nbsp;T S Keshava Prasad,&nbsp;Gerald J Atkins,&nbsp;Akhilesh Pandey,&nbsp;Aditi Chatterjee\",\"doi\":\"10.1155/2012/376470\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":89176,\"journal\":{\"name\":\"Journal of signal transduction\",\"volume\":\"2012 \",\"pages\":\"376470\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2012-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1155/2012/376470\",\"citationCount\":\"31\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of signal transduction\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1155/2012/376470\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2012/5/9 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of signal transduction","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1155/2012/376470","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2012/5/9 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 31

摘要

TNF-related weak inducer of apoptosis (TWEAK)是TNF超家族的新成员。它通过TNFRSF12A(俗称Fn14)发出信号。TWEAK-Fn14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。尽管有报道称TWEAK与自身免疫性疾病、癌症、中风和肾脏相关疾病相关,但在任何信号通路库中尚未发现TWEAK- fn14信号传导的下游分子事件。在本文中,我们从文献中,特别是在人类系统中报道的文献中,手工编译了由TWEAK-Fn14相互作用刺激的下游反应。我们手工积累了TWEAK-Fn14通路,结果编目了46个参与各种生化反应的蛋白,以及TWEAK-Fn14诱导的28个基因的表达。我们已经启用了来自NetPath的各种标准交换格式的数据,这是一个信令路径存储库。我们相信这种复合的分子相互作用途径将能够在TWEAK信号通路中发现新的信号成分。这反过来又可能导致确定与tweak相关疾病的潜在治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

A Bioinformatics Resource for TWEAK-Fn14 Signaling Pathway.

A Bioinformatics Resource for TWEAK-Fn14 Signaling Pathway.

A Bioinformatics Resource for TWEAK-Fn14 Signaling Pathway.

A Bioinformatics Resource for TWEAK-Fn14 Signaling Pathway.

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.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信