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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.

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/a35da7f39bad/JST2012-376470.001.jpg

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