Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/129968
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Type: Journal article
Title: A bioinformatics resource for TWEAK-Fn14 signaling pathway
Author: Bhattacharjee, M.
Raju, R.
Radhakrishnan, A.
Nanjappa, V.
Muthusamy, B.
Singh, K.
Kuppusamy, D.
Lingala, B.T.
Pan, A.
Mathur, P.P.
Harsha, H.C.
Prasad, T.S.K.
Atkins, G.J.
Pandey, A.
Chatterjee, A.
Citation: Journal of Signal Transduction, 2012; 2012:376470-1-376470-10
Publisher: Hindawi Publishing Corporation
Issue Date: 2012
ISSN: 2090-1739
2090-1747
Statement of
Responsibility: 
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, and Aditi Chatterjee
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.
Rights: Copyright © 2012 Mitali Bhattacharjee et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
DOI: 10.1155/2012/376470
Grant ID: http://purl.org/au-research/grants/nhmrc/465419
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Orthopaedics and Trauma publications

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