Table of Contents
Journal of Signal Transduction
Volume 2012, Article ID 376470, 10 pages
Research Article

A Bioinformatics Resource for TWEAK-Fn14 Signaling Pathway

1Institute of Bioinformatics, International Tech Park, Bangalore 560066, India
2Amrita School of Biotechnology, Amrita University, Kollam 690525, India
3Department of Biotechnology, Kuvempu University, Shankaraghatta 577451, India
4Department of Biochemistry and Molecular Biology, Pondicherry University, Puducherry 605014, India
5Centre of Excellence in Bioinformatics, School of Life Sciences, Pondicherry University, Puducherry 605014, India
6Bone Cell Biology Group, Discipline of Orthopaedics and Trauma, University of Adelaide and The Hanson Institute, Adelaide, 5002 SA, Australia
7McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
8Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
9Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
10Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA

Received 22 December 2011; Accepted 3 February 2012

Academic Editor: A. Yoshimura

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.


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.