A Bioinformatics Resource for TWEAK-Fn14 Signaling Pathway

Author:

Bhattacharjee Mitali12,Raju Rajesh13,Radhakrishnan Aneesha14,Nanjappa Vishalakshi12,Muthusamy Babylakshmi15,Singh Kamlendra5,Kuppusamy Dheebika5,Lingala Bhavya Teja5,Pan Archana5,Mathur Premendu Prakash45,Harsha H. C.1,Prasad T. S. Keshava125,Atkins Gerald J.6,Pandey Akhilesh78910,Chatterjee Aditi1

Affiliation:

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

2. Amrita School of Biotechnology, Amrita University, Kollam 690525, India

3. Department of Biotechnology, Kuvempu University, Shankaraghatta 577451, India

4. Department of Biochemistry and Molecular Biology, Pondicherry University, Puducherry 605014, India

5. Centre of Excellence in Bioinformatics, School of Life Sciences, Pondicherry University, Puducherry 605014, India

6. Bone Cell Biology Group, Discipline of Orthopaedics and Trauma, University of Adelaide and The Hanson Institute, Adelaide, 5002 SA, Australia

7. McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA

8. Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA

9. Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA

10. Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA

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.

Funder

Department of Biotechnology, Government of India

Publisher

Hindawi Limited

Subject

Cell Biology,Cellular and Molecular Neuroscience,Biochemistry

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