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Updated: May 21, 2026

Using Human Differentially Expressed Gene Lists to Perform Downstream Pathway Enrichment Analysis and Target Prioritization
Published on: October 3, 2025
A Bioinformatics Resource for TWEAK-Fn14 Signaling Pathway.
Mitali Bhattacharjee1, Rajesh Raju, Aneesha Radhakrishnan
1Institute of Bioinformatics, International Tech Park, Bangalore 560066, India.
This study details the TWEAK-Fn14 signaling pathway, identifying 46 proteins and 28 gene expressions. This curated pathway may reveal new therapeutic targets for TWEAK-associated disorders.
Area of Science:
- Cellular signaling pathways
- Molecular biology
- Immunology
Background:
- TNF-related weak inducer of apoptosis (TWEAK) is a TNF superfamily member signaling via Fn14 (TNFRSF12A).
- TWEAK-Fn14 interactions regulate critical cellular functions like proliferation, inflammation, and apoptosis.
- While TWEAK is linked to diseases, its downstream signaling events are not well-documented.
Purpose of the Study:
- To manually compile and characterize the downstream molecular events of TWEAK-Fn14 signaling from existing literature.
- To create a comprehensive resource for TWEAK-Fn14 pathway interactions, particularly in human systems.
- To make this pathway data available in standard exchange formats via the NetPath repository.
Main Methods:
- Manual curation of scientific literature focusing on TWEAK-Fn14 signaling.
- Identification and cataloging of proteins and gene expressions involved in the pathway.
- Data organization and deposition into the NetPath signaling pathway repository.
Main Results:
- A detailed TWEAK-Fn14 signaling pathway was constructed, involving 46 proteins.
- The pathway encompasses 28 TWEAK-Fn14 induced gene expressions.
- Pathway data is now accessible through NetPath in standard exchange formats.
Conclusions:
- The compiled TWEAK-Fn14 pathway provides a valuable resource for understanding TWEAK signaling.
- This pathway map can facilitate the discovery of novel signaling components.
- Identification of new components may lead to potential therapeutic targets for TWEAK-related diseases.
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