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. 2020 Feb 11;9(2):405. doi: 10.3390/cells9020405

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Tumor necrosis factor-like weak inducer of apoptosis (TWEAK)/ fibroblast growth factor-inducible 14 (Fn14) Signaling. (A) Schematic representation of human TWEAK and Fn14 receptor structure showing full-lengths and TWEAK secreted form. (B) Soluble TWEAK binds to the extracellular domain of the Fn14 receptor and produces its trimerization. This structural change of the receptor triggers the recruitment of TRAF proteins to its cytoplasmic tail and the activation of the different pathways; canonical (p50/RelA) and non-canonical (p52/RelB) NF-kB, ERK/JNK/p38 and AP-1, JAK/STAT and PI3K/AKT. Increased activation of these signaling pathways leads to the regulation of specific target genes with their biological mechanistic role.