Recombinant human TWEAKR/FN14 protein

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

The TWEAKR/FN14 known also as FN14 protein is a receptor primarily involved in cellular signaling. It is found on the cell surface and has a molecular weight of approximately 14 kDa. This receptor expresses in various tissues but its expression is especially high in the liver kidney and muscle tissues. Through its engagement with its ligand TWEAK (Tumor Necrosis Factor-Like Weak Inducer of Apoptosis) TWEAKR/FN14 participates in signal transduction processes that regulate cell survival and proliferation.

Biological function summary

TWEAKR/FN14 influences multiple cellular activities including inflammation proliferation and apoptosis. It does not solely function in isolation often interacting with other proteins in complex networks. In fact FN14 often couples its activity with downstream signaling proteins that impact pathways involved in tissue remodeling and repair. The receptor's ability to mediate these processes makes it a significant regulator of tissue response to damage.

Pathways

Signaling through TWEAKR/FN14 primarily involves the NF-κB and MAPK pathways. These signaling pathways are critical for mediating cellular responses to external stimuli such as stress or injury. The NF-κB pathway in particular plays a role in immune and inflammatory responses where FN14 through its interaction modulates these responses. Additionally proteins such as TRAF (TNF Receptor Associated Factor) are related to FN14 through these pathways contributing to its signaling functions.

Associated diseases and disorders

Dysregulation of TWEAKR/FN14 is linked to pathological conditions such as cancer and fibrosis. Overexpression of FN14 has been observed in several malignancies and its interaction with TWEAK has been implicated in tumorigenic processes. Meanwhile in fibrosis FN14 is associated with excessive tissue repair and scarring connected to the accumulation of extracellular matrix proteins. Altered expression levels and activity of FN14 with its partner proteins can contribute to the progression of these diseases highlighting its potential as a therapeutic target.