TWEAK overexpression 293T lysate (whole cell)

Supplementary information

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

The TNF-like weak inducer of apoptosis (TWEAK) also known as CD255 is a cytokine involved in a variety of cellular processes. This protein has an approximate mass of 24 kDa. TWEAK is expressed in many tissues including the heart brain and spleen. It functions by binding to the fibroblast growth factor-inducible 14 (Fn14) receptor leading to the activation of downstream signaling pathways. TWEAK's role as a ligand places it in the tumor necrosis factor (TNF) superfamily highlighting its involvement in cell death and inflammation signaling.

Biological function summary

TWEAK modulates processes like cell proliferation differentiation and apoptosis. This cytokine affects the immune response and tissue regeneration becoming significant in processes that require tissue remodeling. While acting independently TWEAK does not form part of a larger protein complex. Instead it signals mainly through its exclusive receptor Fn14 on responsive cells triggering cellular responses that influence its biological activities.

Pathways

TWEAK plays an important role in the NF-kB and MAPK signaling pathways. These pathways are important for immune response regulation and cell survival. In these pathways TWEAK closely interacts with TNF receptor-associated factors (TRAFs) which facilitate TWEAK signaling. The connections to pathways involving inflammatory response highlight its significance in maintaining homeostasis within the cellular environment.

TWEAK's activity links to conditions like cancer and rheumatoid arthritis. In cancer excessive TWEAK signaling can contribute to tumor growth and metastasis through its pro-inflammatory and pro-angiogenic effects. In rheumatoid arthritis TWEAK expression relates to joint inflammation and tissue damage where it interacts with proteins like IL-6 and TNF-alpha. These interactions suggest potential therapeutic targets by modulating TWEAK or its signaling partners to treat these diseases.