TWEAK (TNF-related weak inducer of apoptosis), encoded by the TNFSF12 gene, is a type II transmembrane protein in the TNF superfamily. It plays roles in apoptosis, inflammation, and angiogenesis . Antibodies targeting TWEAK are critical for studying its interaction with receptors like TNFRSF12A (TWEAK R/Fn14) and its downstream signaling pathways .
Apoptosis Regulation: TWEAK antibodies block TWEAK-TWEAK R interactions, reducing NF-κB activation and apoptosis in endothelial cells .
Angiogenesis Modulation: TWEAK antibodies inhibit endothelial cell proliferation and migration, critical in cancer and inflammatory diseases .
Structural Epitopes: Antibody-antigen binding involves aromatic residues (e.g., tryptophan, tyrosine) in complementarity-determining regions (CDRs), contributing to high specificity .
Western Blot: Detects TWEAK at ~30 kDa under reducing conditions .
Neutralization Efficacy: IC₅₀ values range from 0.1–1.0 μg/mL in cell-based assays .
TWEAK antibodies are typically generated via hybridoma technology :
Immunization: Human Ig transgenic mice immunized with recombinant TWEAK antigen .
Hybridoma Screening: Clones selected for high affinity (KD < 1 nM) and specificity .
Characterization: Validated via ELISA, surface plasmon resonance (SPR), and functional assays .
Autoimmune Diseases: TWEAK antibodies show potential in rheumatoid arthritis and lupus models by reducing pro-inflammatory cytokines .
Cancer: Targeting TWEAK R inhibits tumor angiogenesis in hepatocellular carcinoma .
KEGG: cel:CELE_F29F11.4
STRING: 6239.F29F11.4