Anti-Human CD255 (TWEAK) Functional Grade Purified

Description: The CARL-1 monoclonal antibody reacts with human TWEAK, a type II transmembrane TNF superfamily member with high identity to TNF in its extracellular portion. TWEAK transcript is expressed broadly in many adult and fetal tissues, however, the staining of human peripheral blood mononuclear cells with monoclonal antibodies shows a more restricted pattern. While freshly isolated PBMCs do not express detectable levels of TWEAK on their surface, IFN-γ-stimulated blood monocytes rapidly upregulate TWEAK surface expression. TWEAK is expressed as membrane bound and secreted forms. Interaction of TWEAK with its counter-receptor promotes secretion of IL-8, activation of NF-κB, proliferation of endothelial cells, and apoptosis in a number of human cell lines. Initially, DR3 was thought to be a receptor for TWEAK, but further studies have shown that TWEAK could induce apoptosis via receptors distinct from DR3. While TWEAK exhibits overlapping signaling functions to TNF, it is generally less effective in inducing apoptosis, giving rise to its name, TNF-like weak inducer of apoptosis. For detection of human TWEAK by sandwich ELISA, a combination of purified CARL-2 for capture and biotinylated CARL-1 for detection is recommended.

References:
Nakayama, M., N. Kayagaki, et al. (2000). "Involvement of TWEAK in Interferon gamma-stimulated Monocyte Cytotoxicity." J. Exp. Med. 192(9): 1373-1380.
Chicheportiche, Y., P. R. Bourdon, et al. (1997). "TWEAK, a new secreted ligand in the tumor necrosis factor family that weakly induces apoptosis." J Biol Chem 272(51): 32401-10.
Kaplan, M. J., D. Ray, et al. (2000). "TRAIL (Apo2 ligand) and TWEAK (Apo3 ligand) mediate CD4+ T cell killing of antigen-presenting macrophages [In Process Citation]." J Immunol 164(6): 2897-904.
Lynch, C. N., Y. C. Wang, et al. (1999). "TWEAK induces angiogenesis and proliferation of endothelial cells." J Biol Chem 274(13): 8455-9.
Schneider, P., R. Schwenzer, et al. (1999). "TWEAK can induce cell death via endogenous TNF and TNF receptor 1." Eur J Immunol 29(6): 1785-92.