CD266 (TWEAK Receptor) Monoclonal Antibody (ITEM-4), Biotin, eBioscience™, Invitrogen™

Description

Description: The ITEM-4 antibody reacts with human TWEAK Receptor/Fn14 (fibroblast growth factor-inducible 14 kDa protein). Fn14 is distantly related to the TNFR family, containing one cysteine-rich domain in the extracellular region and a TNFR-associated factor binding domain but does not contain a death domain (DD) cytoplasmic region. Fn14 plays a role in TWEAK-induced endothelial cell migration, proliferation, and angiogenesis. TWEAK-induced cell death via Fn14 includes both apoptosis and necrosis and can be blocked by an anti-TWEAK antibody, CARL-1. Fn14 is expressed on HUVEC and in some cancer tissues but not on freshly isolated PBMCs. Fn14 mRNA expression has been identified during liver regeneration. It has been reported that ITEM-4 cross-reacts with mouse Fn14. In the mouse, Fn14 is reported to be constitutively expressed by Colon 26 cell line. The ITEM-4 antibody has been show to have blocking function. Applications Reported: The ITEM-4 antibody has been reported for use in flow cytometric analysis. Applications Tested: The ITEM-4 antibody has been tested by flow cytometric analysis on human and mouse Fn14 transfected cells. This can be used at less than or equal to 0.5 μg per test. A test is defined as the amount (μg) of antibody that will stain a cell sample in a final volume of 100 μL. Cell number should be determined empirically but can range from 10^5 to 10^8 cells/test.

TWEAK is a member of the TNF family and was first described as a weak inducer of apoptosis in demonstrate that this relatively small molecule is a fully transformed cell lines. Recently, a receptor for TWEAK was isolated by expression cloning from a HUVEC cell cDNA library. TweakR is a small protein belonging to TNF receptor super family. TweakR is capable of intiating a proliferative signal by binding to TRAF1, 2, and 3. TweakR mRNA is upregulated during tissue regeneration in the aorta and liver. It may also play a role in vascular cell migration and angiogenesis.