Reactivity | HuSpecies Glossary |
Applications | Bioactivity |
Details of Functionality | Measured in a cell proliferation assay using HUVEC human umbilical vein endothelial cells. The ED50 for this effect is 0.200-4.00 ng/mL. |
Source | E. coli-derived human TWEAK/TNFSF12 protein Arg93-His249, with an N-terminal Met and 6-His tag |
Accession # | |
N-terminal Sequence | Met |
Protein/Peptide Type | Recombinant Proteins |
Gene | TNFSF12 |
Purity | >95%, by SDS-PAGE under reducing conditions and visualized by silver stain. |
Endotoxin Note | <0.10 EU per 1 μg of the protein by the LAL method. |
Dilutions |
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Theoretical MW | 18.3 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors. |
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Publications |
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Storage | Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
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Buffer | Lyophilized from a 0.2 μm filtered solution in PBS with BSA as a carrier protein. |
Purity | >95%, by SDS-PAGE under reducing conditions and visualized by silver stain. |
Reconstitution Instructions | Reconstitute at 100 μg/mL in sterile PBS containing at least 0.1% human or bovine serum albumin. |
TWEAK is a type II transmembrane protein belonging to the TNF superfamily (1). It contains a short cytoplasmic domain (aa 1‑18), the transmembrane domain
(aa 19-42) and an extracellular domain (aa 43-249). The extracellular domains of human and murine TWEAK share 89% aa sequence identity. A soluble form of TWEAK is generated from the membrane-associated molecules by proteolytic cleavage after Arg 93 suggesting that TWEAK may have long-range effects. TWEAK is expressed widely in many tissues and cells. At least two receptors that bind TWEAK have been identified (2-4). Death Receptor 3 (DR3), also known as TNFRSF12, Apo-3, LARD, WSL-1 or TRAMP, is a TNF receptor superfamily member that is expressed predominantly in tissues with high lymphocyte content (2). It has been suggested that induction of cell death by TWEAK-DR3 interaction involves the activation of NF-kappa B. In cells that lack DR3, alternate pathways of TWEAK-induced cell death mediated by receptors distinct from DR3 have been suggested (5, 6). TWEAK receptor (TWEAKR, alternatively known as FN14), is a novel TNF receptor superfamily member that also binds TWEAK (3, 4). It is a mitogen-inducible gene that is expressed in fibroblasts, hepetocellular carcinomas and endothelial cells. TWEAK-TWEAKR interaction has been shown to play a role in endothelial cell growth and migration. This effect of TWEAK is not mediated by an up-regulation of VEGF (7).
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