Reactivity | HuSpecies Glossary |
Applications | Bioactivity |
Format | Carrier-Free |
Details of Functionality | Measured by its ability to inhibit the TWEAK-dependent proliferation of HUVEC human umbilical vein endothelial cells. The ED50 for this effect is 10-30 ng/mL in the presence of 15 ng/mL recombinant human TWEAK. |
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Source | Mouse myeloma cell line, NS0-derived human TWEAK R/TNFRSF12 protein
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Accession # | |||||||
N-terminal Sequence | Glu28 |
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Structure / Form | Disulfide-linked homodimer |
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Protein/Peptide Type | Recombinant Proteins |
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Gene | TNFRSF12A |
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Purity | >90%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining. |
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Endotoxin Note | <0.10 EU per 1 μg of the protein by the LAL method. |
Dilutions |
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Theoretical MW | 32 kDa (monomer). 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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SDS-PAGE | 35-45 kDa, reducing conditions |
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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. |
Purity | >90%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining. |
Reconstitution Instructions | Reconstitute at 100 μg/mL in sterile PBS. |
The gene for TNF-related weak inducer of apoptosis receptor (TWEAK R) was originally identified as a fibroblast growth factor-inducible immediate-early response gene Fn14 in mouse NIH 3T3 fibroblasts (1, 2). Human TWEAK R cDNA encodes a 129 amino acid (aa) residue type I transmembrane protein with a 27 aa signal peptide, a 53 aa extracellular domain, a 21 aa transmembrane domain and a 28 aa cytoplasmic domain (1 - 3). Human and mouse TWEAK R share 82% aa sequence identity. TWEAK R is the smallest member of the TNF receptor superfamily and contains only one cysteine-rich region in its extracellular domain. The TWEAK R cytoplasmic domain conatins one TRAF binding motif which binds TRAFs 1, 2, and 3. TWEAK R binds its ligand TWEAK/TNFSF12 with high affinity to initiate a signal transduction cascade that depending upon the cell type, may lead to a variety of cellular responses including cell death, cell proliferation, and angiogenesis (2 - 6). In new born mice, TWEAK R is highly expressed in all tissues examined (heart, intestine, kidney, liver, lung and skin) (1). In adult mice, high TWEAK R expression levels are found in the heart and ovary, while lower expression levels are detected in the lung, kidney, skin. Elevated levels of TWEAK R mRNA were found in human or mouse hepatocellular carcinoma specimens, in regenerating mouse liver and in injured rat arteries (2, 3).
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