Recombinant Mouse TWEAK R/TNFRSF12 Fc Chimera Protein, CF
Recombinant Mouse TWEAK R/TNFRSF12 Fc Chimera Protein, CF Summary
|Mouse TWEAK R
Accession # Q9CR75
CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.
In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.
|Formulation||Lyophilized from a 0.2 μm filtered solution in PBS.|
|Reconstitution||Reconstitute at 100 μg/mL in sterile PBS.|
|Shipping||The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.|
|Stability & Storage:||Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
Background: TWEAK R/TNFRSF12
TNF-related weak inducer of apoptosis receptor (TWEAK R) belongs to the TNF receptor superfamily and is designated TNFRSF12. The gene for TWEAK R was originally identified as a fibroblast growth factor-inducible immediate-early response gene Fn14 in mouse NIH 3T3 fibroblasts (1, 2). Mouse TWEAK R cDNA encodes a 129 amino acid (aa) residues 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 contains 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 by both caspase-dependent apoptosis and cathepsin B-dependent necrosis, cell proliferation, and angiogenesis (2-6). In newborn 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).
- Meighan-Mantha, R. et al. (1999) J. Biol. Chem. 274:33166.
- Feng, S. et al. (2000) Am. J. Pathol. 156:1253.
- Wiley, S. et al. (2001) Immunity 15:837.
- Schneider, P. et al. (1999) Eur. J. Immunol. 29:1785.
- Nakayama, M. et al. (2002) J. Immunol. 168:734.
- Lynch, C.N. et al. (1999) J. Biol. Chem. 274:8455.
Citations for Recombinant Mouse TWEAK R/TNFRSF12 Fc Chimera Protein, CF
R&D Systems personnel manually curate a database that contains references using R&D Systems products. The data collected includes not only links to publications in PubMed, but also provides information about sample types, species, and experimental conditions.
Citations: Showing 1 - 2
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TWEAK/Fn14 pathway is a novel mediator of retinal neovascularization.
Authors: Ameri H, Liu H, Liu R, Ha Y, Paulucci-Holthauzen A, Hu S, Motamedi M, Godley B, Tilton R, Zhang W
Invest Ophthalmol Vis Sci, 2014;55(2):801-13.
Sample Types: In Vivo
Applications: In Vivo
TWEAK/Fn14 interaction regulates RANTES production, BMP-2-induced differentiation, and RANKL expression in mouse osteoblastic MC3T3-E1 cells.
Authors: Ando T, Ichikawa J, Wako M, Hatsushika K, Watanabe Y, Sakuma M, Tasaka K, Ogawa H, Hamada Y, Yagita H, Nakao A
Arthritis Res. Ther., 2006;8(5):R146.
Sample Types: Whole Cells
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