Recombinant Human C1qTNF1 Protein, CF Summary
Product Specifications
ED50 = 0.6-3.6 µg/mL.
Arg26-Pro281, with a C-terminal 6-His tag
Analysis
Product Datasheets
Carrier Free
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.
9268-TN
| Formulation | Lyophilized from a 0.2 μm filtered solution in HEPES and NaCl. |
| Reconstitution | Reconstitute at 250 μg/mL in 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.
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Scientific Data
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When Recombinant Human BAI3 is coated at 4 µg/mL, Recombinant Human C1qTNF1 (Catalog # 9268-TN) binds with an ED50 of 0.6-3.6 µg/mL.
Reconstitution Calculator
Background: CTRP1/C1qTNF1
C1qTNF1 (CTRP1) is an approximately 35 kDa member of the C1q family of secreted proteins and plays a role in energy metabolism and inflammation (1, 2). C1qTNF1 contains a collagen-like region and one C1q-like domain (3). Mature human C1qTNF1 shares 80% aa sequence identity with mouse and rat C1qTNF1. Circulating levels of C1qTNF1 are elevated in obesity, hypertension, and diabetes but can be decreased in the serum of diet-induced obese mice (4-6). C1qTNF1 expression is up-regulated in atherosclerotic plaques or adipose tissue by oxidized LDL or inflammatory cytokines (3, 7, 8). In turn, it induces the expression of inflammatory cytokines (7, 9) and the up-reglation of adhesion proteins on vascular endothelial cells (8). Systemically administered C1qTNF1, in contrast, can limit tissue damage following myocardial infarction (9). In skeletal muscle, C1qTNF1 promotes fatty acid oxidation, energy expenditure, insulin sensitivity, and glucose uptake and glycolysis (6, 10). It also induces the proliferation of immature chondrocytes (11) and aldosterone synthesis in the adrenal cortex (4). R&D Systems in-house testing indicates that C1qTNF1 binds to BAI3, consistent with the reported interactions between BAI3 and C1qL proteins (12).
- Grebrehiwet, B. et al. (2012) Front. Immunol. 5:3.
- Seldin, M.M. et al. (2014) Rev. Endocr. Metab. Disord. 15:111.
- Kim, K.-Y. et al. (2006) FEBS Lett. 580:3953.
- Jeon, J.H. et al. (2008) FASEB J. 22:1502.
- Xin, Y. et al. (2014) Endocr. J. 61:841.
- Peterson, J. M. et al. (2012) J. Biol. Chem. 287:1576.
- Wang, X.Q. et al. (2016) Atherosclerosis 250:38.
- Lu, L. et al. (2016) Eur. Heart J. 37:1762.
- Yuasa, D. et al. (2016) FASEB J. 30:1065.
- Han, S. et al. (2016) J. Nutr. Biochem. 27:43.
- Akiyama, H. et al. (2013) Mol. Cell. Endocrinol. 369:63.
- Bolliger, M.F. et al. (2011) Proc. Natl. Acad. Sci. USA 108:2534.
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