>90%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
<0.10 EU per 1 μg of the protein by the LAL method.
Measured by its binding ability in a functional ELISA. When Recombinant Mouse GSF-15 is immobilized at 2 µg/mL (100 µL/well), the concentration of
Recombinant Mouse Activin RIB/ALK-4 Fc Chimera (Catalog # 1477-AR)
that produces 50% of the optimal binding response is approximately 1-6 μg/mL.
E. coli-derived mouse GDF-15 protein Ser189-Ala303
When Recombinant Mouse GDF-15 (Catalog # 8944-GD) is immobilized at 2 µg/mL (100 µL/well), the concentration of Recombinant Mouse Activin RIB/ALK-4 Fc Chimera (Catalog # 1477-AR) binds with a typical ED50 of 1-6 μg/mL.
1 μg/lane of Recombinant Mouse GDF-15 (Catalog # 8944-GD) was resolved with SDS-PAGE under reducing (R) and non-reducing (NR) conditions and visualized by silver staining, showing bands at 10.5 kDa and 22 kDa, respectively.
Growth Differentiation Factor 15 (GDF-15), also called Macrophage Inhibitory Cytokine 1 (MIC-1), Placental Transforming Growth Factor beta, Prostate-derived Factor, and Placental Bone Morphogenetic Protein, is a divergent member of the TGF-beta superfamily. Cellular responses to TGF-beta proteins are mediated by hetero-oligomeric complexes of type I and type II serine/threonine kinase receptors (1-3). GDF-15 is highly expressed in placenta and brain, and it is expressed at lower levels in kidney, pancreas, prostate, and colon. Similar to other TGF-beta family proteins, GDF-15 is synthesized as a large precursor protein that is cleaved at a dibasic cleavage site (RxxR) to release the mature protein. Mature mouse GDF-15 shares 66% and 97% amino acid sequence identity with the human and rat proteins, respectively. The C-terminal domain of GDF-15 contains seven characteristic conserved cysteine residues necessary for the formation of the cysteine knot and the single inter-chain disulfide bond (4, 5). Biologically active GDF-15 is a disulfide-linked homodimer of the mature protein. GDF-15 has been shown to have various functions, including inhibition of TNF-alpha production from lipopolysaccharide-stimulated macrophages and the induction of cartilage formation (2, 6). GDF-15 also promotes neuronal survival, and hypothalamic expression of GDF-15 causes appetite suppression via modulation of neuropeptide Y and pro-opiomelanocortin levels (7-10). GDF-15 is cardioprotective via inhibition of platelet activation, limiting atherosclerosis, promoting recovery following myocardial infarction, and regulating angiogenesis (11-15). Exposure of cardiomyocytes to GDF-15 results in Smad2 and Smad3 phosphorylation (16).
Unsicker, K. et al. (2013) Cytokine Growth Factor Rev. 24:373.
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Strelau, J. et al. (2000) J. Neurosci. 20:8597.
Breit, S.N. et al. (2011) Growth Factors 29:187.
Strelau, J. et al. (2009) J. Neurosci. 29:13640.
Whitson, R.J. et al. (2013) J. Cell. Biochem. 114:1424.
Rossaint, J. et al. (2013) J. Thromb. Haemost. 11:335.
Song, H. et al. (2012) Mol. Biol. Rep. 39:4017.
Preusch, M.R. et al. (2013) Eur. J. Med. Res. 18:19.
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