GDF15 (human):Fc (mouse) (rec.)
|Synonyms||Growth/Differentiation Factor 15; GDF-15; Macrophage Inhibitory Cytokine 1; MIC-1; NSAID-activated Gene 1 Protein; NAG-1; NRG-1; PTGFB; PLAB; PDF|
|Source/Host||HEK 293 cells|
The extracellular domain of human GDF15 (aa 197-308) is fused to the N-terminus of the Fc region of mouse IgG2a.
|Endotoxin Content||<0.06EU/μg purified protein (LAL test; Lonza).|
|Reconstitution||Reconstitute at 100μg/ml in sterile PBS.|
|Formulation||Lyophilized from 0.2μm-filtered solution in PBS.|
|Other Product Data||
NCBI reference NP_004855.2: GDF15 (human)
|Declaration||Manufactured by Chimerigen.|
|Shipping and Handling|
|Short Term Storage||+4°C|
|Long Term Storage||-20°C|
|Handling Advice||Avoid freeze/thaw cycles.|
Stable for at least 1 year after receipt when stored at -20°C.
Working aliquots are stable for up to 3 months when stored at -20°C.
|Product Specification Sheet|
Growth Differentiation Factor 15 (GDF15) is a divergent member of the TGF-β superfamily. Human GDF15 shares 66% and 68% amino acid sequence identity with the rat and mouse proteins, respectively. GDF15 is highly expressed in placenta and brain, and it is expressed at lower levels in kidney, pancreas, prostate and colon. Similar to other TGF-β family proteins, GDF15 is synthesized as a large precursor protein that is cleaved at a dibasic cleavage site (RxxR) to release the mature protein. Biologically active GDF15 is a disulfide-linked homodimer of the mature protein. GDF15 has been shown to have various functions, including inhibition of TNF-α production from lipopolysaccharide-stimulated macrophages and the induction of cartilage formation. GDF15 promotes neuronal survival, and hypothalamic expression of GDF15 causes appetite suppression via modulation of neuropeptide Y and pro-opiomelanocortin levels. GFRAL and GDF15 signaling is implicated in diet-based obesity and insulin resistance. GDF15 is cardioprotective via inhibition of platelet activation, limiting atherosclerosis, promoting recovery following myocardial infarction, and regulating angiogenesis. Exposure of cardiomyocytes to GDF15 results in Smad2 and Smad3 phosphorylation.