TNF-a (Tumor necrosis factor), being an endogenous pyrogen, is able to induce fever, apoptotic cell death, inflammation and inhibit tumorigenesis. As reported, TNFa could inhibit the proliferation and induce apoptosis of A549 cells, and the concentration of IL-1β in cell supernatant will increase after stimulation. A549 cells were incubated in DMEM with TNFa (1 ng/ml, 10 ng/ml) for 2h, 4h, 8h, 24h, 48h, then cells were observed by inverted microscope.
Lyophilized from 20 mM Tris (pH 8.0) with 150 mM NaCl, 1 mM EDTA, 1 mM DTT, 0.01% SKL, 5% Trehalose, Proclin300. Reconstitute with 20 mM Tris and 150 mM NaCl (pH 8.0) to a concentration of 0.1-1.0 mg/mL. Do not vortex.
For short-term storage (1-2 weeks), store at 4ºC. For long-term storage, store at -20ºC or below. After reconstitution, keep as concentrated solution. Avoid freeze-thaw cycles.
N-terminal His-Tag; Leu80~Leu235 (NP_001265530.1)
< 1 EU/μg
For laboratory use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
tumor necrosis factor , DIF , TNF-a , TNF-alpha , TNFSF2 , TNFalpha , Tnfa , Tnfsf1a , Tnlg1f
This gene encodes a multifunctional proinflammatory cytokine that belongs to the tumor necrosis factor (TNF) superfamily. Members of this family are classified based on primary sequence, function, and structure. This protein is synthesized as a type-II transmembrane protein and is reported to be cleaved into products that exert distinct biological functions. It plays an important role in the innate immune response as well as regulating homeostasis but is also implicated in diseases of chronic inflammation. In mouse deficiency of this gene is associated with defects in response to bacterial infection, with defects in forming organized follicular dendritic cell networks and germinal centers, and with a lack of primary B cell follicles. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jun 2013]