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This product is an unconjugated anti-human TNF-α monoclonal antibody gernerated from the mouse. This antibody can be used for applications: ELISA, Flow Cytometry/FACS.
Please feel free to contact us for a quote and further discussion with our scientists. Datasheets
specifications |
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Antibody Isotype | IgA |
Clone | NGA16M-TT |
Applications | ELISA; FC |
Target | TNF-α |
Host | Mouse |
Clonality | Monoclonal |
Antibody Type | Primary antibody |
Species Reactivity | Human |
Immunogen | Purified recombinant human TNF |
Format | Liquid |
Buffer | PBS |
Storage | Store at 4°C for short-term and -20°C for long-term. Avoid repeated freeze-thaw cycles. |
Target Information |
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Target Name | TNF-α |
Alternative Names | Tumor Necrosis Factor; TNF-Alpha; TNFSF2; Tumor Necrosis Factor Ligand Superfamily Member 2; TNFA; DIF; Tumor Necrosis Factor Ligand 1F; Tumor Necrosis Factor-Alpha; TNF Superfamily Member 2; APC1 Protein; Cachectin; TNLG1F; TNF |
Related Disease | Asthma; Malaria |
Gene ID | 7124 |
UniProt ID | P01375 |
Target Overview | Cytokine that binds to TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. It is mainly secreted by macrophages and can induce cell death of certain tumor cell lines. It is potent pyrogen causing fever by direct action or by stimulation of interleukin-1 secretion and is implicated in the induction of cachexia, Under certain conditions it can stimulate cell proliferation and induce cell differentiation. Impairs regulatory T-cells (Treg) function in individuals with rheumatoid arthritis via FOXP3 dephosphorylation. Upregulates the expression of protein phosphatase 1 (PP1), which dephosphorylates the key 'Ser-418' residue of FOXP3, thereby inactivating FOXP3 and rendering Treg cells functionally defective. Key mediator of cell death in the anticancer action of BCG-stimulated neutrophils in combination with DIABLO/SMAC mimetic in the RT4v6 bladder cancer cell line. Induces insulin resistance in adipocytes via inhibition of insulin-induced IRS1 tyrosine phosphorylation and insulin-induced glucose uptake. Induces GKAP42 protein degradation in adipocytes which is partially responsible for TNF-induced insulin resistance. |
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