TNF-alpha (Tumor Necrosis Factor alpha) Antibody - With BSA and Azide
Purified Mouse Monoclonal Antibody
|Application ||WB, IHC, FC, IP, E|
|Other Names||Tumor necrosis factor, Cachectin, TNF-alpha, Tumor necrosis factor ligand superfamily member 2, TNF-a, Tumor necrosis factor, membrane form, N-terminal fragment, NTF, Intracellular domain 1, ICD1, Intracellular domain 2, ICD2, C-domain 1, C-domain 2, Tumor necrosis factor, soluble form, TNF, TNFA, TNFSF2|
|Target/Specificity||Recombinant human TNF-alpha|
|Application Note||Flow Cytometry : 0.5-1ug/million cells|
Immunofluorescence : 1-2ug/ml
Immunoprecipitation : 1-2ug/500ug protein
Western Blotting (Not tested)
Immunohistology (Frozen & Formalin-paraffin) : 1-2ug/ml for 30 min at RT
(Staining of formalin-fixed tissues requires boiling tissue sections in 10mM Citrate Buffer, pH 6.0, for 10-20 min followed by cooling at RT for 20 minutes).
|Format||0.5 ml at 200ug/ml with BSA and azide|
|Storage||Store at 2 to 8°C.Antibody is stable for 24 months.|
|Precautions||TNF-alpha (Tumor Necrosis Factor alpha) Antibody - With BSA and Azide is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||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 (PubMed:23396208). 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 (PubMed:22517918).|
|Cellular Location||Cell membrane; Single-pass type II membrane protein Tumor necrosis factor, soluble form: Secreted C-domain 2: Secreted.|
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Provided below are standard protocols that you may find useful for product applications.
This MAb recognizes human 17-26kDa protein, which is identified as cytokine TNF-alpha (Tumor Necrosis Factor-alpha). TNF-alpha can be expressed as a 17kDa free molecule, or as a 26kDa membrane protein. TNF-alpha is a protein secreted by lipopolysaccharide-stimulated macrophages, and causes tumor necrosis when injected into tumor bearing mice. TNF alpha is believed to mediate pathogenic shock and tissue injury associated with endotoxemia. TNF alpha exists as a multimer of two, three, or five non-covalently linked units, but shows a single 17kDa band following SDS PAGE under non-reducing conditions. TNF alpha is closely related to the 25kDa protein Tumor Necrosis Factor beta (lymphotoxin), sharing the same receptors and cellular actions. TNF alpha causes cytolysis of certain transformed cells, being synergistic with interferon gamma in its cytotoxicity. Although it has little effect on many cultured normal human cells, TNF alpha appears to be directly toxic to vascular endothelial cells. Other actions of TNF alpha include stimulating growth of human fibroblasts and other cell lines, activating polymorphonuclear neutrophils and osteoclasts, and induction of interleukin 1, prostaglandin E2 and collagenase production. TNF alpha is currently being evaluated in treatment of certain cancers and AIDS Related Complex.
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2. Lindholm C, Naylor A, Johansson EL, Quiding-Järbrink M: Mucosal vaccination increases endothelial expression of mucosal addressin cell adhesion molecule 1 in the human gastrointestinal tract. Infect Immun. 2004;72(2):1004-9.
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4. Yan SR, Qing G, Byers DM, Stadnyk AW, Al-Hertani W, Bortolussi R: Role of MyD88 in diminished tumor necrosis factor alpha production by newborn mononuclear cells in response to lipopolysaccharide. Infect Immun. 2004;72(3):1223-9.
5. Visser J, Graffelman W, Blauw B, Haspels I, Lentjes E, de Kloet ER, Nagelkerken L: LPS-induced IL-10 production in whole blood cultures from chronic fatigue syndrome patients is increased but supersensitive to inhibition by dexamethasone. J Neuroimmunol. 2001;119(2):343-9.
6. Cesaro-Tadic S, Dernick G, Juncker D, Buurman G, Kropshofer H, Michel B, Fattinger C, Delamarche E: High-sensitivity miniaturized immunoassays for tumor necrosis factor alpha using microfluidic systems. Lab Chip. 2004;4(6):563-9.
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