Key Specifications Table
|Species Reactivity||Key Applications||Host||Format||Antibody Type|
|H||ICC, IHC, WB||M||Purified||Monoclonal Antibody|
|Description||Anti-Tumor Necrosis Factor-β Antibody, clone 9B9|
|Presentation||Purified immunoglobulin (Protein A-agarose chormotography). One bottle of lyophilized preparation contains:200ug mouse IgG, 2 mg potassium phosphate buffer, 2.9 mg sodium chloride, and 20 mg raffinose.Reconstitution with 1 ml sterile, distilled water results in an antibody concentration of 200 ug/ml.|
|Safety Information according to GHS|
|Storage and Shipping Information|
|Storage Conditions||Maintain frozen at -20°C in undiluted aliquots for up to 12 months.Freeze only once.|
|Material Size||200 µg|
Anti-Tumor Necrosis Factor-β Antibody, clone 9B9 SDS
|Reference overview||Pub Med ID|
|Monocyte-mediated drug-dependent cellular cytotoxicity: effects on different WEHI 164 target cell lines.|
Austgulen, R, et al.
Cancer Immunol. Immunother., 22: 176-80 (1986) 1986
The contribution of monocyte cytotoxic protein factor (CF) to monocyte-mediated drug-dependent cellular cytotoxicity (DDCC) has been investigated. Cell lines which have been derived from murine WEHI 164 cells (termed WEHI 164 parental) by selecting for high (WEHI 164 clone 3) and low (R-WEHI 164) sensitivity to CF-mediated cytotoxicity were used as target cells in DDCC. By comparing the CF doses which produced 50% dead cells (LD 50) we found that WEHI 164 clone 3 was approximately 30 times more sensitive than WEHI 164 parental which in turn was 70 times more sensitive than R-WEHI 164. Actinomycin D (Act D) treatment of WEHI 164 parental and R-WEHI 164 greatly increase susceptibility to CF-mediated cytotoxicity. The susceptibility of WEHI 164 clone 3 was apparently somewhat increased at low dilutions of CF, whereas no significant increase was observed at high dilutions. The susceptibility to DDCC of the three target cell lines (WEHI 164 parental, WEHI 164 clone 3, and R-WEHI 164) correlated with the sensitivity pattern obtained in CF-mediated cytotoxicity of Act D-treated target cells. Monocyte- and CF-mediated cytotoxicity against Act D-treated WEHI 164 clone 3 and R-WEHI 164 was inhibited by neutralizing CF antiserum. These data indicate that CF is an effector molecule in monocyte-mediated DDCC.
Aggarwal, B B
Meth. Enzymol., 116: 441-8 (1985) 1985
|Human tumor necrosis factor.|
Aggarwal, B B and Kohr, W J
Meth. Enzymol., 116: 448-56 (1985) 1985
|An endotoxin-induced serum factor that causes necrosis of tumors.|
Carswell, E A, et al.
Proc. Natl. Acad. Sci. U.S.A., 72: 3666-70 (1975) 1975
In studying "hemorrhagic necrosis" of tumors produced by endotoxin, it was found that the serum of bacillus Calmette--Guerin (BCG)-infected mice treated with endotoxin contains a substance (tumor necrosis factor; TNF) which mimics the tumor necrotic action of endotoxin itself. TNF-positive serum is as effective as endotoxin itself in causing necrosis of the sarcoma Meth A and other transplanted tumors. A variety of tests indicate that TNF is not residual endotoxin, but a factor released from host cells, probably macrophages, by endotoxin. Corynebacteria and Zymosan, which like BCG induce hyperplasia of the reticulo-endothelial system, can substitute for BCG in priming mice for release of TNF by endotoxin. TNF is toxic in vitro for two neoplastic cell lines; it is not toxic for mouse embryo cultures. We propose that TNF mediates endotoxin-induced tumor necrosis, and that it may be responsible for the suppression of transformed cells by activated macrophages.