Technical datasheet
Description
The monoclonal antibody HM102 reacts with the extra-cellular part of the mouse TNF-RII and with the soluble receptor. TNF-RII is present on most cell types and is considered to play a prominent role in cell stimulation by TNF-alpha. The TNF-RII molecule is shown to be responsible for stimulation of activated T-lymphocytes by TNF-alpha.
Formulation
0.5 ml (100 µg/ml) 0.2 µm filtered biotinylated antibody solution in PBS, containing 0.02% sodium azide and 0.1% bovine serum albumin.
Species
Rat IgG2a
Application
The monoclonal antibody HM102 is an agonistic antibody and can be used for cell culture experiments and for flow cytometry. Furthermore the antibody HM102 is useful for immuno assays, immunoprecipitation and histology on frozen sections. The reactivity of the antibody with soluble TNF-Receptor is not inhibited by high concentrations of mouse TNF-alpha.
Use
For immunohistology and flow cytometry dilutions to be used depend on detection system applied. It is recommended that users test the reagent and determine their own optimal dilutions. The typical starting working dilution is 1:10.
Storage and stability
Product should be stored at 4°C. Under recommended storage conditions, product is stable for one year.
References
1. Tacchini-Cottier, F et al; Role of TNFR1 and TNFR2 in TNF-induced platelet consumption in mice. J Immunol 1998,
160: 6182
2. Mennini, T et al; Glial activation and TNFR-I upregulation precedes motor dysfunction in the spinal cord of mnd mice. Cytokine 2004, 25: 127
3. Bigini, P et al; Immunohistochemical localization of TNFalpha and its receptors in the rodent central nervous system. Methods Mol Med 2004, 98: 73
Precautions
For research use only. Not for use in or on humans or animals or for diagnostics. It is the responsibility of the user to comply with all local/state and Federal rules in the use of this product. Hycult Biotech is not responsible for any patent infringements that might result with the use of or derivation of this product.
Also available
References
1. Tacchini-Cottier, F et al; Role of TNFR1 and TNFR2 in TNF-induced platelet consumption in mice. J Immunol 1998,
160: 6182
2. Mennini, T et al; Glial activation and TNFR-I upregulation precedes motor dysfunction in the spinal cord of mnd mice. Cytokine 2004, 25: 127
3. Bigini, P et al; Immunohistochemical localization of TNFalpha and its receptors in the rodent central nervous system. Methods Mol Med 2004, 98: 73