Anti-Mouse IL-12 – Purified In vivo GOLD™ Functional Grade
Pricing & Details
Purified CHO expressed Recombinant Mouse IL-12 p70
≥ 2.0 mg/ml
≤ 1.0 EU/mg as determined by the LAL method
>95% by SDS-PAGE and HPLC
This monoclonal antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (PBS) pH 7.2 - 7.4, 150 mM NaCl with no carrier protein, potassium, calcium or preservatives added.
Functional grade preclinical antibodies are manufactured in an animal free facility using only In vitro cell culture techniques and are purified by a multi-step process including the use of protein A or G to assure extremely low levels of endotoxins, leachable protein A or aggregates.
Storage and Handling
Functional grade preclinical antibodies may be stored sterile as received at 2-8°C for up to one month. For longer term storage, aseptically aliquot in working volumes without diluting and store at -80°C. Avoid Repeated Freeze Thaw Cycles.
Country of Origin
Each investigator should determine their own optimal working dilution for specific applications. See directions on lot specific datasheets, as information may periodically change.
Clone C17.8 reacts with the p40 subunit of mouse IL-12.
IL-12 plays a role in resistance against pathogens via the differentiation of naive T cells into Th1 cells. It stimulates the growth and function of T cells, blocks formation of new blood vessels, and contributes to antimycobacterial immune response. In addition, it promotes the production of IFN-γ and TNF-α and reduces IL-4 mediated suppression of IFN-γ. Consequently, this enhances the immunostimulatory and immunomodulatory effects of IFN-γ. In addition, there appears to be a link between IL-2 and the signal transduction of IL-12 in NK cells, which enhances the functional response of IL-12 via IFN-γ production and killing of target cells. Furthermore, IL-12 is thought to be associated with autoimmunity. IL-12 was shown to worsen the condition when administered to people already suffering from autoimmune diseases. Comparatively, inhibition of IL-12 (either through IL-12 gene knock-out in mice or treatment of mice with IL-12 mAbs) improved the disease.
NCBI Gene Bank ID
References & Citations
1. Kapsenberg, ML. et al. (1997) J. Immunol. 159: 28
2. Ritz, J. et al. (2001) Blood. 97(12):3860-6.
3. Barnes, PF. et al. (1994) J Clin Invest. 93(4):1733-9.
Products are for research use only. Not for use in diagnostic or therapeutic procedures.