Product Information
| MW (kDa) | 31-36 |
| Purity | >98% as determined by SDS-PAGE of 6 μg reduced (+) and non-reduced (-) recombinant mHis6IL-6. All lots are greater than 98% pure. |
| Endotoxin | Less than 0.01 ng endotoxin/1 μg mHis6IL-6. |
| Activity | The bioactivity of recombinant mIL-6 was determined in a B9 cell proliferation assay. The ED50 of each lot is between 0.5 and 5 pg/ml. |
| Molecular Formula | Recombinant N-terminally His6-tagged mIL-6 has a calculated MW of 24,311. DTT-reduced and non-reduced protein migrate as 31-36 kDa polypeptides. Lower mobility and heterogeneity in SDS-PAGE are due to glycosylation. The expected amino terminus of recombinant mHis6IL-6 was verified by amino acid sequencing. |
Recombinant mouse His6IL-6 (mHis6IL-6) Phe25-Thr211 (Accession #NP_112445) was expressed in human 293 cells at Cell Signaling Technology.
IL-6 is a potent inducer of the acute phase response and is produced by T cells, macrophages, fibroblasts, endothelial, and other cells (1,2). IL-6 induces proliferation and differentiation and acts on B cells, T cells, thymocytes, among others. IL-6 in concert with TGF-β is important for developing Th17 responses. IL-6 binds to IL-6Rα and through this association induces gp130 homodimerization (1). gp130 homodimerization triggers the Jak/Stat cascade and the SHP2/MAPK (Erk) cascade (1,3,4). IL-6 also forms a complex with an IL-6Rα splice variant that is non-membrane associated (3). This IL-6/soluble IL-6Rα complex can activate the gp130 signaling pathway on cells that express gp130, but not IL-6Rα (3). Research studies have shown that IL-6 may contribute to metastatic breast cancer by increasing expression of proangiogenic VEGF (5).
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