Cat: MF-1006
Cat: MF-1006
IL6, Mouse, HEK293 Cells,Tag Free: Product Information
P08505
Human embryonic kidney cell, HEK293-derived mouse IL-6 protein
Phe25-Thr211
21.8 kDa
Solution protein.
Dissolved in sterile PBS buffer. This solution can be diluted into other aqueous buffers. Centrifuge the vial prior to opening.
Avoid repeated freeze-thaw cycles. It is recommended that the protein be aliquoted for optimal storage. 12 months from date of receipt, -20 to -70 °C as supplied.
Shipping with dry ice.
> 95%, determined by SDS-PAGE.
<0.010 EU per 1 ug of the protein by the LAL method.
Measured in a cell proliferation assay using T1165.85.2.1 mouse plasmacytoma cells. The EC50 for this effect is 0.01-0.05 ng/mL.
IL6, Mouse, HEK293 Cells,Tag Free:SDS-PAGE & Bioactivity
IL6, Mouse, HEK293 Cells,Tag Free:Synonyms
BSF2; BSF-2; CDF; CTL differentiation factor ; HSF; IFNB2; IFN-beta-2; IL6; IL-6
IL6, Mouse, HEK293 Cells,Tag Free:Background
Interleukin-6 (IL-6) plays important roles in the acute phase reaction, inflammation, hematopoiesis, bone metabolism, and cancer progression (1 - 5).
Mature mouse IL-6 is 187 amino acids (aa) in length and shares 39% and 85% aa sequence identity with human and rat IL-6, respectively (6 - 8). IL-6
induces signaling through a cell surface heterodimeric receptor complex composed of a ligand binding subunit (IL-6 R alpha) and a signal transducing
subunit (gp130). IL-6 binds to IL-6 R alpha, triggering IL-6 R alpha association with gp130 and gp130 dimerization (9). Soluble forms of IL-6 R alpha are
generated by both alternative splicing and proteolytic cleavage (5). In a mechanism known as trans-signaling, complexes of soluble IL-6 and IL-6 R alpha
elicit responses from gp130-expressing cells that lack cell surface IL-6 R alpha (5). Trans-signaling enables a wider range of cell types to respond to IL-6, as the expression of gp130 is ubiquitous, while that of IL-6 R alpha is predominantly restricted to hepatocytes, monocytes, and resting lymphocytes (2, 5).
IL-6, along with TNF-alpha and IL-1, drives the acute inflammatory response and the transition from acute inflammation to either acquired immunity or
chronic inflammatory disease (1 - 5). When dysregulated, it contributes to chronic inflammation in obesity, insulin resistance, inflammatory bowel disease,
arthritis, sepsis, and atherosclerosis (1, 2, 5). IL-6 can also function as an anti-inflammatory molecule, as in skeletal muscle where it is secreted in responseto exercise (2). In addition, it enhances hematopoietic stem cell proliferation and the differentiation of Th17 cells, memory B cells, and plasma cells (1, 10).
1. Mansell, A. and B.J. Jenkins (2013) Cytokine Growth Factor Rev. 24:249.
2. Schuett, H. et al. (2009) Thromb. Haemost. 102:215.
3. Erta, M. et al. (2012) Int. J. Biol. Sci. 8:1254.
4. Garbers, C. et al. (2012) Cytokine Growth Factor Rev. 23:85.
5. Mihara, M. et al. (2012) Clin. Sci. (Lond.) 122:143.
6. Chiu, C.P. et al. (1988) Proc. Natl. Acad. Sci. USA 85:7099.
7. Simpson, R.J. et al. (1988) Eur. J. Biochem. 176:187.
8. Van Snick, J. et al. (1988) Eur. J. Immunol. 18:193.
9. Murakami, M. et al. (1993) Science 260:1808.
10. Cerutti, A. et al. (1998) J. Immunol. 160:2145.