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Recombinant Human Interleukin-6 (IL6)
(Cat. No.: C009)
Background:
Cytokines of the IL6/GCSF/MGF family are glycoproteins of about 170 to 180 amino acid residues that contain four conserved cysteine residues involved in two disulphide bonds. They have a compact, globular fold (similar to other interleukins), stabilized by the 2 disulphide bonds. One half of the structure is dominated by a 4 alpha-helix bundle with a left-handed twist: the helices are anti-parallel, with 2 overhand connections, which fall into a 2-stranded anti-parallel beta-sheet. The fourth alpha helix is important to the biological activity of the molecule.
Interleukin (IL)-6 is an important proinflammatory and immunoregulatory cytokine expressed by various cells. Interleukin-6 has been shown to inhibit the growth of early stage and to promote the proliferation of advanced stage melanoma cells in vitro.
Description:
Recombinant Human IL-6 produced in E. coli is a single, non-glycosylated polypeptide chain containing 185 amino acids and having a molecular mass of 21.0 kDa.
Quality Control:
Biological activity: rHuIL-6 is fully biologically active when compared to standard. The ED50 as determined by the dose-dependant stimulation of human TF-1 cells is less then 0.1 ng/ml, corresponding to a Specific Activity of 5.0 x 107 IU/mg.
Purity: Greater than 98.0% as determined by:
(a) Analysis by RP-HPLC.
(b) Anion-exchange FPLC.
(c) Analysis by reducing and non-reducing SDS-PAGE Silver Stained gel.
Molecular weight: 21 KD+/-10% determined by reduced SDS-PAGE.
Amino-Acid Sequence: The sequence of the first five N-terminal amino acids was determined and was found to be Ser-Pro-Val-Pro-Pro.
Endotoxin: Less than 0.3ng/µg (0.3IEU/µg) determined by LAL test.
Formulation: Lyophilized from a concentrated (1mg/ml) solution in water containing 43µg/ml sodium chloride.
Storage: Lyophilized rHuIL-6 although stable at room temperature for 3 weeks, should be stored desiccated below -18oC. Upon reconstitution rHuIL-6 should be stored at 4oC between 2-7 days and for future use below -18oC. For long-term storage it is recommended to add a carrier protein (0.1% HSA or BSA).
Please avoid freeze-thaw cycles.
Reconstitution: It is recommended to reconstitute the lyophilized rHuIL-6 in sterile 18MΩ-cm H2O not less than 100µg/ml, which can then be further diluted to other aqueous solutions.
Latest Publications:
1: Diab Vasc Dis Res 2009 Jan;Vol 6(1)
Circulating soluble CD36 is associated with glucose metabolism and interleukin-6 in glucose-intolerant men.
[Abstract] Recently, soluble CD36 (sCD36) levels were reported to be elevated in type 2 diabetes, and to be tightly correlated with insulin resistance. Our aim was to obtain further insight into the relationship between insulin sensitivity, low-grade inflammation and sCD36. We studied glucose-tolerant (n=90) and glucose-intolerant (n=57) moderately obese men. Insulin sensitivity was measured by the frequent sample intravenous glucose tolerance test, and sCD36 by an in-house ELISA assay. In glucose-intolerant subjects, sCD36 was negatively associated with insulin sensitivity and positively with interleukin-6 (IL-6), fasting glucose, fasting triglycerides, fat-free mass and platelet count. On multiple linear regression analyses, insulin sensitivity contributed 22% of sCD36
variance, independent of age, body mass index (BMI) and IL-6, in glucose-intolerant subjects. The level of sCD36 in subjects with glycosylated haemoglobin (HbA1C) above the mean was higher than in those with HbA1C values below the mean. Insulin sensitivity is a predictor of sCD36 in men with impaired glucose tolerance. IL-6 is related to sCD36 but does not predict sCD36 independent of insulin sensitivity and BMI.
2: PLoS ONE 2009 ;Vol 4(1)
IL-1beta, IL-6, and RANTES as biomarkers of Chikungunya severity.
[Abstract] BACKGROUND: Little is known about the immunopathogenesis of Chikungunya virus. Circulating levels of immune mediators and growth factors were analyzed from patients infected during the first Singaporean Chikungunya fever outbreak in early 2008 to establish biomarkers associated with infection and/or disease severity. METHODS AND FINDINGS: Adult patients with laboratory-confirmed Chikungunya fever infection, who were referred to the Communicable Disease Centre/Tan Tock Seng Hospital during the period from January to February 2008, were included in this retrospective study. Plasma fractions were analyzed using a multiplex-microbead immunoassay. Among the patients, the most common clinical features were fever (100%), arthralgia (90%), rash (50%) and
conjunctivitis (40%). Profiles of 30 cytokines, chemokines, and growth factors were able to discriminate the clinical forms of Chikungunya from healthy controls, with patients classified as non-severe and severe disease. Levels of 8 plasma cytokines and 4 growth factors were significantly elevated. Statistical analysis showed that an increase in IL-1beta, IL-6 and a decrease in RANTES were associated with disease severity. CONCLUSIONS: This is the first comprehensive report on the production of cytokines, chemokines, and growth factors during acute Chikungunya virus infection. Using these biomarkers, we were able to distinguish between mild disease and more severe forms of Chikungunya fever, thus enabling the identification of patients with poor prognosis and monitoring of the disease.
3: Cancer Res 2009 Jan;
{beta}1 Integrin Adhesion Enhances IL-6-Mediated STAT3 Signaling in Myeloma Cells: Implications for Microenvironment Influence on Tumor Survival and Proliferation.
[Abstract] The bone marrow microenvironmental components interleukin (IL)-6 and fibronectin (FN) individually influence the proliferation and survival of multiple myeloma (MM) cells; however, in vivo, these effectors most likely work together. We examined signaling events, cell cycle progression, and levels of drug response in MM cells either adhered to FN via beta1 integrins, stimulated with IL-6, or treated with the two combined. Although G1-S cell cycle arrest associated with FN adhesion was overcome when IL-6 was added, the cell adhesion-mediated drug resistance (CAM-DR) was maintained in the presence of IL-6. Concomitant exposure of MM cells to IL-6 and FN adhesion revealed a dramatic increase in signal transducers and activators of transcription 3 (STAT3)
phosphorylation, nuclear translocation, and DNA binding, compared with either IL-6 or FN adhesion alone in four MM cell lines. Importantly, this increase in STAT3 activation correlated with a novel association between STAT3 and gp130 in cells adhered to FN before stimulation with IL-6, relative to nonadherent cells. Taken together, these results suggest a mechanism by which collaborative signaling by beta1 integrin and gp130 confers an increased survival advantage to MM cells. [Cancer Res 2009;69(3):1009-15].
4: Comp Med 2008
Dec;Vol 58(6)
Quantitative tomography of early-onset spontaneous AA amyloidosis in interleukin 6 transgenic mice.
[Abstract] Mice that constitutively express the human interleukin 6 (huIL6) protein from a heritable transgene (H2-L(d)-IL-6) express high levels of the acute-phase reactant, serum amyloid protein A, a liver-derived apoprotein of high-density lipoprotein that is the precursor of AA amyloid. Typically at approximately 5 mo of age B6(C)- Tg(H2-L(d)-IL-6)Kish (H2/huIL-6) animals begin to develop splenic deposits of AA amyloid, which progress to involve the liver, kidney, and vasculature, ultimately resulting in death due to severe systemic AA amyloidosis at 8 to 9 mo of age. These mice provide a robust model in which to study novel therapeutic and diagnostic imaging agents for AA amyloidosis. We recently have noted a change in onset of spontaneous disease, as evidenced by 2
female transgenic mice that were found moribund at only 5 mo of age. Extensive hepatosplenic amyloid deposits in both mice were identified and quantified by single-photon emission computed tomography, which further revealed heterogeneous distribution of radiotracer in the spleen indicating a distinction between amyloid-laden red pulp and the disease-free lymphoid follicles. The AA nature of the deposits was evidenced immunohistochemically and by mass spectrometric analyses of extracted amyloid fibrils. Our studies have documented the manifestation of early-onset, severe, spontaneous AA amyloidosis in 2- to 5-mo-old H2/ huIL-6 mice; we hypothesize that this disease is due to genetic rather than environmental factors.
Domain Info
GeneBank Entry:
NM_000600
Protein Accession No.:
NP_000591
Protein Sequence:
SPVPP GEDSK DVAAP HRQPL TSSER IDKQI RYILD GISAL RKETC NKSNM CESSK EALAE NNLNL PKMAE KDGCF QSGFN EETCL VKIIT GLLEF EVYLE YLQNR FESSE EQARA VQMST KVLIQ FLQKK AKNLD AITTP DPTTN ASLLT KLQAQ NQWLQ DMTTH LILRS FKEFL QSSLR ALRQM
Transcript Info
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