Search results for: Recombinant Human IL-6R alpha Proteins
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Modular organization of Interleukin-6 and Interleukin-11 α-receptors.Interleukin (IL)-6 and IL-11 are the only canonical members of the IL-6 family of cytokines that induce signaling through a homodimer of the common β-receptor glycoprotein (gp)130. A pre-requisite for signal transduction is the initial binding of the cytokines to their unique α-receptors, IL-6R and IL-11R. The cell-type specific expression of the two receptors determines the target cells of IL-6 and IL-11, because gp130 is ubiquitously expressed. However, ciliary neurotrophic factor (CNTF) and IL-27p28/IL-30 have been described as additional ligands for the IL-6R, underlining a remarkable plasticity among the cytokines of the IL-6 family and their receptors. In this study, we show that neither IL-6 nor IL-11 can bind to and signal through the α-receptor of the respective other cytokine. We further create eight chimeric IL-6/IL-11 receptors, which are all biologically active. We find that the domains D1 to D3, which contain the cytokine binding module (CBM), determine which cytokine can activate the chimeric receptor, whereas the stalk region, the transmembrane region, or the intracellular region do not participate in the ligand selectivity of the receptor and are therefore interchangeable between IL-6R and IL-11R. These results suggest a modular organization of the IL-6R and IL-11R, and a similar signal transduction complex of the two cytokines.
Human Interleukin-11 IL-1 Mouse Interleukin-11 IL-1 Recombinant Human Interle Recombinant Human Interle Recombinant Mouse Interle Recombinant Mouse Interle (3β)-Androsta-5,16-diene Rat monoclonal anti mouse Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti HCV core 2 119aa recombin HCV NS3 1192 1456aa recom
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Alternative intronic polyadenylation generates the interleukin-6 trans-signaling inhibitor sgp130-E10.Interleukin (IL)-6 signals via a receptor complex composed of the signal-transducing β-receptor gp130 and the non-signaling membrane-bound or soluble IL-6 receptor α (IL-6R, sIL-6R), which is referred to as classic and trans-signaling, respectively. IL-6 trans-signaling is functionally associated with the development of chronic inflammatory diseases and cancer. Soluble gp130 (sgp130) variants are natural inhibitors of trans-signaling. Differential splicing yields sgp130 isoforms. Here, we describe that alternative intronic polyadenylation in intron 10 of the gp130 transcript results in a novel mRNA coding for an sgp130 protein isoform (sgp130-E10) of 70-80 kDa. The sgp130-E10 protein was expressed in vivo in human peripheral blood mononuclear cells. To assess the biological activity of sgp130-E10, we expressed this variant as Fc-tagged fusion protein (sgp130-E10Fc). Recombinant sgp130-E10Fc binds to a complex of IL-6 and sIL-6R, but not to IL-6 alone, and specifically inhibits IL-6 trans-signaling. Thus, it might play an important role in the regulation of trans-signaling in vivo.
2906 related Products with: Alternative intronic polyadenylation generates the interleukin-6 trans-signaling inhibitor sgp130-E10.PI3-Kɣ Inhibitor, AS-605 PI3-Kɣ Inhibitor, AS-605 FAAH Inhibitor, PF-622 FAAH Inhibitor, PF-622; A FAAH Inhibitor, PF-622 FAAH Inhibitor, PF-622; A AZD-6244 Mechanisms: MEK TAE-684 Mechanisms: ALK i BI-6727 Mechanisms: Polo- 3-Aminocyclohexanol (cis rac-trans 3’-Aminomethy (6R-trans)-7-Amino-8-oxo-
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Efficacy and safety implications of molecular constructs of biological agents for rheumatoid arthritis.Targeted biologic immunomodulatory therapies have had a major impact in rheumatoid arthritis (RA) treatment, including tumor necrosis factor (TNF)-α inhibition, B-cell depletion, interference in T-cell costimulation and interleukin (IL)-1 and IL-6 inhibition. Along with the recognition of the importance of early, aggressive disease-modifying antirheumatic drugs (DMARDs) grounded in the use of methotrexate, the introduction of biologic DMARDs (bDMARDs) has provided significantly improved outcomes in patients with RA with a goal of true remission, or at least a state of very low disease activity, now possible in many. There are a number of methods to inhibit cytokines, cellular receptors and pathways of signal transduction that have been used thus far and are in development. In some cases, the method of target inhibition and differences in molecular construct has impacted efficacy and/or safety; whereas, in other cases, similar safety and/or efficacy signals across compounds have demonstrated class- or target-related effects. As the development of targeted therapies moves forward, it is increasingly important to understand the role of the target both in RA disease pathogenesis and normal host defense and the mechanisms of target inhibition.
1418 related Products with: Efficacy and safety implications of molecular constructs of biological agents for rheumatoid arthritis.Growth Differentiation Fa RANK Ligand Soluble, Huma RANK Ligand Soluble, Huma Formamide Molecular biolo Formamide Molecular biolo Ofloxacin CAS Number [824 Cellufine Formyl , 50 ml Cellufine Formyl Media Cellufine Formyl , 500 ml Cellufine Formyl Media Cellufine Formyl Media Cytokeratin, High Molecu
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Functional implications of large backbone amplitude motions of the glycoprotein 130-binding epitope of interleukin-6.Human interleukin (IL)-6 plays a pivotal role in the immune response, hematopoiesis, the acute-phase response, and inflammation. IL-6 has three distinct receptor epitopes, termed sites I, II, and III, that facilitate the formation of a signaling complex. IL-6 signals via a homodimer of glycoprotein 130 (gp130) after initially forming a heterodimer with the nonsignaling α-receptor [IL-6 α-receptor (IL-6R)] via site I. Here, we present the backbone dynamics of apo-IL-6 as determined by analysis of NMR relaxation data with the extended model-free formalism of Lipari and Szabo. To alleviate significant resonance overlap in the HSQC-type spectra, cell-free protein synthesis was used to selectively (15) N-label residues, thereby ensuring a complete set of residue-specific dynamics. The calculated order parameters [square of the generalized model-free order parameter (S(2))] showed significant conformational heterogeneity among clusters of residues in IL-6. In particular, the N-terminal region of the long AB-loop, which corresponds spatially to one of the gp130 receptor binding epitopes (i.e. site III), experiences substantial fluctuations along the conformation of the main chain (S(2) = 0.3-0.8) that are not observed at the other two epitopes or in other cytokines. Thus, we postulate that dynamic properties of the AB-loop are responsible for inhibiting the interaction of IL-6 with gp130 in the absence of the IL-6R, and that binding of IL-6R at site I shifts the dynamic equilibrium to favor interaction with gp130 at site III. In addition, molecular dynamics simulations corroborated the NMR-derived dynamics, and showed that the BC-loop adopts different substates that possibly play a role in facilitating receptor assembly.
2332 related Products with: Functional implications of large backbone amplitude motions of the glycoprotein 130-binding epitope of interleukin-6.Ofloxacin CAS Number [824 anti HBcAg core IgG2a (mo Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti ELISA Binding Buffer ELISA Binding Buffer ELISA Binding Buffer Acyl CoA binding Protein Actin binding EGFP E. coli SSB (Single Stran E. coli SSB (Single Stran E. coli SSB (Single Stran
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A translational approach to micro-inflammation in end-stage renal disease: molecular effects of low levels of interleukin-6.Inflammation plays a key role in the progression of cardiovascular disease, the leading cause of mortality in ESRD (end-stage renal disease). Over recent years, inflammation has been greatly reduced with treatment, but mortality remains high. The aim of the present study was to assess whether low (<2 pg/ml) circulating levels of IL-6 (interleukin-6) are necessary and sufficient to activate the transcription factor STAT3 (signal transducer and activator of transcription 3) in human hepatocytes, and if this micro-inflammatory state was associated with changes in gene expression of some acute-phase proteins involved in cardiovascular mortality in ESRD. Human hepatocytes were treated for 24 h in the presence and absence of serum fractions from ESRD patients and healthy subjects with different concentrations of IL-6. The specific role of the cytokine was also evaluated by cell experiments with serum containing blocked IL-6. Furthermore, a comparison of the effects of IL-6 from patient serum and rIL-6 (recombinant IL-6) at increasing concentrations was performed. Confocal microscopy and Western blotting demonstrated that STAT3 activation was associated with IL-6 cell-membrane-bound receptor overexpression only in hepatocytes cultured with 1.8 pg/ml serum IL-6. A linear activation of STAT3 and IL-6 receptor expression was also observed after incubation with rIL-6. Treatment of hepatocytes with 1.8 pg/ml serum IL-6 was also associated with a 31.6-fold up-regulation of hepcidin gene expression and a 8.9-fold down-regulation of fetuin-A gene expression. In conclusion, these results demonstrated that low (<2 pg/ml) circulating levels of IL-6, as present in non-inflamed ESRD patients, are sufficient to activate some inflammatory pathways and can differentially regulate hepcidin and fetuin-A gene expression.
1244 related Products with: A translational approach to micro-inflammation in end-stage renal disease: molecular effects of low levels of interleukin-6.Renal disease spectrum ti Male genitourinary system Anti 3 DG imidazolone Mon Liver disease spectrum ti Lung disease spectrum tis Colon disease spectrum ti Breast disease spectrum t Breast disease spectrum t Breast disease spectrum t Brain disease spectrum (b Cervical carcinoma tissue Tissue array of uterine c
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Overproduced interleukin 6 decreases blood lipid levels via upregulation of very-low-density lipoprotein receptor.Interleukin 6 (IL6) blockade raises blood lipid levels in patients with rheumatoid arthritis.
1635 related Products with: Overproduced interleukin 6 decreases blood lipid levels via upregulation of very-low-density lipoprotein receptor.Low Density Lipoprotein Low Density Lipoprotein Low Density Lipoprotein Primary antibody low den Lipoprotein, Human Plasma Lipoproteins, Human Plasm Rabbit Anti-HDL high dens Mouse Anti-Human Low Dens Mouse Anti-Human Interleu anti B human blood antige Blood Group Antibodies a anti B human blood group
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Pretreatment levels of sTNF-R1 and sIL-6R are associated with a higher vulnerability for IFN-alpha-induced depressive symptoms in patients with malignant melanoma.Immunomodulatory therapy with interferon-alpha (IFN-alpha) often leads to neuropsychiatric side effects, especially depression. An activation of the immune system is discussed to trigger neurotransmitter changes and depressive illness. So far, few data are available about biologic markers, who may predict the individual risk for developing depressive symptoms during IFN-alpha therapy. The aim of the present study was to investigate the predictive role of certain immunologic markers for the development of IFN-alpha-induced depression. We hypothesized that patients characterized by a proinflammatory and TH1-accentuated immune response before treatment might have an increased risk for developing depressive mood changes. Thirty-three melanoma patients were prospectively investigated during adjuvant treatment with IFN-alpha-2a/2b (3 x 3 Mio units/wk). Depressive mood changes were assessed with the self-rating depression scale (SDS, Zung-scale) before and during IFN-alpha treatment. Serum concentrations of soluble tumor necrosis factor-R1 (sTNF-R1), soluble interleukin-6R (sIL-6R), sIL-4R, and neopterin were measured before and after 3 months of treatment. sIL-6R, which was negatively associated with SDS scores, significantly predicted higher depression scores in the first 3 months of IFN-alpha treatment. sTNF-R1, which was positively associated with SDS scores, significantly predicted the development of late depressive symptoms after 6 months of therapy. In contrast to the initial hypothesis, patients characterized by high sTNF-R1 and low sIL-6R baseline levels, indicating an anti-inflammatory condition before therapy, had a higher vulnerability for depression during IFN-alpha therapy.
1087 related Products with: Pretreatment levels of sTNF-R1 and sIL-6R are associated with a higher vulnerability for IFN-alpha-induced depressive symptoms in patients with malignant melanoma.Interleukins Recombinant Interleukins Recombinant Interleukins Recombinant Interleukins Recombinant Malignant melanoma, metas Malignant melanoma, metas Malignant melanoma, metas Malignant melanoma tissue Malignant melanoma tissue Multiple malignant melano Low density malignant mel Malignant melanoma tissue
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