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sgp130fc  (R&D Systems)


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    Structured Review

    R&D Systems sgp130fc
    Sgp130fc, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/sgp130fc/Recombinant+Rat+gp130+Fc+Chimera+Protein%2C+CF/pm41962618-55-8-9
    Average 94 stars, based on 7 article reviews
    sgp130fc - by Bioz Stars, 2026-09
    94/100 stars

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    Related Articles

    Recombinant:

    Article Title: Sgp130Fc regulates IL-6/JAK2/STAT3 trans-signaling pathway in rat vocal fold fibroblast activation.
    Article Snippet: Acute vocal fold injury activates rat vocal fold fibroblasts (VFFs) and upregulates IL-6 expression.. We investigated whether soluble gp130Fc (sgp130Fc) modulates IL-6 trans-signaling via the JAK2/STAT3 pathway.. We established a vocal fold injury model, isolated primary VFFs, and silenced JAK2 expression using siRNA.

    Article Title: IL-6 dysregulation originates in dendritic cells and mediates graft-versus-host disease via classical signaling.
    Article Snippet: For IL-6R blockade studies, rat anti-mouse IL-6R monoclonal antibody (MR16-1; Chugai Pharmaceutical Co.) was administered intraperitoneally at 500mg per dose on day 1 and days 13 and 17 posttransplantation as described.22 Rat immunoglobulin G was used as an isotype control (Sigma-Aldrich). .. Serum soluble receptor and cytokines Soluble receptor levels were assessed by commercial enzymelinked immunosorbent assay kits (R&D Systems): murine sIL-6R (Mouse IL-6R a DuoSet ELISA), sgp130 (Mouse gp130 DuoSet ELISA), and sgp130Fc (Human sgp130 DuoSet ELISA; with recombinant human sgp130Fc chimera protein [R&D Systems] as the standard). .. Serum cytokine levels were measured by Flex Array (BD Biosciences).

    Article Title: Nonspecific Inhibition of IL6 Family Cytokine Signalling by Soluble gp130
    Article Snippet: .. Recombinant human (rh)CNTF (257-NT, R&D Systems, Minneapolis, MN, USA), rhCT1 (612-CD, R&D Systems, Minneapolis, MN, USA), rhIL6 (206-IL, R&D Systems, Minneapolis, MN, USA), rhIL11 (Z03108, Genscript, Minneapolis, MN, USA), rhLIF (7734-LF, R&D Systems, Minneapolis, MN, USA), rhOSM (PHC5015, ThermoFisher Scientific, San Francisco, CA, USA), sgp130Fc (671-GP, R&D Systems, Minneapolis, MN, USA). ..

    Transduction:

    Article Title: Sgp130Fc regulates IL-6/JAK2/STAT3 trans-signaling pathway in rat vocal fold fibroblast activation.
    Article Snippet: Acute vocal fold injury activates rat vocal fold fibroblasts (VFFs) and upregulates IL-6 expression.. We investigated whether soluble gp130Fc (sgp130Fc) modulates IL-6 trans-signaling via the JAK2/STAT3 pathway.. We established a vocal fold injury model, isolated primary VFFs, and silenced JAK2 expression using siRNA.

    Enzyme-linked Immunosorbent Assay:

    Article Title: IL-6 dysregulation originates in dendritic cells and mediates graft-versus-host disease via classical signaling.
    Article Snippet: For IL-6R blockade studies, rat anti-mouse IL-6R monoclonal antibody (MR16-1; Chugai Pharmaceutical Co.) was administered intraperitoneally at 500mg per dose on day 1 and days 13 and 17 posttransplantation as described.22 Rat immunoglobulin G was used as an isotype control (Sigma-Aldrich). .. Serum soluble receptor and cytokines Soluble receptor levels were assessed by commercial enzymelinked immunosorbent assay kits (R&D Systems): murine sIL-6R (Mouse IL-6R a DuoSet ELISA), sgp130 (Mouse gp130 DuoSet ELISA), and sgp130Fc (Human sgp130 DuoSet ELISA; with recombinant human sgp130Fc chimera protein [R&D Systems] as the standard). .. Serum cytokine levels were measured by Flex Array (BD Biosciences).

    Injection:

    Article Title: Interleukin-6 trans-signaling inhibition prevents oxidative stress in a mouse model of early diabetic retinopathy
    Article Snippet: .. After eight weeks of hyperglycemia, appropriate treatment groups received 5 mg/kg sgp130Fc (mouse sgp130Fc protein, R&D Systems, Minneapolis, MN) [ , ], by intraperitoneal injection twice weekly for 2 weeks. ..

    Article Title: Diabetes Induced Alterations in Murine Vitreous Proteome Are Mitigated by IL-6 Trans-Signaling Inhibition
    Article Snippet: .. Treated mice received 5 mg/kg sgp130Fc (Mouse sgp130Fc Chimera Protein; R&D Systems, Minneapolis, MN, USA) by intraperitoneal injection twice weekly for the last 2 weeks of study. ..

    Binding Assay:

    Article Title: Interleukin-6 Downregulates the Expression of Vascular Endothelial-Cadherin and Increases Permeability in Renal Glomerular Endothelial Cells via the Trans-Signaling Pathway.
    Article Snippet: .. Additionally, sgp130Fc (671-GP, R&D, USA) specifically inhibits the IL-6 trans-signaling pathway by binding to the IL-6/IL-6R complex [17]. ..

    Article Title: Interleukin-6 Downregulates the Expression of Vascular Endothelial-Cadherin and Increases Permeability in Renal Glomerular Endothelial Cells via the Trans-Signaling Pathway
    Article Snippet: .. Additionally, sgp130Fc (671-GP, R&D, USA) specifically inhibits the IL-6 trans-signaling pathway by binding to the IL-6/IL-6R complex [ ]. ..

    Inhibition:

    Article Title: Blockade of interleukin-6 trans-signaling prevents mitochondrial dysfunction and cellular senescence in retinal endothelial cells.
    Article Snippet: IL-6 trans-signaling (IL-6 TS) was activated with IL-6 (50 ng/mL) and sIL-6R (150 ng/mL; PeproTech, Rocky Hill, NJ, USA) or with Hyper IL-6 (50 ng/mL; kindly provided by Dr. Stefan Rose-John) overnight. .. For inhibition of IL-6 TS, cells were pretreated with sgp130Fc (10 μg/mL, Cat# 671-GP-100, R&D Systems, Minneapolis, MN, USA) 1 h prior to activation of IL-6 TS. .. RNA was isolated from cells using phenol-chloroform extraction with TRIzol reagent (Invitrogen, Carlsbad, CA, USA) as described previously (Rio et al., 2010).

    Activation Assay:

    Article Title: Blockade of interleukin-6 trans-signaling prevents mitochondrial dysfunction and cellular senescence in retinal endothelial cells.
    Article Snippet: IL-6 trans-signaling (IL-6 TS) was activated with IL-6 (50 ng/mL) and sIL-6R (150 ng/mL; PeproTech, Rocky Hill, NJ, USA) or with Hyper IL-6 (50 ng/mL; kindly provided by Dr. Stefan Rose-John) overnight. .. For inhibition of IL-6 TS, cells were pretreated with sgp130Fc (10 μg/mL, Cat# 671-GP-100, R&D Systems, Minneapolis, MN, USA) 1 h prior to activation of IL-6 TS. .. RNA was isolated from cells using phenol-chloroform extraction with TRIzol reagent (Invitrogen, Carlsbad, CA, USA) as described previously (Rio et al., 2010).



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    R&D Systems sgp130fc (recombinant human gp130 fc chimera - cat# 671-gp)
    miR-449a directly targets IL-6R and switches off IL-6 trans -signaling (A) The putative miR-449a binding sites in IL-6R were predicted using online bioinformatics tools. The interaction between miR-449a and IL-6R was verified using a dual luciferase reporter assay. ∗p < 0.05; ∗∗p < 0.001; ∗∗∗p < 0.0005; ∗∗∗∗p < 0.0001 Student’s t test vs. control group. Each experiment was repeated three times. Bars indicate SDs. (B) RIP assay of the enrichment of Ago2 on IL-6R and miR-449a transcripts normalized to a negative control irrelevant IgG antibody (CTR) in HNO-210 cell line overexpressing miR-449a. (C) Levels of sIL-6R and IL-6R in HNO-210 cell culture medium by quantitative ELISA (left and right) and expression levels of sIL-6R in HNO-210 cells by qRT-PCR (last panel). The experiments were repeated three times in triplicate. Bars, SDs. (D) Western blots analysis of transduced HNO-210 cell models in different experimental conditions: (i) 0.1% serum starvation, (ii) Hyper IL-6 stimulation (20 ng/mL for 30 min), (iii) <t>sgp130fc</t> treatment (1,000 ng/mL for 1 h), and sgp130fc pretreatment followed by Hyper IL-6 stimulation. miR-449a modulation of IL-6 trans -signaling mediated by pStat3 Tyr705 – pERK (Thr202; Tyr204)—pAKT Ser473. Vinculin was used as loading control. The experiments were repeated at least three times giving always similar results. Columns represent the intensity of the different bands evaluated as arbitrary units. Bars are SDs. ANOVA ∗p < 0.01; ∗∗p < 0.05; ∗∗∗p < 0.005; ∗∗∗∗p < 0.0001. (E) Relative expression levels of SNAI2, E-cadherin, and N-cadherin of transduced HNO-210 cell models in different experimental conditions: (i) 0.1% serum starvation, (ii) Hyper IL-6 stimulation (20 ng/mL for 30 min), (iii) sgp130fc treatment (1,000 ng/mL for 1 h) and sgp130fc pretreatment followed by Hyper IL-6 stimulation. ANOVA ∗<0.01 ∗∗p < 0.05; ∗∗∗p < 0.005; ∗∗∗∗p < 0.0001. All data are representative of three independent experiments.
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    Image Search Results


    miR-449a directly targets IL-6R and switches off IL-6 trans -signaling (A) The putative miR-449a binding sites in IL-6R were predicted using online bioinformatics tools. The interaction between miR-449a and IL-6R was verified using a dual luciferase reporter assay. ∗p < 0.05; ∗∗p < 0.001; ∗∗∗p < 0.0005; ∗∗∗∗p < 0.0001 Student’s t test vs. control group. Each experiment was repeated three times. Bars indicate SDs. (B) RIP assay of the enrichment of Ago2 on IL-6R and miR-449a transcripts normalized to a negative control irrelevant IgG antibody (CTR) in HNO-210 cell line overexpressing miR-449a. (C) Levels of sIL-6R and IL-6R in HNO-210 cell culture medium by quantitative ELISA (left and right) and expression levels of sIL-6R in HNO-210 cells by qRT-PCR (last panel). The experiments were repeated three times in triplicate. Bars, SDs. (D) Western blots analysis of transduced HNO-210 cell models in different experimental conditions: (i) 0.1% serum starvation, (ii) Hyper IL-6 stimulation (20 ng/mL for 30 min), (iii) sgp130fc treatment (1,000 ng/mL for 1 h), and sgp130fc pretreatment followed by Hyper IL-6 stimulation. miR-449a modulation of IL-6 trans -signaling mediated by pStat3 Tyr705 – pERK (Thr202; Tyr204)—pAKT Ser473. Vinculin was used as loading control. The experiments were repeated at least three times giving always similar results. Columns represent the intensity of the different bands evaluated as arbitrary units. Bars are SDs. ANOVA ∗p < 0.01; ∗∗p < 0.05; ∗∗∗p < 0.005; ∗∗∗∗p < 0.0001. (E) Relative expression levels of SNAI2, E-cadherin, and N-cadherin of transduced HNO-210 cell models in different experimental conditions: (i) 0.1% serum starvation, (ii) Hyper IL-6 stimulation (20 ng/mL for 30 min), (iii) sgp130fc treatment (1,000 ng/mL for 1 h) and sgp130fc pretreatment followed by Hyper IL-6 stimulation. ANOVA ∗<0.01 ∗∗p < 0.05; ∗∗∗p < 0.005; ∗∗∗∗p < 0.0001. All data are representative of three independent experiments.

    Journal: Molecular Therapy. Nucleic Acids

    Article Title: MiR-449a antagonizes EMT through IL-6-mediated trans -signaling in laryngeal squamous cancer

    doi: 10.1016/j.omtn.2024.102140

    Figure Lengend Snippet: miR-449a directly targets IL-6R and switches off IL-6 trans -signaling (A) The putative miR-449a binding sites in IL-6R were predicted using online bioinformatics tools. The interaction between miR-449a and IL-6R was verified using a dual luciferase reporter assay. ∗p < 0.05; ∗∗p < 0.001; ∗∗∗p < 0.0005; ∗∗∗∗p < 0.0001 Student’s t test vs. control group. Each experiment was repeated three times. Bars indicate SDs. (B) RIP assay of the enrichment of Ago2 on IL-6R and miR-449a transcripts normalized to a negative control irrelevant IgG antibody (CTR) in HNO-210 cell line overexpressing miR-449a. (C) Levels of sIL-6R and IL-6R in HNO-210 cell culture medium by quantitative ELISA (left and right) and expression levels of sIL-6R in HNO-210 cells by qRT-PCR (last panel). The experiments were repeated three times in triplicate. Bars, SDs. (D) Western blots analysis of transduced HNO-210 cell models in different experimental conditions: (i) 0.1% serum starvation, (ii) Hyper IL-6 stimulation (20 ng/mL for 30 min), (iii) sgp130fc treatment (1,000 ng/mL for 1 h), and sgp130fc pretreatment followed by Hyper IL-6 stimulation. miR-449a modulation of IL-6 trans -signaling mediated by pStat3 Tyr705 – pERK (Thr202; Tyr204)—pAKT Ser473. Vinculin was used as loading control. The experiments were repeated at least three times giving always similar results. Columns represent the intensity of the different bands evaluated as arbitrary units. Bars are SDs. ANOVA ∗p < 0.01; ∗∗p < 0.05; ∗∗∗p < 0.005; ∗∗∗∗p < 0.0001. (E) Relative expression levels of SNAI2, E-cadherin, and N-cadherin of transduced HNO-210 cell models in different experimental conditions: (i) 0.1% serum starvation, (ii) Hyper IL-6 stimulation (20 ng/mL for 30 min), (iii) sgp130fc treatment (1,000 ng/mL for 1 h) and sgp130fc pretreatment followed by Hyper IL-6 stimulation. ANOVA ∗<0.01 ∗∗p < 0.05; ∗∗∗p < 0.005; ∗∗∗∗p < 0.0001. All data are representative of three independent experiments.

    Article Snippet: Cells was analyzed in different experimental conditions: 0.1% Serum Starvation, Hyper IL-6 R&D Systems (Recombinant Human IL-6/IL-6R Complex Chimera - Cat# 8954-SR) stimulation (20 ng/mL for 30 min), sgp130fc (Recombinant Human gp130 Fc Chimera - Cat# 671-GP) treatment (1,000 ng/mL for 1 h), sgp130fc pretreatment followed by Hyper IL-6 stimulation.

    Techniques: Binding Assay, Luciferase, Reporter Assay, Negative Control, Cell Culture, Enzyme-linked Immunosorbent Assay, Expressing, Quantitative RT-PCR, Western Blot