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reporter cell  (InvivoGen)


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    InvivoGen reporter cell
    Reporter Cell, supplied by InvivoGen, used in various techniques. Bioz Stars score: 94/100, based on 80 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/b16+blue+ifn+%CE%B1+%CE%B2+reporter+cells/B16-Blue+IFN-%CE%B1+%CE%B2+cells/us12551460-384-14-19
    Average 94 stars, based on 80 article reviews
    reporter cell - by Bioz Stars, 2026-09
    94/100 stars

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    Related Articles

    CCK-8 Assay:

    Article Title: Identification of Histone Deacetylase Inhibitor Targeting Type I Interferon and B Cell Abnormalities in Systemic Lupus Erythematosus
    Article Snippet: .. IFN‐I production was evaluated using HEK‐Blue IFN‐α/β, HEK‐Blue TNF‐α, HEK‐Blue IL‐6, and B16‐Blue IFN‐α/β reporter cells (InvivoGen) as previously described, and cell viability was measured using the cell counting kit‐8 (Dojindo Laboratories, Tokyo, Japan). ..

    Article Title: Identification of histone deacetylase inhibitor targeting type I interferon and B-cell abnormalities in systemic lupus erythematosus.
    Article Snippet: THP1-Blue ISG cells purchased from InvivoGen (San Diego, CA, USA) and peripheral blood mononuclear cells (PBMCs) were seeded and treated with compounds from the Prestwick Chemical Library (Prestwick Chemical, San Diego, CA, USA) at 1 μM in the presence of resiquimod (R848; 10 μg/mL), 2’3’-cyclic GMP-AMP (2’3’-cGAMP; 5 μg/mL), or IFN-I (Universal IFN-I 200 U/mL) for 24 h. Universal IFN-I was used with the expectation of IFN-αA activity, confirmed in our previous experiments to exhibit stable effects. .. IFN-I production was evaluated using HEK-Blue IFN-α/β, HEK-BlueTM TNF-α, HEK-BlueTM IL-6, and B16-Blue IFN-α/β reporter cells (InvivoGen) as previously described1, and cell viability was measured using the cell counting kit-8 (Dojindo Laboratories, Tokyo, Japan). ..

    Cell Culture:

    Article Title: Systemic Delivery of a STING Agonist-Loaded Positively Charged Liposome Selectively Targets Tumor Immune Microenvironment and Suppresses Tumor Angiogenesis.
    Article Snippet: Although stimulator of interferon genes (STING) agonists has shown great promise in preclinical studies, the clinical development of STING agonist therapy is challenged by its limited systemic delivery.. Here, positively charged fusogenic liposomes loaded with a STING agonist (PoSTING) are designed for systemic delivery and to preferentially target the tumor microenvironment.. When PoSTING is administered intravenously, it selectively targets not only tumor cells but also immune and tumor endothelial cells (ECs).

    Control:

    Article Title: Klebsiella pneumoniae hijacks the Toll-IL-1R protein SARM1 in a type I IFN-dependent manner to antagonize host immunity
    Article Snippet: .. Murine type I IFNs were detected using B16-Blue IFN-α/β reporter cells (Invivogen) which carry an SEAP reporter gene under the control of the IFN-α/β- of inducible ISG54 promoter and that have an inactivation of the IFN-γ receptor. .. Supernatants from iBMDM cells were incubated with the reporter cell line, and levels of SEAP in the supernatants were determined using the detection medium QUANTI-Blue (Invivogen) after 24 h as per the manufacturer’s instructions using recombinant mouse IFN-β (PBL Assay Science, catalogue number 12401-1) as a standard.

    Article Title: Klebsiella pneumoniae hijacks the Toll-IL-1R protein SARM1 in a type I IFN-dependent manner to antagonize host immunity
    Article Snippet: .. Murine type I IFNs were detected using B16-Blue IFN-α/β reporter cells (InvivoGen) which carry an SEAP reporter gene under the control of the IFN-α/β-inducible ISG54 promoter and that have an inactivation of the IFN-γ receptor. .. Supernatants from iBMDM cells were incubated with the reporter cell line, and levels of SEAP in the supernatants were determined using the detection medium QUANTI-Blue (InvivoGen) after 24 h as per the manufacturer’s instructions using recombinant mouse IFN-β (PBL Assay Science, catalogue number 12401-1) as a standard.

    Article Title: Klebsiella pneumoniae Reduces SUMOylation To Limit Host Defense Responses
    Article Snippet: .. Murine type I IFNs were detected using B16-Blue IFN-α/β reporter cells (Invivogen) which carry an SEAP reporter gene under the control of the IFN-α/β-inducible ISG54 promoter and that have an inactivation of the IFN-γ receptor. .. Briefly, supernatants from iBMDM infections were incubated with the reporter cell line, and levels of SEAP in the supernatants were determined using the detection medium QUANTI-Blue (Invivogen) after 24 h as per the manufacturer’s instructions using recombinant mouse IFN-β (PBL Assay Science, catalog number 12401-1) as a standard.



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    Vorinostat ameliorates disease phenotypes in STING‐associated vasculopathy with onset in infancy mice. (A) Pharmacokinetic analysis of vorinostat in C57BL/6J mice following single intraperitoneal administration (20 mg/kg). Mice were intraperitoneally administered vorinostat (20 mg/kg) once daily for eight weeks. (B) Lung tissue sections stained with Azan from both vorinostat‐treated and control mice, with a quantifiable reduction in histology scores that indicate disease severity (scale bar: 100 μm). (C) Serum IFN‐I levels, assessed using <t>the</t> <t>B16‐Blue</t> IFN‐αβ reporter assay, were significantly reduced in the vorinostat‐treated group, demonstrating the efficacy of the drug in moderating IFN‐I overproduction. (D) The urinary activity of N ‐acetyl‐beta‐D‐glucosaminidase, a marker of interstitial renal damage, was decreased in the vorinostat group, indicating improved renal function. (E) Quantitative real‐time polymerase chain reaction analysis of lung and kidney tissues revealed down‐regulation of IFN‐I–related and inflammatory gene expression in mice treated with vorinostat. Data are presented as mean ± SEM; * P < 0.05, ** P < 0.01, and *** P < 0.001, denoting different levels of significance. IFN, interferon. Color figure can be viewed in the online issue, which is available at http://onlinelibrary.wiley.com/doi/10.1002/art.43434/abstract .
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    Vorinostat ameliorates disease phenotypes in STING‐associated vasculopathy with onset in infancy mice. (A) Pharmacokinetic analysis of vorinostat in C57BL/6J mice following single intraperitoneal administration (20 mg/kg). Mice were intraperitoneally administered vorinostat (20 mg/kg) once daily for eight weeks. (B) Lung tissue sections stained with Azan from both vorinostat‐treated and control mice, with a quantifiable reduction in histology scores that indicate disease severity (scale bar: 100 μm). (C) Serum IFN‐I levels, assessed using <t>the</t> <t>B16‐Blue</t> IFN‐αβ reporter assay, were significantly reduced in the vorinostat‐treated group, demonstrating the efficacy of the drug in moderating IFN‐I overproduction. (D) The urinary activity of N ‐acetyl‐beta‐D‐glucosaminidase, a marker of interstitial renal damage, was decreased in the vorinostat group, indicating improved renal function. (E) Quantitative real‐time polymerase chain reaction analysis of lung and kidney tissues revealed down‐regulation of IFN‐I–related and inflammatory gene expression in mice treated with vorinostat. Data are presented as mean ± SEM; * P < 0.05, ** P < 0.01, and *** P < 0.001, denoting different levels of significance. IFN, interferon. Color figure can be viewed in the online issue, which is available at http://onlinelibrary.wiley.com/doi/10.1002/art.43434/abstract .
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    Vorinostat ameliorates disease phenotypes in STING‐associated vasculopathy with onset in infancy mice. (A) Pharmacokinetic analysis of vorinostat in C57BL/6J mice following single intraperitoneal administration (20 mg/kg). Mice were intraperitoneally administered vorinostat (20 mg/kg) once daily for eight weeks. (B) Lung tissue sections stained with Azan from both vorinostat‐treated and control mice, with a quantifiable reduction in histology scores that indicate disease severity (scale bar: 100 μm). (C) Serum IFN‐I levels, assessed using the B16‐Blue IFN‐αβ reporter assay, were significantly reduced in the vorinostat‐treated group, demonstrating the efficacy of the drug in moderating IFN‐I overproduction. (D) The urinary activity of N ‐acetyl‐beta‐D‐glucosaminidase, a marker of interstitial renal damage, was decreased in the vorinostat group, indicating improved renal function. (E) Quantitative real‐time polymerase chain reaction analysis of lung and kidney tissues revealed down‐regulation of IFN‐I–related and inflammatory gene expression in mice treated with vorinostat. Data are presented as mean ± SEM; * P < 0.05, ** P < 0.01, and *** P < 0.001, denoting different levels of significance. IFN, interferon. Color figure can be viewed in the online issue, which is available at http://onlinelibrary.wiley.com/doi/10.1002/art.43434/abstract .

    Journal: Arthritis & Rheumatology (Hoboken, N.j.)

    Article Title: Identification of Histone Deacetylase Inhibitor Targeting Type I Interferon and B Cell Abnormalities in Systemic Lupus Erythematosus

    doi: 10.1002/art.43434

    Figure Lengend Snippet: Vorinostat ameliorates disease phenotypes in STING‐associated vasculopathy with onset in infancy mice. (A) Pharmacokinetic analysis of vorinostat in C57BL/6J mice following single intraperitoneal administration (20 mg/kg). Mice were intraperitoneally administered vorinostat (20 mg/kg) once daily for eight weeks. (B) Lung tissue sections stained with Azan from both vorinostat‐treated and control mice, with a quantifiable reduction in histology scores that indicate disease severity (scale bar: 100 μm). (C) Serum IFN‐I levels, assessed using the B16‐Blue IFN‐αβ reporter assay, were significantly reduced in the vorinostat‐treated group, demonstrating the efficacy of the drug in moderating IFN‐I overproduction. (D) The urinary activity of N ‐acetyl‐beta‐D‐glucosaminidase, a marker of interstitial renal damage, was decreased in the vorinostat group, indicating improved renal function. (E) Quantitative real‐time polymerase chain reaction analysis of lung and kidney tissues revealed down‐regulation of IFN‐I–related and inflammatory gene expression in mice treated with vorinostat. Data are presented as mean ± SEM; * P < 0.05, ** P < 0.01, and *** P < 0.001, denoting different levels of significance. IFN, interferon. Color figure can be viewed in the online issue, which is available at http://onlinelibrary.wiley.com/doi/10.1002/art.43434/abstract .

    Article Snippet: IFN‐I production was evaluated using HEK‐Blue IFN‐α/β, HEK‐Blue TNF‐α, HEK‐Blue IL‐6, and B16‐Blue IFN‐α/β reporter cells (InvivoGen) as previously described, and cell viability was measured using the cell counting kit‐8 (Dojindo Laboratories, Tokyo, Japan).

    Techniques: Staining, Control, Reporter Assay, Activity Assay, Marker, Real-time Polymerase Chain Reaction, Gene Expression

    Therapeutic effects of vorinostat through IFN‐I suppression in New Zealand Black/White F1 lupus‐prone mice. Effects of vorinostat (20 mg/kg, intraperitoneal, five times/week for 16 weeks) in New Zealand Black/White F1 mice. (A) Kaplan–Meier survival curves show improved survival in the vorinostat‐treated group (log‐rank test, P = 0.0359). (B) Reduced proteinuria scores (log‐rank test, P = 0.0087). (C) Improvement in serum anti‐dsDNA antibody titers, C3 levels, and proteinuria (n = 7 per group). (D) Decreased histopathological scores of nephritis. (E) Reduced glomerular deposition of IgM, IgG, and C3 by immunofluorescence analysis. (F) Decreased serum IFN‐I levels measured by B16‐Blue IFN‐α/β reporter cells. (G) Vorinostat suppresses IFN‐I–related gene expression in the spleen and bone marrow. (H) Vorinostat reduced the number of splenic pDCs. (I) Vorinostat decreased the number of B cells in the spleen. (J) Vorinostat decreased the percentage of ABCs among B cells in the spleen. (K) Vorinostat treatment reduced the number of pre‐B cells but did not affect pro‐B cells. (L) Suppressed Vpreb1 expression in bone marrow B cells. Data are expressed as mean ± SEM; * P < 0.05, ** P < 0.01, and *** P < 0.001. ABC, age‐associated B cell; dsDNA, double‐stranded DNA; IFN, interferon; pDC, plasmacytoid dendritic cell. Color figure can be viewed in the online issue, which is available at http://onlinelibrary.wiley.com/doi/10.1002/art.43434/abstract .

    Journal: Arthritis & Rheumatology (Hoboken, N.j.)

    Article Title: Identification of Histone Deacetylase Inhibitor Targeting Type I Interferon and B Cell Abnormalities in Systemic Lupus Erythematosus

    doi: 10.1002/art.43434

    Figure Lengend Snippet: Therapeutic effects of vorinostat through IFN‐I suppression in New Zealand Black/White F1 lupus‐prone mice. Effects of vorinostat (20 mg/kg, intraperitoneal, five times/week for 16 weeks) in New Zealand Black/White F1 mice. (A) Kaplan–Meier survival curves show improved survival in the vorinostat‐treated group (log‐rank test, P = 0.0359). (B) Reduced proteinuria scores (log‐rank test, P = 0.0087). (C) Improvement in serum anti‐dsDNA antibody titers, C3 levels, and proteinuria (n = 7 per group). (D) Decreased histopathological scores of nephritis. (E) Reduced glomerular deposition of IgM, IgG, and C3 by immunofluorescence analysis. (F) Decreased serum IFN‐I levels measured by B16‐Blue IFN‐α/β reporter cells. (G) Vorinostat suppresses IFN‐I–related gene expression in the spleen and bone marrow. (H) Vorinostat reduced the number of splenic pDCs. (I) Vorinostat decreased the number of B cells in the spleen. (J) Vorinostat decreased the percentage of ABCs among B cells in the spleen. (K) Vorinostat treatment reduced the number of pre‐B cells but did not affect pro‐B cells. (L) Suppressed Vpreb1 expression in bone marrow B cells. Data are expressed as mean ± SEM; * P < 0.05, ** P < 0.01, and *** P < 0.001. ABC, age‐associated B cell; dsDNA, double‐stranded DNA; IFN, interferon; pDC, plasmacytoid dendritic cell. Color figure can be viewed in the online issue, which is available at http://onlinelibrary.wiley.com/doi/10.1002/art.43434/abstract .

    Article Snippet: IFN‐I production was evaluated using HEK‐Blue IFN‐α/β, HEK‐Blue TNF‐α, HEK‐Blue IL‐6, and B16‐Blue IFN‐α/β reporter cells (InvivoGen) as previously described, and cell viability was measured using the cell counting kit‐8 (Dojindo Laboratories, Tokyo, Japan).

    Techniques: Immunofluorescence, Gene Expression, Expressing