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il 1 receptor antagonist il 1ra  (R&D Systems)


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    Structured Review

    R&D Systems il 1 receptor antagonist il 1ra
    Il 1 Receptor Antagonist Il 1ra, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 56 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/il+1+receptor+antagonist+il+1ra/Recombinant+Human+IL-1ra%2FIL-1F3+Protein/pmc12585178-372-16-21
    Average 94 stars, based on 56 article reviews
    il 1 receptor antagonist il 1ra - by Bioz Stars, 2026-09
    94/100 stars

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    Related Articles

    other:

    Article Title: Cell-autonomous and non-cell-autonomous effects of arginase-II on cardiac aging
    Article Snippet: To study effects of IL-1β in CM-RAW on cardiac cells apoptosis, myocytes were pre-treated with IL-1 receptor antagonist IL-1ra (280-RA, R&D systems) for 2 hours.

    Article Title: Cell-autonomous and non-cell-autonomous effects of Arginase 2 on cardiac aging
    Article Snippet: To study the effects of IL-1β in CM-RAW on cardiac cells apoptosis, myocytes were pre-treated with IL-1 receptor antagonist IL-1RA (280-RA, R&D systems) for 2 hr.

    Article Title: Role of pulmonary epithelial arginase-II in activation of fibroblasts and lung inflammaging.
    Article Snippet: Reagents were purchased from the following sources: TGF- β receptor 1 inhibitor SB431542 (S1067, Selleckchem, Houston, USA), IL- 1 receptor antagonist IL- 1ra (280- RA) and human IL- 1β (201- LB/CF) from R&D systems (Minnesota, USA), Wheat Germ Agglutinin– Alexa Fluor 488 (W11261) from Invitrogen (Lucerne, Switzerland).

    Clinical Proteomics:

    Article Title: Fueling the FIRES: Hemophagocytic lymphohistiocytosis in febrile infection-related epilepsy syndrome.
    Article Snippet: Department of Neurology, Division of Pediatric Neurology, Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee, Wisconsin Departments of Neurology and Immunology, Center for MS and Autoimmune Neurology, Translational Neuroimmunology Lab, Mayo Clinic, Rochester, Minnesota Clinical Epilepsy Section and Division of Neuroimmunology and Neurovirology, National Institute of Neurological Disorders and Stroke National Institute of Health, Bethesda, Maryland Department of Neurology, Children's National Health System, Washington, District of Columbia Department of Hematology, Children's National Health System, Washington, District of Columbia

    Enzyme-linked Immunosorbent Assay:

    Article Title: Fueling the FIRES: Hemophagocytic lymphohistiocytosis in febrile infection-related epilepsy syndrome.
    Article Snippet: Department of Neurology, Division of Pediatric Neurology, Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee, Wisconsin Departments of Neurology and Immunology, Center for MS and Autoimmune Neurology, Translational Neuroimmunology Lab, Mayo Clinic, Rochester, Minnesota Clinical Epilepsy Section and Division of Neuroimmunology and Neurovirology, National Institute of Neurological Disorders and Stroke National Institute of Health, Bethesda, Maryland Department of Neurology, Children's National Health System, Washington, District of Columbia Department of Hematology, Children's National Health System, Washington, District of Columbia



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    Blocking IL-1β in the RA serum attenuates glycolysis-HIF-1α axis mediated IL-1β. (A) qPCR analysis of HK2, HIF-1α, and IL-1β mRNA expression in HMDMs stimulated for 24 h with IL-1β, TNF-α, GM-CSF, IFN-γ, or IL-6 ( n = 7).( B )Representative image of IL-1β and HIF-1α expression in HMDMs pretreated with or without 2-DG (5 mM, 3 h) followed by 24 h stimulation with IL-1β, TNF-α, or GM-CSF ( n = 4).( C )Extracellular acidification rate (ECAR) measured by Seahorse assay in HMDMs exposed to RA serum with or without <t>IL-1RN,</t> infliximab, or lenzilumab ( n = 6).( D-E ) Western blot analysis of HIF-1α and IL-1β expression in macrophages treated with RA serum in the presence or absence of ( D ) IL-1RN or ( E ) infliximab for 24 h ( n = 6).Data were shown as mean ± SEM and were analyzed using one-way ANOVA or Two-tailed student’s t-test. *, p < 0.05; **, p < 0.01. 2-DG: 2-Deoxy-D-glucose; <t>IL-1RN:</t> <t>Interleukin-1</t> receptor antagonist; IFX: Infliximab
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    Blocking IL-1β in the RA serum attenuates glycolysis-HIF-1α axis mediated IL-1β. (A) qPCR analysis of HK2, HIF-1α, and IL-1β mRNA expression in HMDMs stimulated for 24 h with IL-1β, TNF-α, GM-CSF, IFN-γ, or IL-6 ( n = 7).( B )Representative image of IL-1β and HIF-1α expression in HMDMs pretreated with or without 2-DG (5 mM, 3 h) followed by 24 h stimulation with IL-1β, TNF-α, or GM-CSF ( n = 4).( C )Extracellular acidification rate (ECAR) measured by Seahorse assay in HMDMs exposed to RA serum with or without <t>IL-1RN,</t> infliximab, or lenzilumab ( n = 6).( D-E ) Western blot analysis of HIF-1α and IL-1β expression in macrophages treated with RA serum in the presence or absence of ( D ) IL-1RN or ( E ) infliximab for 24 h ( n = 6).Data were shown as mean ± SEM and were analyzed using one-way ANOVA or Two-tailed student’s t-test. *, p < 0.05; **, p < 0.01. 2-DG: 2-Deoxy-D-glucose; <t>IL-1RN:</t> <t>Interleukin-1</t> receptor antagonist; IFX: Infliximab
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    Image Search Results


    GCDCA-mediated hepatocyte IL-1β secretion activates HSCs. ( A ) Western blot analysis ofα-SMA and Collagen-I in LX2 cells treated with conditioned medium (CM) from GCDCA/LPS-stimulated L02 hepatocytes. ( B ) The protein levels of α-SMA and Collagen-I in LX2 cells with treatment of IL-1 receptor antagonist (IL-1RA, 200 ng/mL) upon CM exposure. ( C and D ) Representative images and quantification of LX2 migration upon CM exposure detected by wound healing assay. ( E ) CCK-8 assay of LX2 proliferation by CM treatment. n ≥ 3 for each group. a P < 0.05.

    Journal: Journal of Inflammation Research

    Article Title: Glycochenodeoxycholic acid induces the release of IL-1beta from L02 cells via the NLRP3/caspase-1/GSDMD pathway to activate LX2 cells

    doi: 10.2147/JIR.S532042

    Figure Lengend Snippet: GCDCA-mediated hepatocyte IL-1β secretion activates HSCs. ( A ) Western blot analysis ofα-SMA and Collagen-I in LX2 cells treated with conditioned medium (CM) from GCDCA/LPS-stimulated L02 hepatocytes. ( B ) The protein levels of α-SMA and Collagen-I in LX2 cells with treatment of IL-1 receptor antagonist (IL-1RA, 200 ng/mL) upon CM exposure. ( C and D ) Representative images and quantification of LX2 migration upon CM exposure detected by wound healing assay. ( E ) CCK-8 assay of LX2 proliferation by CM treatment. n ≥ 3 for each group. a P < 0.05.

    Article Snippet: Conditioned media from treated L02 cells were co-cultured with LX2 cells in the presence/absence of Interleukin-1 receptor antagonist (IL-1RA) (200 ng/mL, HY-P7029A, MCE).

    Techniques: Western Blot, Migration, Wound Healing Assay, CCK-8 Assay

    Blocking IL-1β in the RA serum attenuates glycolysis-HIF-1α axis mediated IL-1β. (A) qPCR analysis of HK2, HIF-1α, and IL-1β mRNA expression in HMDMs stimulated for 24 h with IL-1β, TNF-α, GM-CSF, IFN-γ, or IL-6 ( n = 7).( B )Representative image of IL-1β and HIF-1α expression in HMDMs pretreated with or without 2-DG (5 mM, 3 h) followed by 24 h stimulation with IL-1β, TNF-α, or GM-CSF ( n = 4).( C )Extracellular acidification rate (ECAR) measured by Seahorse assay in HMDMs exposed to RA serum with or without IL-1RN, infliximab, or lenzilumab ( n = 6).( D-E ) Western blot analysis of HIF-1α and IL-1β expression in macrophages treated with RA serum in the presence or absence of ( D ) IL-1RN or ( E ) infliximab for 24 h ( n = 6).Data were shown as mean ± SEM and were analyzed using one-way ANOVA or Two-tailed student’s t-test. *, p < 0.05; **, p < 0.01. 2-DG: 2-Deoxy-D-glucose; IL-1RN: Interleukin-1 receptor antagonist; IFX: Infliximab

    Journal: Arthritis Research & Therapy

    Article Title: The Glycolysis-HIF-1α axis induces IL-1β of macrophages in rheumatoid arthritis

    doi: 10.1186/s13075-025-03647-z

    Figure Lengend Snippet: Blocking IL-1β in the RA serum attenuates glycolysis-HIF-1α axis mediated IL-1β. (A) qPCR analysis of HK2, HIF-1α, and IL-1β mRNA expression in HMDMs stimulated for 24 h with IL-1β, TNF-α, GM-CSF, IFN-γ, or IL-6 ( n = 7).( B )Representative image of IL-1β and HIF-1α expression in HMDMs pretreated with or without 2-DG (5 mM, 3 h) followed by 24 h stimulation with IL-1β, TNF-α, or GM-CSF ( n = 4).( C )Extracellular acidification rate (ECAR) measured by Seahorse assay in HMDMs exposed to RA serum with or without IL-1RN, infliximab, or lenzilumab ( n = 6).( D-E ) Western blot analysis of HIF-1α and IL-1β expression in macrophages treated with RA serum in the presence or absence of ( D ) IL-1RN or ( E ) infliximab for 24 h ( n = 6).Data were shown as mean ± SEM and were analyzed using one-way ANOVA or Two-tailed student’s t-test. *, p < 0.05; **, p < 0.01. 2-DG: 2-Deoxy-D-glucose; IL-1RN: Interleukin-1 receptor antagonist; IFX: Infliximab

    Article Snippet: For cytokine blocking, HMDMs were incubated with RA serum with 100ng/ml of Interleukin-1 receptor antagonist (IL-1RN, HY-P7029, MedChemExpress), 10 μg/ml of Infliximab (HY-P9970, MedChemExpress), or Lenzilumab (HY-P99207, MedChemExpress) for 24 h, respectively.

    Techniques: Blocking Assay, Expressing, Western Blot, Two Tailed Test