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interleukin 6 il 6 receptor antibody  (MedChemExpress)


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    MedChemExpress interleukin 6 il 6 receptor antibody
    Interleukin 6 Il 6 Receptor Antibody, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-p0317/Interleukin+(IL)-6+Receptor/pm34693451-46-12-19
    Average 93 stars, based on 1 article reviews
    interleukin 6 il 6 receptor antibody - by Bioz Stars, 2026-10
    93/100 stars

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    Related Articles

    Injection:

    Article Title: Targeting SPHK1 in macrophages remodels the tumor microenvironment and enhances anti‐PD‐1 immunotherapy efficacy in colorectal cancer liver metastasis
    Article Snippet: Anti‐PD‐1 antibody (clone RMP1‐14, 200 mg; BioXcell) or isotype IgG (200 mg; BioXcell) combined with or without PF543 (5 mg/kg) or SKI II (50 mg/kg) was injected intraperitoneally into each mouse. .. For anti‐interleukin 1 receptor (IL‐1R) treatment of liver tumors, BALB/c mice with CT26 intrasplenic inoculation were administered 500 μg IL‐1R antagonist anakinra (MedChemExpress), by intraperitoneal injection on days 4, 7, 10, 13, and 16. ..

    Recombinant:

    Article Title: Targeting DCLK1 attenuates tumor stemness and evokes antitumor immunity in triple-negative breast cancer by inhibiting IL-6/STAT3 signaling
    Article Snippet: .. Chemotherapy drugs including doxorubicin and cisplatin were from Solarbio (China); IL-6 receptor antagonist, Tocilizumab, was purchased from MCE (USA); STAT3 pathway inhibitor, S31-201, was from Selleck (USA); Recombinant Human IL-6 was from PeproTech (USA). ..

    Radio Immunoprecipitation:

    Article Title: Stattic sensitizes osteosarcoma cells to epidermal growth factor receptor inhibitors via blocking the interleukin 6-induced STAT3 pathway.
    Article Snippet: Osteosarcoma (OS), the most common malignant bone tumor with high metastatic potential, frequently affects children and adolescents.. Epidermal growth factor receptor (EGFR)-targeted tyrosine kinase inhibitors exhibit encouraging anti-tumor activity for patients with solid tumors, whereas their effects on OS remain controversial.. In the present study, we aimed to elucidate the anti-tumor activity of gefitinib for OS, as well as to explore the underlying mechanisms.

    Lysis:

    Article Title: Stattic sensitizes osteosarcoma cells to epidermal growth factor receptor inhibitors via blocking the interleukin 6-induced STAT3 pathway.
    Article Snippet: Osteosarcoma (OS), the most common malignant bone tumor with high metastatic potential, frequently affects children and adolescents.. Epidermal growth factor receptor (EGFR)-targeted tyrosine kinase inhibitors exhibit encouraging anti-tumor activity for patients with solid tumors, whereas their effects on OS remain controversial.. In the present study, we aimed to elucidate the anti-tumor activity of gefitinib for OS, as well as to explore the underlying mechanisms.

    Bicinchoninic Acid Protein Assay:

    Article Title: Stattic sensitizes osteosarcoma cells to epidermal growth factor receptor inhibitors via blocking the interleukin 6-induced STAT3 pathway.
    Article Snippet: Osteosarcoma (OS), the most common malignant bone tumor with high metastatic potential, frequently affects children and adolescents.. Epidermal growth factor receptor (EGFR)-targeted tyrosine kinase inhibitors exhibit encouraging anti-tumor activity for patients with solid tumors, whereas their effects on OS remain controversial.. In the present study, we aimed to elucidate the anti-tumor activity of gefitinib for OS, as well as to explore the underlying mechanisms.



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    DCLK1 activates <t>IL-6/JAK1/STAT3</t> signaling. a Gene set variation analysis (GSVA) showing DCLK1-associated pathways in TNBC. b Gene set enrichment analysis (GSEA) revealing the significant activation of IL-6/JAK/STAT3 pathway in DCLK1-high expressed TNBC patients. c Spearman correlation analysis showing the positive association between DCLK1 expression and IL6 expression. d, e Western blotting to determine expression levels of phosphorylated STAT3 (Tyr705) and total STAT3 as well as CSC-associated markers ( d ) and EMT-associated markers ( e ) in TNBC cells treated with exogenous IL-6 stimulation for 24 h. f TIDE analysis showing a lower response in TNBC patients with a higher IL-6 expression (left, 21%, 38/180) than patients with a lower IL-6 expression (right, 32%, 58/122) in the FUSCC dataset. g CFSE-based T-cell proliferation assay revealing a lower activity of CD8+ T cell treated with exogenous IL-6 stimulation for 72 h compared to the control group. h Real-time qPCR determination of the effects of DCLK1 on IL-6 mRNA expression levels. i Western blotting detection of activated IL-6/JAK1/STAT3 signaling in DCLK1-overexpressing MDA-MB-468 cells (left) and inactivated IL-6/JAK1/STAT3 signaling in DCLK1-knockout BT549 cells (middle), 4T1 cell (right). j IHC examination of DCLK1, IL-6, phosphorylated STAT3 (Tyr705) and CD8 in the control and DCLK1-knockout 4T1 subcutaneous tumors
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    DCLK1 activates <t>IL-6/JAK1/STAT3</t> signaling. a Gene set variation analysis (GSVA) showing DCLK1-associated pathways in TNBC. b Gene set enrichment analysis (GSEA) revealing the significant activation of IL-6/JAK/STAT3 pathway in DCLK1-high expressed TNBC patients. c Spearman correlation analysis showing the positive association between DCLK1 expression and IL6 expression. d, e Western blotting to determine expression levels of phosphorylated STAT3 (Tyr705) and total STAT3 as well as CSC-associated markers ( d ) and EMT-associated markers ( e ) in TNBC cells treated with exogenous IL-6 stimulation for 24 h. f TIDE analysis showing a lower response in TNBC patients with a higher IL-6 expression (left, 21%, 38/180) than patients with a lower IL-6 expression (right, 32%, 58/122) in the FUSCC dataset. g CFSE-based T-cell proliferation assay revealing a lower activity of CD8+ T cell treated with exogenous IL-6 stimulation for 72 h compared to the control group. h Real-time qPCR determination of the effects of DCLK1 on IL-6 mRNA expression levels. i Western blotting detection of activated IL-6/JAK1/STAT3 signaling in DCLK1-overexpressing MDA-MB-468 cells (left) and inactivated IL-6/JAK1/STAT3 signaling in DCLK1-knockout BT549 cells (middle), 4T1 cell (right). j IHC examination of DCLK1, IL-6, phosphorylated STAT3 (Tyr705) and CD8 in the control and DCLK1-knockout 4T1 subcutaneous tumors
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    DCLK1 activates IL-6/JAK1/STAT3 signaling. a Gene set variation analysis (GSVA) showing DCLK1-associated pathways in TNBC. b Gene set enrichment analysis (GSEA) revealing the significant activation of IL-6/JAK/STAT3 pathway in DCLK1-high expressed TNBC patients. c Spearman correlation analysis showing the positive association between DCLK1 expression and IL6 expression. d, e Western blotting to determine expression levels of phosphorylated STAT3 (Tyr705) and total STAT3 as well as CSC-associated markers ( d ) and EMT-associated markers ( e ) in TNBC cells treated with exogenous IL-6 stimulation for 24 h. f TIDE analysis showing a lower response in TNBC patients with a higher IL-6 expression (left, 21%, 38/180) than patients with a lower IL-6 expression (right, 32%, 58/122) in the FUSCC dataset. g CFSE-based T-cell proliferation assay revealing a lower activity of CD8+ T cell treated with exogenous IL-6 stimulation for 72 h compared to the control group. h Real-time qPCR determination of the effects of DCLK1 on IL-6 mRNA expression levels. i Western blotting detection of activated IL-6/JAK1/STAT3 signaling in DCLK1-overexpressing MDA-MB-468 cells (left) and inactivated IL-6/JAK1/STAT3 signaling in DCLK1-knockout BT549 cells (middle), 4T1 cell (right). j IHC examination of DCLK1, IL-6, phosphorylated STAT3 (Tyr705) and CD8 in the control and DCLK1-knockout 4T1 subcutaneous tumors

    Journal: Breast Cancer Research : BCR

    Article Title: Targeting DCLK1 attenuates tumor stemness and evokes antitumor immunity in triple-negative breast cancer by inhibiting IL-6/STAT3 signaling

    doi: 10.1186/s13058-023-01642-3

    Figure Lengend Snippet: DCLK1 activates IL-6/JAK1/STAT3 signaling. a Gene set variation analysis (GSVA) showing DCLK1-associated pathways in TNBC. b Gene set enrichment analysis (GSEA) revealing the significant activation of IL-6/JAK/STAT3 pathway in DCLK1-high expressed TNBC patients. c Spearman correlation analysis showing the positive association between DCLK1 expression and IL6 expression. d, e Western blotting to determine expression levels of phosphorylated STAT3 (Tyr705) and total STAT3 as well as CSC-associated markers ( d ) and EMT-associated markers ( e ) in TNBC cells treated with exogenous IL-6 stimulation for 24 h. f TIDE analysis showing a lower response in TNBC patients with a higher IL-6 expression (left, 21%, 38/180) than patients with a lower IL-6 expression (right, 32%, 58/122) in the FUSCC dataset. g CFSE-based T-cell proliferation assay revealing a lower activity of CD8+ T cell treated with exogenous IL-6 stimulation for 72 h compared to the control group. h Real-time qPCR determination of the effects of DCLK1 on IL-6 mRNA expression levels. i Western blotting detection of activated IL-6/JAK1/STAT3 signaling in DCLK1-overexpressing MDA-MB-468 cells (left) and inactivated IL-6/JAK1/STAT3 signaling in DCLK1-knockout BT549 cells (middle), 4T1 cell (right). j IHC examination of DCLK1, IL-6, phosphorylated STAT3 (Tyr705) and CD8 in the control and DCLK1-knockout 4T1 subcutaneous tumors

    Article Snippet: Chemotherapy drugs including doxorubicin and cisplatin were from Solarbio (China); IL-6 receptor antagonist, Tocilizumab, was purchased from MCE (USA); STAT3 pathway inhibitor, S31-201, was from Selleck (USA); Recombinant Human IL-6 was from PeproTech (USA).

    Techniques: Activation Assay, Expressing, Western Blot, Proliferation Assay, Activity Assay, Control, Knock-Out

    DCLK1 is a promising target in mesenchymal-like subtype of TNBC. a, b High mRNA expression of DCLK1 ( a ) and IL-6 ( b ) predicts reduced recurrence-free survival (RFS) in TNBC (n = 392) subtype rather than Luminal A (n = 522), Luminal B (n = 332) or HER2 (n = 315) subtype according to KM-potter database. c High mRNA expression of DCLK1 and predicts reduced overall survival (OS) in TNBC tissues according to KM-plotter database (n = 153). d The boxplot showing a significantly higher expression of DCLK1 in the MES subtype than the other three subtypes. e Receiver operating characteristic (ROC) curve for using DCLK1 expression to identify the MES subtype. f CCK8 assays to determine the toxicity of DCLK1 inhibitor, DCLK1-IN-1, on TNBC cells. g CCK8 assays to determine the cell viability of mesenchymal-like cells BT549 and basal-like cells MDA-MB-468 with different treatment as indicated (left and middle), and the cells surviving different treatments were also showed by crystal violet (right). h Western blotting showing the effects of DCLK1-IN-1 on EMT and CSC-associated marker in BT549 cells. i Transwell assays showing the inhibited migratory/invasive abilities in BT549 cells treated with DCLK1-IN-1. j Tumor growth curves showing the anti-tumor effects after DCLK1-IN-1 or S31-201 treatment (left), tumors from the indicated treatments were removed and photographed (right). (n = 6 per group). k Excised tumor weights showing a significant decrease after DCLK1-IN-1 or S31-201 treatment. l Flow cytometry analyzing the percentage of CD8+ T cells in subcutaneous tumor tissues after the indicated treatments

    Journal: Breast Cancer Research : BCR

    Article Title: Targeting DCLK1 attenuates tumor stemness and evokes antitumor immunity in triple-negative breast cancer by inhibiting IL-6/STAT3 signaling

    doi: 10.1186/s13058-023-01642-3

    Figure Lengend Snippet: DCLK1 is a promising target in mesenchymal-like subtype of TNBC. a, b High mRNA expression of DCLK1 ( a ) and IL-6 ( b ) predicts reduced recurrence-free survival (RFS) in TNBC (n = 392) subtype rather than Luminal A (n = 522), Luminal B (n = 332) or HER2 (n = 315) subtype according to KM-potter database. c High mRNA expression of DCLK1 and predicts reduced overall survival (OS) in TNBC tissues according to KM-plotter database (n = 153). d The boxplot showing a significantly higher expression of DCLK1 in the MES subtype than the other three subtypes. e Receiver operating characteristic (ROC) curve for using DCLK1 expression to identify the MES subtype. f CCK8 assays to determine the toxicity of DCLK1 inhibitor, DCLK1-IN-1, on TNBC cells. g CCK8 assays to determine the cell viability of mesenchymal-like cells BT549 and basal-like cells MDA-MB-468 with different treatment as indicated (left and middle), and the cells surviving different treatments were also showed by crystal violet (right). h Western blotting showing the effects of DCLK1-IN-1 on EMT and CSC-associated marker in BT549 cells. i Transwell assays showing the inhibited migratory/invasive abilities in BT549 cells treated with DCLK1-IN-1. j Tumor growth curves showing the anti-tumor effects after DCLK1-IN-1 or S31-201 treatment (left), tumors from the indicated treatments were removed and photographed (right). (n = 6 per group). k Excised tumor weights showing a significant decrease after DCLK1-IN-1 or S31-201 treatment. l Flow cytometry analyzing the percentage of CD8+ T cells in subcutaneous tumor tissues after the indicated treatments

    Article Snippet: Chemotherapy drugs including doxorubicin and cisplatin were from Solarbio (China); IL-6 receptor antagonist, Tocilizumab, was purchased from MCE (USA); STAT3 pathway inhibitor, S31-201, was from Selleck (USA); Recombinant Human IL-6 was from PeproTech (USA).

    Techniques: Expressing, Western Blot, Marker, Flow Cytometry

    DCLK1-activated IL-6/STAT3 pathway plays critical roles in CSC-like properties and anti-tumor immunity in TNBC. DCLK1 upregulates IL-6 expression and activates JAK1/STAT3 signaling, which promotes tumor cell stemness and inhibits CD8+ T cell-mediated antitumor immunity. DCLK1-IN-1 may be a promising treatment for TNBC patients with high DCLK1 expressions

    Journal: Breast Cancer Research : BCR

    Article Title: Targeting DCLK1 attenuates tumor stemness and evokes antitumor immunity in triple-negative breast cancer by inhibiting IL-6/STAT3 signaling

    doi: 10.1186/s13058-023-01642-3

    Figure Lengend Snippet: DCLK1-activated IL-6/STAT3 pathway plays critical roles in CSC-like properties and anti-tumor immunity in TNBC. DCLK1 upregulates IL-6 expression and activates JAK1/STAT3 signaling, which promotes tumor cell stemness and inhibits CD8+ T cell-mediated antitumor immunity. DCLK1-IN-1 may be a promising treatment for TNBC patients with high DCLK1 expressions

    Article Snippet: Chemotherapy drugs including doxorubicin and cisplatin were from Solarbio (China); IL-6 receptor antagonist, Tocilizumab, was purchased from MCE (USA); STAT3 pathway inhibitor, S31-201, was from Selleck (USA); Recombinant Human IL-6 was from PeproTech (USA).

    Techniques: Expressing