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tnfα hz 1014  (Proteintech)


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    Proteintech tnfα hz 1014
    Tnfα Hz 1014, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 71 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tnfα hz 1014/product/Proteintech
    Average 94 stars, based on 71 article reviews
    tnfα hz 1014 - by Bioz Stars, 2026-03
    94/100 stars

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    Fig. 5. Validation the <t>IL-6-STAT3-TNFα-NF-κB</t> interaction pathway between the chordoma cells and macrophages. (A)–(B) The migration and invasion of UM-chor1 cells was significantly increased after TNFα treatment (n = 3). (C)–(D) The migration and invasion of Uch1 cells was significantly increased after TNFα treatment. (E) The expression levels of NF-κB and CTSB were elevated after TNFα treatment both in UM-chor1 and Uch1 cells. (F)–(G) Histograms of CD206 and TNFα in macrophages under different induction conditions. The MFI was shown in the right of each line. (H) The relative expression level of M2 markers CD163, CD206, ARG-1 and IL-10 in IL-6M. (I) The secretion level of TNFα in macrophages induced under different IL-6 concentrations (n = 3). (J) The expression levels of pSTAT3, STAT3, TNFα and CTSB were elevated in macrophages induced under different IL-6 concentrations. (K)-(L) The secretion level of IL-6 was increased after TNFα treatment in UM-chor1 and Uch1 cells (n = 3). **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05. ns, no significance. CTSB, cathepsin <t>B.</t> <t>UM-TAM,</t> UM-chor1- derived tumor-associated macrophage. UC-TAM, Uch1-derived tumor-associated macrophage. IL-6M, IL-6-derived macrophages. MFI, mean fluorescence intensity.
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    Fig. 5. Validation the IL-6-STAT3-TNFα-NF-κB interaction pathway between the chordoma cells and macrophages. (A)–(B) The migration and invasion of UM-chor1 cells was significantly increased after TNFα treatment (n = 3). (C)–(D) The migration and invasion of Uch1 cells was significantly increased after TNFα treatment. (E) The expression levels of NF-κB and CTSB were elevated after TNFα treatment both in UM-chor1 and Uch1 cells. (F)–(G) Histograms of CD206 and TNFα in macrophages under different induction conditions. The MFI was shown in the right of each line. (H) The relative expression level of M2 markers CD163, CD206, ARG-1 and IL-10 in IL-6M. (I) The secretion level of TNFα in macrophages induced under different IL-6 concentrations (n = 3). (J) The expression levels of pSTAT3, STAT3, TNFα and CTSB were elevated in macrophages induced under different IL-6 concentrations. (K)-(L) The secretion level of IL-6 was increased after TNFα treatment in UM-chor1 and Uch1 cells (n = 3). **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05. ns, no significance. CTSB, cathepsin B. UM-TAM, UM-chor1- derived tumor-associated macrophage. UC-TAM, Uch1-derived tumor-associated macrophage. IL-6M, IL-6-derived macrophages. MFI, mean fluorescence intensity.

    Journal: International immunopharmacology

    Article Title: Tumor-derived IL-6 promotes chordoma invasion by stimulating tumor-associated macrophages M2 polarization and TNFα secretion.

    doi: 10.1016/j.intimp.2024.113315

    Figure Lengend Snippet: Fig. 5. Validation the IL-6-STAT3-TNFα-NF-κB interaction pathway between the chordoma cells and macrophages. (A)–(B) The migration and invasion of UM-chor1 cells was significantly increased after TNFα treatment (n = 3). (C)–(D) The migration and invasion of Uch1 cells was significantly increased after TNFα treatment. (E) The expression levels of NF-κB and CTSB were elevated after TNFα treatment both in UM-chor1 and Uch1 cells. (F)–(G) Histograms of CD206 and TNFα in macrophages under different induction conditions. The MFI was shown in the right of each line. (H) The relative expression level of M2 markers CD163, CD206, ARG-1 and IL-10 in IL-6M. (I) The secretion level of TNFα in macrophages induced under different IL-6 concentrations (n = 3). (J) The expression levels of pSTAT3, STAT3, TNFα and CTSB were elevated in macrophages induced under different IL-6 concentrations. (K)-(L) The secretion level of IL-6 was increased after TNFα treatment in UM-chor1 and Uch1 cells (n = 3). **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05. ns, no significance. CTSB, cathepsin B. UM-TAM, UM-chor1- derived tumor-associated macrophage. UC-TAM, Uch1-derived tumor-associated macrophage. IL-6M, IL-6-derived macrophages. MFI, mean fluorescence intensity.

    Article Snippet: Chordoma cells were harvested and re-suspended either in TAM CM or in complete medium with different concentration of TNFα (HZ-1014, Proteintech, China).

    Techniques: Biomarker Discovery, Migration, Expressing, Derivative Assay, Fluorescence

    Fig. 6. The interaction between chordoma cells and macrophages increased immune checkpoints expression and inhibited CD8 þ T cells proliferation and function. (A) The relative expression levels of immune checkpoints in UM-chor1 cells were up-regulated after co-cultured with macrophages. (B)-(C) The relative expression levels of PD-L1 and PD-L2 in UM-chor1 and Uch1 cells were increased after TNFα treatment. (D) The relative expression levels of immune checkpoints in UM-TAMs were up-regulated compared with M0 cells. (E) The Histograms of PD-L1 in macrophages under different induction conditions. The MFI was shown in the right of each line. (F) The ratio of CD8+/CD3 + T cells was significantly decreased when T cells co-cultured with macrophages under different induction conditions (n = 4). (G) The expression of Granzyme B was significantly decreased in CD8 + T cells when T cells co-cultured with macrophages under different induction conditions (n = 3). **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05. ns, no significance. UM-TAM, UM-chor1-derived tumor-associated macrophage. UC-TAM, Uch1-derived tumor-associated macrophage. IL-6M, IL-6-derived macrophages. MFI, mean fluorescence intensity.

    Journal: International immunopharmacology

    Article Title: Tumor-derived IL-6 promotes chordoma invasion by stimulating tumor-associated macrophages M2 polarization and TNFα secretion.

    doi: 10.1016/j.intimp.2024.113315

    Figure Lengend Snippet: Fig. 6. The interaction between chordoma cells and macrophages increased immune checkpoints expression and inhibited CD8 þ T cells proliferation and function. (A) The relative expression levels of immune checkpoints in UM-chor1 cells were up-regulated after co-cultured with macrophages. (B)-(C) The relative expression levels of PD-L1 and PD-L2 in UM-chor1 and Uch1 cells were increased after TNFα treatment. (D) The relative expression levels of immune checkpoints in UM-TAMs were up-regulated compared with M0 cells. (E) The Histograms of PD-L1 in macrophages under different induction conditions. The MFI was shown in the right of each line. (F) The ratio of CD8+/CD3 + T cells was significantly decreased when T cells co-cultured with macrophages under different induction conditions (n = 4). (G) The expression of Granzyme B was significantly decreased in CD8 + T cells when T cells co-cultured with macrophages under different induction conditions (n = 3). **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05. ns, no significance. UM-TAM, UM-chor1-derived tumor-associated macrophage. UC-TAM, Uch1-derived tumor-associated macrophage. IL-6M, IL-6-derived macrophages. MFI, mean fluorescence intensity.

    Article Snippet: Chordoma cells were harvested and re-suspended either in TAM CM or in complete medium with different concentration of TNFα (HZ-1014, Proteintech, China).

    Techniques: Expressing, Cell Culture, Derivative Assay, Fluorescence

    Fig. 7. Block IL-6/STAT3 pathway could attenuate the interaction between chordoma cells and macrophages. (A)The phosphorylation of STAT3 induced by chordoma cells or IL-6 could be attenuated by ST and Toci. (B)-(C) The expression levels of pSTAT3, TNFα, CD163, CD206 PD-L1 and PD-L2 in UM-TAM and UC-TAM were significantly decreased after ST treatment. (D)-(E) The expression of M2 markers (CD163 and CD206), immune checkpoints (PD-L1 and PD-L2) and TNFα in IL- 6M cells were significantly decreased after ST treatment. **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05. ns, no significance. Toci, Tocilizumab.ST, Sttatic. UM-TAM, UM-chor1-derived tumor-associated macrophage. UC-TAM, Uch1-derived tumor-associated macrophage. IL-6M, IL-6-derived macrophages. MFI, mean fluorescence intensity.

    Journal: International immunopharmacology

    Article Title: Tumor-derived IL-6 promotes chordoma invasion by stimulating tumor-associated macrophages M2 polarization and TNFα secretion.

    doi: 10.1016/j.intimp.2024.113315

    Figure Lengend Snippet: Fig. 7. Block IL-6/STAT3 pathway could attenuate the interaction between chordoma cells and macrophages. (A)The phosphorylation of STAT3 induced by chordoma cells or IL-6 could be attenuated by ST and Toci. (B)-(C) The expression levels of pSTAT3, TNFα, CD163, CD206 PD-L1 and PD-L2 in UM-TAM and UC-TAM were significantly decreased after ST treatment. (D)-(E) The expression of M2 markers (CD163 and CD206), immune checkpoints (PD-L1 and PD-L2) and TNFα in IL- 6M cells were significantly decreased after ST treatment. **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05. ns, no significance. Toci, Tocilizumab.ST, Sttatic. UM-TAM, UM-chor1-derived tumor-associated macrophage. UC-TAM, Uch1-derived tumor-associated macrophage. IL-6M, IL-6-derived macrophages. MFI, mean fluorescence intensity.

    Article Snippet: Chordoma cells were harvested and re-suspended either in TAM CM or in complete medium with different concentration of TNFα (HZ-1014, Proteintech, China).

    Techniques: Blocking Assay, Phospho-proteomics, Expressing, Derivative Assay, Fluorescence

    The regulation of transcription factors to the promoter of CD55 . (A) The mRNA level of TFCP2 by RT-PCR after HCT116 cells transfected with si- TFCP2 or siRNA control for 24 h. (B) The protein expression of TFCP2 by Western blotting after HCT116 cells transfected with si- TFCP2 or siRNA control for 48 h. (C) Dual-luciferase assay of pGL3- CD55 pro -Wt in HCT116 cells after co-transfected with si- TFCP2. (D) The mRNA level of NF-κB in HCT116 cells treated with NF-κB inhibitor and that in LOVO cells treated with NF-κB activator for 24 h. (E) The luciferase activity of pGL3- CD55 pro -Wt in HCT116 cells treated with or without NF-κB inhibitor. (F) The luciferase activity of pGL3- CD55 pro -Wt and pGL3- CD55 pro - NF-κB -Mut in LOVO cells treated with or without NF-κB activator (TNFα). (G) CD55 promoter activity assay in pGL3- CD55 pro -Wt, pGL3- CD55 pro - NF-κB -Mut, and pGL3- CD55 pro - TFCP2 -Mut plasmids. Luciferase activity was normalized to Renilla luciferase activity (L/R). (H) The binding of TFCP2 and NF-κB to the promoter of CD55 by ChIP. IgG from rabbits served as a control (* p < 0.05, ** p < 0.01, *** p < 0.001, ns, no significance). ChIP, chromatin immunoprecipitation.

    Journal: Frontiers in Immunology

    Article Title: The genetic and epigenetic regulation of CD55 and its pathway analysis in colon cancer

    doi: 10.3389/fimmu.2022.947136

    Figure Lengend Snippet: The regulation of transcription factors to the promoter of CD55 . (A) The mRNA level of TFCP2 by RT-PCR after HCT116 cells transfected with si- TFCP2 or siRNA control for 24 h. (B) The protein expression of TFCP2 by Western blotting after HCT116 cells transfected with si- TFCP2 or siRNA control for 48 h. (C) Dual-luciferase assay of pGL3- CD55 pro -Wt in HCT116 cells after co-transfected with si- TFCP2. (D) The mRNA level of NF-κB in HCT116 cells treated with NF-κB inhibitor and that in LOVO cells treated with NF-κB activator for 24 h. (E) The luciferase activity of pGL3- CD55 pro -Wt in HCT116 cells treated with or without NF-κB inhibitor. (F) The luciferase activity of pGL3- CD55 pro -Wt and pGL3- CD55 pro - NF-κB -Mut in LOVO cells treated with or without NF-κB activator (TNFα). (G) CD55 promoter activity assay in pGL3- CD55 pro -Wt, pGL3- CD55 pro - NF-κB -Mut, and pGL3- CD55 pro - TFCP2 -Mut plasmids. Luciferase activity was normalized to Renilla luciferase activity (L/R). (H) The binding of TFCP2 and NF-κB to the promoter of CD55 by ChIP. IgG from rabbits served as a control (* p < 0.05, ** p < 0.01, *** p < 0.001, ns, no significance). ChIP, chromatin immunoprecipitation.

    Article Snippet: NF-κB inhibitor (B5556) and NF-κB activator (TNFα) (HZ-1014) were purchased from Sigma-Aldrich (New Jersey, USA) and ProteinTech (Chicago, USA), respectively.

    Techniques: Reverse Transcription Polymerase Chain Reaction, Transfection, Control, Expressing, Western Blot, Luciferase, Activity Assay, Binding Assay, Chromatin Immunoprecipitation