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nfκb antibody kit  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc nfκb antibody kit
    Nfκb Antibody Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 92/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nf%CE%BAb+antibody+kit/pmc11197201-29-21-37?v=Cell+Signaling+Technology+Inc
    Average 92 stars, based on 8 article reviews
    nfκb antibody kit - by Bioz Stars, 2026-07
    92/100 stars

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    Image Search Results


    BB inhibits LPS-inducted NF-κB activation and inflammatory cytokine production. LPS induced NF-κB activation and the release of inflammatory cytokines in a dose-dependent manner. LPS stimulation significantly increased the phosphorylation of (A) IκBα and (B) p65, (C) elevated p65 DNA-binding activity and (D) promoted the production of IL-1β, IL-6 and TNF-α. Preincubation with BB (10 and 20 µM) markedly diminished the effects of LPS. The results are presented as the mean ± SEM. All the experiments were performed in triplicate and repeated three times. DMSO was used as the control. * P<0.05 vs. control; # P<0.05 vs. LPS; Δ P<0.05 vs. LPS + BB 10 µM. BB, bilobalide; LPS, lipopolysaccharide; p-, phosphorylated.

    Journal: Experimental and Therapeutic Medicine

    Article Title: Bilobalide attenuates lipopolysaccharide‑induced HepG2 cell injury by inhibiting TLR4‑NF‑κB signaling via the PI3K/Akt pathway

    doi: 10.3892/etm.2023.12312

    Figure Lengend Snippet: BB inhibits LPS-inducted NF-κB activation and inflammatory cytokine production. LPS induced NF-κB activation and the release of inflammatory cytokines in a dose-dependent manner. LPS stimulation significantly increased the phosphorylation of (A) IκBα and (B) p65, (C) elevated p65 DNA-binding activity and (D) promoted the production of IL-1β, IL-6 and TNF-α. Preincubation with BB (10 and 20 µM) markedly diminished the effects of LPS. The results are presented as the mean ± SEM. All the experiments were performed in triplicate and repeated three times. DMSO was used as the control. * P<0.05 vs. control; # P<0.05 vs. LPS; Δ P<0.05 vs. LPS + BB 10 µM. BB, bilobalide; LPS, lipopolysaccharide; p-, phosphorylated.

    Article Snippet: IL-6 (cat. no. CSB-E04638h), IL-1β (cat. no. CSB-E08053h) and TNF-α (cat. no. CSB-E04740h) ELISA kits were obtained from CUSABIO TECHNOLOGY LLC. β-actin (cat. no. 4970S), IκBα (cat. no. 4812S), NF-κB p65 (cat. no. 8242S), phosphorylated (p)-IκBα (cat. no. 2859S) and p-p65 (cat. no. 3033S) antibodies were purchased from Cell Signaling Technology, Inc. Horseradish peroxidase-conjugated anti-rabbit IgG secondary antibody (cat. no. BA1054) was purchased from Wuhan Boster Biological Technology, Ltd. TransAM NF-κB p65 kit (cat. no. 40096) was obtained from Active Motif, Inc.

    Techniques: Activation Assay, Phospho-proteomics, Binding Assay, Activity Assay, Control

    Toll-like receptor 4 is involved in LPS-induced HepG2 cell injury, NF-κB activation and inflammatory cytokine release. CLI-095 significantly decreased LPS-induced increase in (A) IκBα phosphorylation, (B) p65 phosphorylation, (C) p65 DNA-binding activity and (D) IL-1β, IL-6 and TNF-α levels. (E) CLI-095 attenuated LPS-induced cell injury. The results are presented as the mean ± SEM. All the experiments were performed in triplicate and repeated three times. DMSO was used as the control. * P<0.05 vs. control; # P<0.05 vs. LPS. LPS, lipopolysaccharide; p-, phosphorylated.

    Journal: Experimental and Therapeutic Medicine

    Article Title: Bilobalide attenuates lipopolysaccharide‑induced HepG2 cell injury by inhibiting TLR4‑NF‑κB signaling via the PI3K/Akt pathway

    doi: 10.3892/etm.2023.12312

    Figure Lengend Snippet: Toll-like receptor 4 is involved in LPS-induced HepG2 cell injury, NF-κB activation and inflammatory cytokine release. CLI-095 significantly decreased LPS-induced increase in (A) IκBα phosphorylation, (B) p65 phosphorylation, (C) p65 DNA-binding activity and (D) IL-1β, IL-6 and TNF-α levels. (E) CLI-095 attenuated LPS-induced cell injury. The results are presented as the mean ± SEM. All the experiments were performed in triplicate and repeated three times. DMSO was used as the control. * P<0.05 vs. control; # P<0.05 vs. LPS. LPS, lipopolysaccharide; p-, phosphorylated.

    Article Snippet: IL-6 (cat. no. CSB-E04638h), IL-1β (cat. no. CSB-E08053h) and TNF-α (cat. no. CSB-E04740h) ELISA kits were obtained from CUSABIO TECHNOLOGY LLC. β-actin (cat. no. 4970S), IκBα (cat. no. 4812S), NF-κB p65 (cat. no. 8242S), phosphorylated (p)-IκBα (cat. no. 2859S) and p-p65 (cat. no. 3033S) antibodies were purchased from Cell Signaling Technology, Inc. Horseradish peroxidase-conjugated anti-rabbit IgG secondary antibody (cat. no. BA1054) was purchased from Wuhan Boster Biological Technology, Ltd. TransAM NF-κB p65 kit (cat. no. 40096) was obtained from Active Motif, Inc.

    Techniques: Activation Assay, Phospho-proteomics, Binding Assay, Activity Assay, Control

    BB inhibits LPS-induced TLR4 mRNA expression, NF-κB activation and inflammatory cytokine release through the PI3K/Akt pathway. (A) LY294002 attenuated the inhibitory effects of BB on TLR4 mRNA expression in LPS-stimulated HepG2 cells. LY294002 abolished the effects of BB on (B) p65 DNA-binding activity, (C) IκBα phosphorylation, (D) p65 phosphorylation and (E) inflammatory cytokine release. (F) The cytoprotective effect of BB was also abolished by LY294002. The results are presented as the mean ± SEM. All the experiments were performed in triplicate and repeated three times. DMSO was used as the control. * P<0.05 vs. control; # P<0.05 vs. LPS; Δ P<0.05 vs. LPS + BB 20 µM. BB, bilobalide; TLR4, toll-like receptor 4; p-, phosphorylated; LPS, lipopolysaccharide.

    Journal: Experimental and Therapeutic Medicine

    Article Title: Bilobalide attenuates lipopolysaccharide‑induced HepG2 cell injury by inhibiting TLR4‑NF‑κB signaling via the PI3K/Akt pathway

    doi: 10.3892/etm.2023.12312

    Figure Lengend Snippet: BB inhibits LPS-induced TLR4 mRNA expression, NF-κB activation and inflammatory cytokine release through the PI3K/Akt pathway. (A) LY294002 attenuated the inhibitory effects of BB on TLR4 mRNA expression in LPS-stimulated HepG2 cells. LY294002 abolished the effects of BB on (B) p65 DNA-binding activity, (C) IκBα phosphorylation, (D) p65 phosphorylation and (E) inflammatory cytokine release. (F) The cytoprotective effect of BB was also abolished by LY294002. The results are presented as the mean ± SEM. All the experiments were performed in triplicate and repeated three times. DMSO was used as the control. * P<0.05 vs. control; # P<0.05 vs. LPS; Δ P<0.05 vs. LPS + BB 20 µM. BB, bilobalide; TLR4, toll-like receptor 4; p-, phosphorylated; LPS, lipopolysaccharide.

    Article Snippet: IL-6 (cat. no. CSB-E04638h), IL-1β (cat. no. CSB-E08053h) and TNF-α (cat. no. CSB-E04740h) ELISA kits were obtained from CUSABIO TECHNOLOGY LLC. β-actin (cat. no. 4970S), IκBα (cat. no. 4812S), NF-κB p65 (cat. no. 8242S), phosphorylated (p)-IκBα (cat. no. 2859S) and p-p65 (cat. no. 3033S) antibodies were purchased from Cell Signaling Technology, Inc. Horseradish peroxidase-conjugated anti-rabbit IgG secondary antibody (cat. no. BA1054) was purchased from Wuhan Boster Biological Technology, Ltd. TransAM NF-κB p65 kit (cat. no. 40096) was obtained from Active Motif, Inc.

    Techniques: Expressing, Activation Assay, Binding Assay, Activity Assay, Phospho-proteomics, Control