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mouse monoclonal nf κb antibody  (Santa Cruz Biotechnology)
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anti p nf κb p50  (Santa Cruz Biotechnology)
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anti nfκb p65 p s536 antibody  (Bioss)
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OMVs upregulate tumor MHC I expression via the TLR4–NF‐κB–NLRC5 axis. (A) Relative mRNA expression of H‐2K and H‐2D in B16 cells after 24 h treatment with different OMV concentrations. (B) Representative plots for flow cytometry analysis of MHC‐I⁺ B16 tumor cell. (C) Proportions of MHC I + B16 cells after indicated treatments. (D) Volcano plot of differentially expressed genes in OMV versus control groups (red: significantly upregulated ≥2‐fold; blue: significantly downregulated ≥2‐fold). (E) GO enrichment of upregulated genes. (F) KEGG pathway enrichment of genes associated with innate and adaptive immune responses. (G‐H) Heat maps of MHC I–related genes detected by RNA‐seq (G) and qPCR (H). (I) Western blot analysis of TLR4 (≈100 kDa), <t>p‐p65</t> (≈70 kDa), NLRC5 (≈225 kDa), and β‐actin (≈48 kDa) in tumor cells. (J) Proportions of MHC I + tumor cells after indicated treatments. (K) Proposed mechanism of OMV‐induced MHC I upregulation through the TLR–NF‐κB–NLRC5 pathway. Created in BioRender. Zhang, F. (2026) https://BioRender.com/97sw6s6 . Data are mean ± SD (n = 3). Statistical significance was determined using Student's t‐test or One‐way ANOVA. **** p < 0.0001.
Anti Nfκb P65 P S536 Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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p nf ĸb p65  (Santa Cruz Biotechnology)
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OMVs upregulate tumor MHC I expression via the TLR4–NF‐κB–NLRC5 axis. (A) Relative mRNA expression of H‐2K and H‐2D in B16 cells after 24 h treatment with different OMV concentrations. (B) Representative plots for flow cytometry analysis of MHC‐I⁺ B16 tumor cell. (C) Proportions of MHC I + B16 cells after indicated treatments. (D) Volcano plot of differentially expressed genes in OMV versus control groups (red: significantly upregulated ≥2‐fold; blue: significantly downregulated ≥2‐fold). (E) GO enrichment of upregulated genes. (F) KEGG pathway enrichment of genes associated with innate and adaptive immune responses. (G‐H) Heat maps of MHC I–related genes detected by RNA‐seq (G) and qPCR (H). (I) Western blot analysis of TLR4 (≈100 kDa), <t>p‐p65</t> (≈70 kDa), NLRC5 (≈225 kDa), and β‐actin (≈48 kDa) in tumor cells. (J) Proportions of MHC I + tumor cells after indicated treatments. (K) Proposed mechanism of OMV‐induced MHC I upregulation through the TLR–NF‐κB–NLRC5 pathway. Created in BioRender. Zhang, F. (2026) https://BioRender.com/97sw6s6 . Data are mean ± SD (n = 3). Statistical significance was determined using Student's t‐test or One‐way ANOVA. **** p < 0.0001.
P Nf ĸb P65, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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nf κb  (Active Motif)
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OMVs upregulate tumor MHC I expression via the TLR4–NF‐κB–NLRC5 axis. (A) Relative mRNA expression of H‐2K and H‐2D in B16 cells after 24 h treatment with different OMV concentrations. (B) Representative plots for flow cytometry analysis of MHC‐I⁺ B16 tumor cell. (C) Proportions of MHC I + B16 cells after indicated treatments. (D) Volcano plot of differentially expressed genes in OMV versus control groups (red: significantly upregulated ≥2‐fold; blue: significantly downregulated ≥2‐fold). (E) GO enrichment of upregulated genes. (F) KEGG pathway enrichment of genes associated with innate and adaptive immune responses. (G‐H) Heat maps of MHC I–related genes detected by RNA‐seq (G) and qPCR (H). (I) Western blot analysis of TLR4 (≈100 kDa), <t>p‐p65</t> (≈70 kDa), NLRC5 (≈225 kDa), and β‐actin (≈48 kDa) in tumor cells. (J) Proportions of MHC I + tumor cells after indicated treatments. (K) Proposed mechanism of OMV‐induced MHC I upregulation through the TLR–NF‐κB–NLRC5 pathway. Created in BioRender. Zhang, F. (2026) https://BioRender.com/97sw6s6 . Data are mean ± SD (n = 3). Statistical significance was determined using Student's t‐test or One‐way ANOVA. **** p < 0.0001.
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sc 8008  (Santa Cruz Biotechnology)
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OMVs upregulate tumor MHC I expression via the TLR4–NF‐κB–NLRC5 axis. (A) Relative mRNA expression of H‐2K and H‐2D in B16 cells after 24 h treatment with different OMV concentrations. (B) Representative plots for flow cytometry analysis of MHC‐I⁺ B16 tumor cell. (C) Proportions of MHC I + B16 cells after indicated treatments. (D) Volcano plot of differentially expressed genes in OMV versus control groups (red: significantly upregulated ≥2‐fold; blue: significantly downregulated ≥2‐fold). (E) GO enrichment of upregulated genes. (F) KEGG pathway enrichment of genes associated with innate and adaptive immune responses. (G‐H) Heat maps of MHC I–related genes detected by RNA‐seq (G) and qPCR (H). (I) Western blot analysis of TLR4 (≈100 kDa), <t>p‐p65</t> (≈70 kDa), NLRC5 (≈225 kDa), and β‐actin (≈48 kDa) in tumor cells. (J) Proportions of MHC I + tumor cells after indicated treatments. (K) Proposed mechanism of OMV‐induced MHC I upregulation through the TLR–NF‐κB–NLRC5 pathway. Created in BioRender. Zhang, F. (2026) https://BioRender.com/97sw6s6 . Data are mean ± SD (n = 3). Statistical significance was determined using Student's t‐test or One‐way ANOVA. **** p < 0.0001.
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OMVs upregulate tumor MHC I expression via the TLR4–NF‐κB–NLRC5 axis. (A) Relative mRNA expression of H‐2K and H‐2D in B16 cells after 24 h treatment with different OMV concentrations. (B) Representative plots for flow cytometry analysis of MHC‐I⁺ B16 tumor cell. (C) Proportions of MHC I + B16 cells after indicated treatments. (D) Volcano plot of differentially expressed genes in OMV versus control groups (red: significantly upregulated ≥2‐fold; blue: significantly downregulated ≥2‐fold). (E) GO enrichment of upregulated genes. (F) KEGG pathway enrichment of genes associated with innate and adaptive immune responses. (G‐H) Heat maps of MHC I–related genes detected by RNA‐seq (G) and qPCR (H). (I) Western blot analysis of TLR4 (≈100 kDa), <t>p‐p65</t> (≈70 kDa), NLRC5 (≈225 kDa), and β‐actin (≈48 kDa) in tumor cells. (J) Proportions of MHC I + tumor cells after indicated treatments. (K) Proposed mechanism of OMV‐induced MHC I upregulation through the TLR–NF‐κB–NLRC5 pathway. Created in BioRender. Zhang, F. (2026) https://BioRender.com/97sw6s6 . Data are mean ± SD (n = 3). Statistical significance was determined using Student's t‐test or One‐way ANOVA. **** p < 0.0001.
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OMVs upregulate tumor MHC I expression via the TLR4–NF‐κB–NLRC5 axis. (A) Relative mRNA expression of H‐2K and H‐2D in B16 cells after 24 h treatment with different OMV concentrations. (B) Representative plots for flow cytometry analysis of MHC‐I⁺ B16 tumor cell. (C) Proportions of MHC I + B16 cells after indicated treatments. (D) Volcano plot of differentially expressed genes in OMV versus control groups (red: significantly upregulated ≥2‐fold; blue: significantly downregulated ≥2‐fold). (E) GO enrichment of upregulated genes. (F) KEGG pathway enrichment of genes associated with innate and adaptive immune responses. (G‐H) Heat maps of MHC I–related genes detected by RNA‐seq (G) and qPCR (H). (I) Western blot analysis of TLR4 (≈100 kDa), <t>p‐p65</t> (≈70 kDa), NLRC5 (≈225 kDa), and β‐actin (≈48 kDa) in tumor cells. (J) Proportions of MHC I + tumor cells after indicated treatments. (K) Proposed mechanism of OMV‐induced MHC I upregulation through the TLR–NF‐κB–NLRC5 pathway. Created in BioRender. Zhang, F. (2026) https://BioRender.com/97sw6s6 . Data are mean ± SD (n = 3). Statistical significance was determined using Student's t‐test or One‐way ANOVA. **** p < 0.0001.
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p p65  (Santa Cruz Biotechnology)
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OMVs upregulate tumor MHC I expression via the TLR4–NF‐κB–NLRC5 axis. (A) Relative mRNA expression of H‐2K and H‐2D in B16 cells after 24 h treatment with different OMV concentrations. (B) Representative plots for flow cytometry analysis of MHC‐I⁺ B16 tumor cell. (C) Proportions of MHC I + B16 cells after indicated treatments. (D) Volcano plot of differentially expressed genes in OMV versus control groups (red: significantly upregulated ≥2‐fold; blue: significantly downregulated ≥2‐fold). (E) GO enrichment of upregulated genes. (F) KEGG pathway enrichment of genes associated with innate and adaptive immune responses. (G‐H) Heat maps of MHC I–related genes detected by RNA‐seq (G) and qPCR (H). (I) Western blot analysis of TLR4 (≈100 kDa), <t>p‐p65</t> (≈70 kDa), NLRC5 (≈225 kDa), and β‐actin (≈48 kDa) in tumor cells. (J) Proportions of MHC I + tumor cells after indicated treatments. (K) Proposed mechanism of OMV‐induced MHC I upregulation through the TLR–NF‐κB–NLRC5 pathway. Created in BioRender. Zhang, F. (2026) https://BioRender.com/97sw6s6 . Data are mean ± SD (n = 3). Statistical significance was determined using Student's t‐test or One‐way ANOVA. **** p < 0.0001.
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Image Search Results


Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet:

Article Snippet: Anti-p-NF-κB p50(ser337) mouse antibody , Santa Cruz Biotechnology , sc-271908; RRID: AB_10612088.

Techniques: Cell-Signaling, Virus, Tissue, Microarray, Recombinant, cDNA Synthesis, Enzyme-linked Immunosorbent Assay, Software, Biomarker Discovery, In Vivo Imaging

OMVs upregulate tumor MHC I expression via the TLR4–NF‐κB–NLRC5 axis. (A) Relative mRNA expression of H‐2K and H‐2D in B16 cells after 24 h treatment with different OMV concentrations. (B) Representative plots for flow cytometry analysis of MHC‐I⁺ B16 tumor cell. (C) Proportions of MHC I + B16 cells after indicated treatments. (D) Volcano plot of differentially expressed genes in OMV versus control groups (red: significantly upregulated ≥2‐fold; blue: significantly downregulated ≥2‐fold). (E) GO enrichment of upregulated genes. (F) KEGG pathway enrichment of genes associated with innate and adaptive immune responses. (G‐H) Heat maps of MHC I–related genes detected by RNA‐seq (G) and qPCR (H). (I) Western blot analysis of TLR4 (≈100 kDa), p‐p65 (≈70 kDa), NLRC5 (≈225 kDa), and β‐actin (≈48 kDa) in tumor cells. (J) Proportions of MHC I + tumor cells after indicated treatments. (K) Proposed mechanism of OMV‐induced MHC I upregulation through the TLR–NF‐κB–NLRC5 pathway. Created in BioRender. Zhang, F. (2026) https://BioRender.com/97sw6s6 . Data are mean ± SD (n = 3). Statistical significance was determined using Student's t‐test or One‐way ANOVA. **** p < 0.0001.

Journal: Advanced Science

Article Title: Intratumoral Fusogenic Outer Membrane Vesicles Enhance Antitumor Immunity Through Tumor MHC‐I Upregulation and Tumor Bacterization

doi: 10.1002/advs.78279

Figure Lengend Snippet: OMVs upregulate tumor MHC I expression via the TLR4–NF‐κB–NLRC5 axis. (A) Relative mRNA expression of H‐2K and H‐2D in B16 cells after 24 h treatment with different OMV concentrations. (B) Representative plots for flow cytometry analysis of MHC‐I⁺ B16 tumor cell. (C) Proportions of MHC I + B16 cells after indicated treatments. (D) Volcano plot of differentially expressed genes in OMV versus control groups (red: significantly upregulated ≥2‐fold; blue: significantly downregulated ≥2‐fold). (E) GO enrichment of upregulated genes. (F) KEGG pathway enrichment of genes associated with innate and adaptive immune responses. (G‐H) Heat maps of MHC I–related genes detected by RNA‐seq (G) and qPCR (H). (I) Western blot analysis of TLR4 (≈100 kDa), p‐p65 (≈70 kDa), NLRC5 (≈225 kDa), and β‐actin (≈48 kDa) in tumor cells. (J) Proportions of MHC I + tumor cells after indicated treatments. (K) Proposed mechanism of OMV‐induced MHC I upregulation through the TLR–NF‐κB–NLRC5 pathway. Created in BioRender. Zhang, F. (2026) https://BioRender.com/97sw6s6 . Data are mean ± SD (n = 3). Statistical significance was determined using Student's t‐test or One‐way ANOVA. **** p < 0.0001.

Article Snippet: AF647‐conjugated anti‐Escherichia coli LPS antibody (Cat. No. bs‐8000R‐AF647), anti‐NFκB p65 (p‐S536) antibody (Cat. No. bs‐0982R), and anti‐Hexokinase 2 antibody (Cat. No. bs‐9455R) were obtained from Bioss (China).

Techniques: Expressing, Flow Cytometry, Analysis, Control, RNA Sequencing, Western Blot