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anti p nf κb p50  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology anti p nf κb p50

    Anti P Nf κb P50, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 191 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nf+%CE%BAb+p50/p-NF%CE%BAB+p50+Antibody/pmc13657245-69-0-5
    Average 93 stars, based on 191 article reviews
    anti p nf κb p50 - by Bioz Stars, 2026-10
    93/100 stars

    Images

    1) Product Images from "M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy"

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

    Journal: iScience

    doi: 10.1016/j.isci.2026.117695


    Figure Legend Snippet:

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

    Related Articles

    Blocking Assay:

    Article Title: Anti‐Cancer Effect of Sulforaphane in Human Pancreatic Cancer Cells Mia PaCa ‐2
    Article Snippet: Then, it was transferred to 0.45 μm Immobilon‐P transfer membranes (Merk Millipore, Darmstadt, Germany). .. After transfer, it was blocked in a 2.5% BSA blocking buffer for 1 h. After blocking, primary antibodies such as anti‐glycogen synthase kinase‐3 beta (GSK‐3β; #5558, 1:1000, Cell Signaling Technology, Beverly, MA, USA), phosphorylated (p‐)GSK‐3β (Ser9; #12456, 1:1000, Cell Signaling), phosphorylated (p‐)NF‐κB p65 (#3033, 1:1000, Cell Signaling), NF‐κB p65 (#8242, 1:1000, Cell Signaling), NF‐κB p50 (E‐10; sc‐8414, 1:200, Santa Cruz Biotechnology, CA, USA), B‐cell lymphoma 2 (BCL‐2; sc‐130 307, 1:200, Santa Cruz), glyceraldehyde 3‐phosphate dehydrogenase (GAPDH; sc‐47 724, 1:200, Santa Cruz), BCL‐2 associated X (BAX; K001593, 1:500, Solarbio Life Sciences, Beijing, China), caspase‐3 (sc‐271 028, 1:100, Santa Cruz), poly‐adenosine diphosphate ribose polymerase (PARP; #9542, 1:1000, Cell Signaling), β‐catenin (#9562, 1:1000, Cell Signaling), cMyc (K002749; 1:500, Solarbio Life Sciences), lamin A/C (#4777, 1:2000, Cell Signaling), and β‐actin (K200058M, 1:5000, Solarbio Life Sciences) were treated and stored overnight at 4°C. .. After washing four times for 10 min each with Tris‐buffered saline containing 0.1% Tween‐20 (TBST; pH 7.6), secondary antibodies, horseradish peroxidase (HRP)‐conjugated anti‐rabbit immunoglobulin gamma (IgG; #7074, 1:2000, Cell Signaling) or HRP‐conjugated anti‐mouse IgG (#7076, 1:2000, Cell Signaling), were treated and cultured for 1 h and 30 min, respectively.

    Membrane:

    Article Title: An Adhesive Peptide Derived from Mussel Protein Alleviates LL37-Induced Rosacea Through Anti-Inflammatory and Anti-Angiogenic Mechanisms
    Article Snippet: .. Subsequently, the membrane was incubated overnight at 4 ◦C with primary antibodies against TLR2, KLK5, MMP9, NF-κB (p65), p-NF-κB (p-p65), NF-κB (p50), p-NF-κB (p-p50), IκB-α, p-IκB-α, AKT, p-AKT, ERK1/2, p-ERK1/2, JNK, p-JNK, Involucrin, Claudin-4, Claudin-1, Filaggrin, Occludin, VEGF-A, transforming growth factor beta (TGF-β), PECAM (CD31), and β-actin (Santa Cruz, Dallas, Texas, USA). .. After washing, the membranes were incubated with secondary antibodies for 2 h at room temperature and then treated with the ClarityTM Western ECL substrate (BIO-RAD, Hercules, CA, USA) for 30 s. Images were obtained using the Amersham Imager 680 system (GE Healthcare Life Sciences, Chicago, IL, USA).

    Incubation:

    Article Title: An Adhesive Peptide Derived from Mussel Protein Alleviates LL37-Induced Rosacea Through Anti-Inflammatory and Anti-Angiogenic Mechanisms
    Article Snippet: .. Subsequently, the membrane was incubated overnight at 4 ◦C with primary antibodies against TLR2, KLK5, MMP9, NF-κB (p65), p-NF-κB (p-p65), NF-κB (p50), p-NF-κB (p-p50), IκB-α, p-IκB-α, AKT, p-AKT, ERK1/2, p-ERK1/2, JNK, p-JNK, Involucrin, Claudin-4, Claudin-1, Filaggrin, Occludin, VEGF-A, transforming growth factor beta (TGF-β), PECAM (CD31), and β-actin (Santa Cruz, Dallas, Texas, USA). .. After washing, the membranes were incubated with secondary antibodies for 2 h at room temperature and then treated with the ClarityTM Western ECL substrate (BIO-RAD, Hercules, CA, USA) for 30 s. Images were obtained using the Amersham Imager 680 system (GE Healthcare Life Sciences, Chicago, IL, USA).

    other:

    Article Title: Physalin A Suppresses Human Oral Squamous Carcinoma Cell Migration and Invasion Through Inhibiting Grb2/Ras and MMP/uPA Signaling Pathways.
    Article Snippet: The quantified proteins were electrophoretically separated by 8-12% SDSPAGE gel (based on different KDa), and were transferred to polyvinylidene difluoride (PVDF; Cat. No. IPVH00010; Merck Millipore, Burlington, MA, USA) membranes, which were blocked with 5% albumin.

    Article Title: Physalin A Suppresses Human Oral Squamous Carcinoma Cell Migration and Invasion Through Inhibiting Grb2/Ras and MMP/uPA Signaling Pathways
    Article Snippet: The membranes were then stained using primary antibodies [anti- plasminogen activator inhibitor 1 (PAI-1; sc-5297; Santa Cruz Biotechnology), -uPA (sc-59727; Santa Cruz Biotechnology), -E-cad (sc-374067; Santa Cruz Biotechnology), -α-tubulin (α-tub; sc-8035; Santa Cruz Biotechnology), -MMP-1 (sc-21731; Santa Cruz Biotechnology), -MMP-2 (sc-13595; Santa Cruz Biotechnology), -MMP-3 (sc-21732; Santa Cruz Biotechnology), -MMP-9 (sc-393859; Santa Cruz Biotechnology), -tissue inhibitor of metalloprotease (TIMP-1; sc-365905; Santa Cruz Biotechnology), -TIMP-2 (sc-21735; Santa Cruz Biotechnology), -p-IKK (p-IKK; sc-293135; Santa Cruz Biotechnology), -IKK (sc-8032; Santa Cruz Biotechnology), -p-IκB (sc-8404; Santa Cruz Biotechnology), -IκB (sc-1643; Santa Cruz Biotechnology), -NF-κB p65 (sc-8008; Santa Cruz Biotechnology), -NF-κB p50 (sc-8414; Santa Cruz Biotechnology), -p-ERK (9911; Cell Signaling Technology), -ERK (9911; Cell Signaling Technology), -p-c-Jun N-terminal kinase (-p-JNK; 4668; Cell Signaling Technology), -JNK (9252; Cell Signaling Technology), -p-p38 (9211; Cell Signaling Technology), -p38 (9212; Cell Signaling Technology), -p-c-Jun (3270; Cell Signaling Technology), -c-Jun (9165; Cell Signaling Technology), -Grb2 (3972; Cell Signaling Technology), -Ras (3965; Cell Signaling Technology), -p-PI3K (4228; Cell Signaling Technology), -PI3K (4292; Cell Signaling Technology), -p-Akt (9271; Cell Signaling Technology), -Akt (9272; Cell Signaling Technology), -PCNA (sc-56; Santa Cruz Biotechnology) and -β-actin (sc-47778; Santa Cruz Biotechnology)] in 4°C overnight.



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    AA inhibits IκBα phosphorylation and degradation in stimulated COLO 205 and RAW 264.7 cells. COLO 205 (a) and RAW 264.7 (b) cells were pretreated with AA (10 or 30 μM) for 24 h or treated with vehicle (0.1% dimethyl sulfoxide [DMSO]). After pretreatment, COLO 205 cells were stimulated with TNF-α (10 ng/mL), and RAW 264.7 cells with LPS (10 μg/mL) for 30 min. Phosphorylated IκBα and IκBα levels were analyzed by Western blotting. β-actin served as a loading control. AA treatment reduced phosphorylated IκBα and preserved IκBα levels, consistent with suppression of nuclear factor-κB <t>(NF-κB)</t> activation. Blots are representative of a single experiment ( n = 1) and were used for qualitative confirmation only. Full-sized, uncropped Western blot images are provided in Supplemental Figure 2 .
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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

    AA inhibits IκBα phosphorylation and degradation in stimulated COLO 205 and RAW 264.7 cells. COLO 205 (a) and RAW 264.7 (b) cells were pretreated with AA (10 or 30 μM) for 24 h or treated with vehicle (0.1% dimethyl sulfoxide [DMSO]). After pretreatment, COLO 205 cells were stimulated with TNF-α (10 ng/mL), and RAW 264.7 cells with LPS (10 μg/mL) for 30 min. Phosphorylated IκBα and IκBα levels were analyzed by Western blotting. β-actin served as a loading control. AA treatment reduced phosphorylated IκBα and preserved IκBα levels, consistent with suppression of nuclear factor-κB (NF-κB) activation. Blots are representative of a single experiment ( n = 1) and were used for qualitative confirmation only. Full-sized, uncropped Western blot images are provided in Supplemental Figure 2 .

    Journal: International Journal of Immunopathology and Pharmacology

    Article Title: Asiatic acid inhibits NF-κB signaling and ameliorates experimental acute and chronic colitis in mice

    doi: 10.1177/03946320251398285

    Figure Lengend Snippet: AA inhibits IκBα phosphorylation and degradation in stimulated COLO 205 and RAW 264.7 cells. COLO 205 (a) and RAW 264.7 (b) cells were pretreated with AA (10 or 30 μM) for 24 h or treated with vehicle (0.1% dimethyl sulfoxide [DMSO]). After pretreatment, COLO 205 cells were stimulated with TNF-α (10 ng/mL), and RAW 264.7 cells with LPS (10 μg/mL) for 30 min. Phosphorylated IκBα and IκBα levels were analyzed by Western blotting. β-actin served as a loading control. AA treatment reduced phosphorylated IκBα and preserved IκBα levels, consistent with suppression of nuclear factor-κB (NF-κB) activation. Blots are representative of a single experiment ( n = 1) and were used for qualitative confirmation only. Full-sized, uncropped Western blot images are provided in Supplemental Figure 2 .

    Article Snippet: To confirm the specificity of DNA-protein interactions, a supershift assay was performed using anti-NF-κB p50 antibodies (Santa Cruz Biotechnology, Dallas, TX, USA).

    Techniques: Phospho-proteomics, Western Blot, Control, Activation Assay

    AA suppresses NF-κB DNA-binding activity in TNF-α-stimulated COLO 205 cells. COLO 205 cells were treated with AA (10 or 30 μM) for 24 h and then stimulated with TNF-α (10 ng/mL) for 30 min. Nuclear extracts were analyzed by electrophoretic mobility shift assay (EMSA) using a biotin-labeled NF-κB consensus probe. AA pretreatment led to a dose-dependent reduction in NF-κB DNA-binding activity. Results shown are representative of n = 2 independent experiments.

    Journal: International Journal of Immunopathology and Pharmacology

    Article Title: Asiatic acid inhibits NF-κB signaling and ameliorates experimental acute and chronic colitis in mice

    doi: 10.1177/03946320251398285

    Figure Lengend Snippet: AA suppresses NF-κB DNA-binding activity in TNF-α-stimulated COLO 205 cells. COLO 205 cells were treated with AA (10 or 30 μM) for 24 h and then stimulated with TNF-α (10 ng/mL) for 30 min. Nuclear extracts were analyzed by electrophoretic mobility shift assay (EMSA) using a biotin-labeled NF-κB consensus probe. AA pretreatment led to a dose-dependent reduction in NF-κB DNA-binding activity. Results shown are representative of n = 2 independent experiments.

    Article Snippet: To confirm the specificity of DNA-protein interactions, a supershift assay was performed using anti-NF-κB p50 antibodies (Santa Cruz Biotechnology, Dallas, TX, USA).

    Techniques: Binding Assay, Activity Assay, Electrophoretic Mobility Shift Assay, Labeling

    NF-κB p65 immunohistochemistry (IHC) in DSS-induced acute colitis and IL-10⁻/⁻ chronic colitis. (a) Representative IHC images of colon sections from the DSS model (×400 magnification; scale bar = 50 μm). AA-treated mice showed visibly reduced nuclear p65 staining compared with the vehicle group (antibody diluted 1:400). (b) Immunoreactivity score (IRS) for nuclear NF-κB p65 in the DSS model. AA significantly lowered nuclear p65 immunoreactivity compared with the vehicle group. Data are shown as mean ± SD. (c) Representative IHC images from the IL-10⁻/⁻ model (×400 magnification; scale bar = 50 μm). AA treatment decreased nuclear p65 positivity relative to the vehicle group (antibody diluted 1:400). (d) IRS for nuclear NF-κB p65 in the IL-10⁻/⁻ model. AA significantly decreased the immunoreactivity compared to the vehicle group. Data are shown as mean ± SD. DSS and IL-10⁻/⁻: Control, Vehicle, AA ( n = 4/group). Significance: * p < 0.05; ** p < 0.01 (vs vehicle).

    Journal: International Journal of Immunopathology and Pharmacology

    Article Title: Asiatic acid inhibits NF-κB signaling and ameliorates experimental acute and chronic colitis in mice

    doi: 10.1177/03946320251398285

    Figure Lengend Snippet: NF-κB p65 immunohistochemistry (IHC) in DSS-induced acute colitis and IL-10⁻/⁻ chronic colitis. (a) Representative IHC images of colon sections from the DSS model (×400 magnification; scale bar = 50 μm). AA-treated mice showed visibly reduced nuclear p65 staining compared with the vehicle group (antibody diluted 1:400). (b) Immunoreactivity score (IRS) for nuclear NF-κB p65 in the DSS model. AA significantly lowered nuclear p65 immunoreactivity compared with the vehicle group. Data are shown as mean ± SD. (c) Representative IHC images from the IL-10⁻/⁻ model (×400 magnification; scale bar = 50 μm). AA treatment decreased nuclear p65 positivity relative to the vehicle group (antibody diluted 1:400). (d) IRS for nuclear NF-κB p65 in the IL-10⁻/⁻ model. AA significantly decreased the immunoreactivity compared to the vehicle group. Data are shown as mean ± SD. DSS and IL-10⁻/⁻: Control, Vehicle, AA ( n = 4/group). Significance: * p < 0.05; ** p < 0.01 (vs vehicle).

    Article Snippet: To confirm the specificity of DNA-protein interactions, a supershift assay was performed using anti-NF-κB p50 antibodies (Santa Cruz Biotechnology, Dallas, TX, USA).

    Techniques: Immunohistochemistry, Staining, Control