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p p65 nf κb ser536 (Cell Signaling Technology Inc)

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Cell Signaling Technology Inc p p65 nf κb ser536

Sch B <t>inhibits</t> <t>NF-κB</t> signaling pathway expression. mRNA expression levels of (A) IL-6, (B) IL-8 (C) and TNF-α were measured in CCA cells treated with different concentrations of Sch B (0, 40, 80, 160 µmol/l). Statistical analysis was performed using Welch's ANOVA followed by Dunnett's T3 post hoc test. (D) NF-κB expression in CCA cells was evaluated using a double luciferase assay with different concentrations of Sch B (0, 10, 20, 40, 80, 160 µmol/l). (E) Hoechst immunofluorescence staining of <t>p65</t> expression in CCA cells. (F) CCA cell activity was assessed after treatment with Sch B and Bay 11–7082, a targeted NF-κB inhibitor. Statistical analysis was performed using ANOVA and Dunnett's post hoc test. *P<0.05, **P<0.01, ***P<0.001. Sch B, Schisandrin B; CCA, cholangiocarcinoma.

P P65 Nf κb Ser536, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/p+p65+ser536/pmc13051282-7-0-8
Average 86 stars, based on 1 article reviews

p p65 nf κb ser536 - by Bioz Stars, 2026-10

86/100 stars

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1) Product Images from "Schisandrin B suppresses cholangiocarcinoma by targeting the ROS/p38 MAPK/NF-κB axis"

Article Title: Schisandrin B suppresses cholangiocarcinoma by targeting the ROS/p38 MAPK/NF-κB axis

Journal: Oncology Letters

doi: 10.3892/ol.2026.15551

Sch B inhibits NF-κB signaling pathway expression. mRNA expression levels of (A) IL-6, (B) IL-8 (C) and TNF-α were measured in CCA cells treated with different concentrations of Sch B (0, 40, 80, 160 µmol/l). Statistical analysis was performed using Welch's ANOVA followed by Dunnett's T3 post hoc test. (D) NF-κB expression in CCA cells was evaluated using a double luciferase assay with different concentrations of Sch B (0, 10, 20, 40, 80, 160 µmol/l). (E) Hoechst immunofluorescence staining of p65 expression in CCA cells. (F) CCA cell activity was assessed after treatment with Sch B and Bay 11–7082, a targeted NF-κB inhibitor. Statistical analysis was performed using ANOVA and Dunnett's post hoc test. *P<0.05, **P<0.01, ***P<0.001. Sch B, Schisandrin B; CCA, cholangiocarcinoma.

Figure Legend Snippet: Sch B inhibits NF-κB signaling pathway expression. mRNA expression levels of (A) IL-6, (B) IL-8 (C) and TNF-α were measured in CCA cells treated with different concentrations of Sch B (0, 40, 80, 160 µmol/l). Statistical analysis was performed using Welch's ANOVA followed by Dunnett's T3 post hoc test. (D) NF-κB expression in CCA cells was evaluated using a double luciferase assay with different concentrations of Sch B (0, 10, 20, 40, 80, 160 µmol/l). (E) Hoechst immunofluorescence staining of p65 expression in CCA cells. (F) CCA cell activity was assessed after treatment with Sch B and Bay 11–7082, a targeted NF-κB inhibitor. Statistical analysis was performed using ANOVA and Dunnett's post hoc test. *P<0.05, **P<0.01, ***P<0.001. Sch B, Schisandrin B; CCA, cholangiocarcinoma.

Techniques Used: Expressing, Luciferase, Immunofluorescence, Staining, Activity Assay

Incubation:

Article Title:
Article Snippet: .. Primary antibodies IKBα (Cell Signaling Technology, catalog # 9242S,1:1000), p65 (Cell Signaling Technology, catalog # 8242S,1:1000), p-p65-Ser536 (Cell Signaling Technology, catalog # 3033S,1:1000), ERK-1/2 (Cell Signaling Technology, catalog # 4695S,1:1000), pERK1/2- Thr202/Tyr204 (Cell Signaling Technology, catalog # 4370S,1:1000), p38 (Cell Signaling Technology, catalog # 9212S,1:1000), p-p38-Thr180/Tyr182 (Cell Signaling Technology, catalog # 9211S,1:1000), p100/52 (Cell Signaling Technology, catalog # 4882S,1:1000), AKT (Cell Signaling Technology, catalog # 9272S,1:1000), p-AKT-T450 (Cell Signaling Technology, catalog # 9267S,1:1000), c-Fos (Cell Signaling Technology, catalog # 2250S,1:1000), NFATc-1 (Sant Cruz Biotechnology, catalog # sc7294,1:500), CathepsinK (Sant Cruz Biotechnology, catalog # sc48353,1:500), CathepsinL (Sant Cruz Biotechnology, catalog # sc390367,1:500), Lamp2 (Sant Cruz Biotechnology, catalog # sc20004,1:500), TRAF3 (Sant Cruz Biotechnology, catalog # sc6933,1:200), GAPDH(Sant Cruz Biotechnology, catalog # sc365062,1:1000), were incubated overnight. ..

Article Title: Avenanthramide-C Mitigates High-Fat Diet-Accelerated Alzheimer’s Pathologies via NOD1-Driven Neuroinflammation in 5×FAD Mice
Article Snippet: A total of 30–40 μg of protein was separated on 8–10% SDS–polyacrylamide gels and electrotransferred onto PVDF membranes (Millipore, Bedford, MA, USA). .. The blots were incubated for 16 h at 4 °C with primary antibodies (at 1:1000 dilutions) specific for p-GSK3β (Ser9) (#5558, D85E12, Cell Signaling, Danvers, MA, USA), GSK-3β (#5676, D75D3, Cell Signaling), p-Akt (Ser473) (#4060, D9E, Cell Signaling), Akt (#9272, C67E7, Cell Signaling), p-IRS-1 (Tyr612) (#44-816G, polyclonal antibody, Invitrogen, California, CA, USA), IRS-1 (#PA1-1057, polyclonal antibody, Invitrogen), Shank3 (#sc-377088, C-4, Santa Cruz, Dallas, TX, USA), PSD95 (#3450, D27E11, Cell Signaling), GluA1 (#13185, 13185, Cell Signaling), GluN1 (#5704, D65B7, Cell Signaling), GluN2B (#4212, D15B3, Cell Signaling), TNF-α (#11948, D2D4, Cell Signaling), IL-1β (#12507, D3H1Z, Cell Signaling), IL-6 (#12153, D3K2N, Cell Signaling), IL-10 (#12163, D13A11, Cell Signaling), NOD1 (#3545, polyclonal antibody, Cell Signaling), RIP2 (#4142, D10B11, Cell Signaling), p-p65 (Ser536) (#3033, 93H1, Cell Signaling), NF-κB (p65) (#8242, D14E12, Cell Signaling), or β-actin (#ab8227, polyclonal antibody, Abcam, Cambridge, MA, USA). .. The immunoblots were then incubated with specific secondary antibodies (Abcam) for 2 h at RT, and the bands were detected with an enhanced chemiluminescence device (Millipore, Billerica, MA, USA).

Article Title: Ginsenoside Rh2 Suppresses the Fanconi Anemia Pathway by Inhibiting NF-κB-Mediated FANCL Transcription in Bladder Cancer
Article Snippet: .. Membranes were incubated with the following primary antibodies at 1:2000 dilution overnight at 4°C: FANCI (Thermo Fisher Scientific, Cat. A300-212 A), FANCD2 (Thermo Fisher Scientific, Cat. MA1-16570), FANCP/SLX4 (Thermo Fisher Scientific, Cat. PA5-45039), FANCQ/XPF (Thermo Fisher Scientific, Cat. PA5-117118), PCNA (Thermo Fisher Scientific, Cat. 13-3900), FANCA (Thermo Fisher Scientific, Cat. 14657), FANCC (Thermo Fisher Scientific, Cat. H00002176-B01P), FANCM (Thermo Fisher Scientific, Cat. PA5-68191), FANCF (Abcam, USA, Cat. ab105266), FAAP24 (Abcam, Cat. ab122800), FAAP100 (Abcam, Cat. ab224178), FANCL (Abcam, Cat. ab272618), FANCB (Abcam, Cat. ab84536), USP1 (Cell Signaling Technology, USA, Cat. 4933), UAF1/WDR48 (Abcam, Cat. ab97343), GAPDH (Cell Signaling Technology, Cat. 2118), p65 (Cell Signaling Technology, Cat. 8242), p-p65 Ser536 (Cell Signaling Technology, Cat. 3033), β-catenin (Cell Signaling Technology, Cat. 8480), p-β-catenin Ser37 (Cell Signaling Technology, Cat. 9561), Akt (Cell Signaling Technology, Cat. 9272), p-Akt Thr308 (Cell Signaling Technology, Cat. 9275), JNK (Cell Signaling Technology, Cat. 9252), p-JNK Thr183/Tyr185 (Cell Signaling Technology, Cat. 4671), STAT3 (Cell Signaling Technology, Cat. 4904), and p-STAT3 Tyr705 (Cell Signaling Technology, Cat. 9145). .. After washing, membranes were incubated with HRP-conjugated secondary antibodies (anti-rabbit IgG or anti-mouse IgG, depending on host species; Cell Signaling Technology, Cat. 7074 for rabbit, Cat. 7076 for mouse) at 1:5000 dilution for 1 h at room temperature.

Article Title: Xin-Fu-Kang oral liquid improves cardiac function and attenuates miR-223–associated NF-κB/NLRP3 pyroptotic signaling in chronic heart failure
Article Snippet: .. Membranes were blocked (5% nonfat milk or 5% BSA in TBST, 1.5 h, RT) and incubated with primary antibodies overnight (4 °C): NLRP3 (#ab214185, Abcam, United Kingdom); IL-1β (#16806-1-AP, Proteintech, United States); GSDMD (#ab209845, Abcam, United Kingdom); pro-caspase-1 (#ab179515, Abcam, United Kingdom); p65 (#10745-1-AP, Proteintech, United States); P-p65 (Ser536) (#3033, Cell Signaling Technology, United States); GAPDH (#60004-1-Ig, Proteintech, United States). ..

other:

Article Title: Senotherapeutic Potential of Araliadiol in Senescent Human Dermal Fibroblasts: An In Vitro Study Using Three Senescence Models
Article Snippet: p-p65 (Ser536) , Rabbit , Monoclonal (Human, Mouse, Rat) , 1:1000 , CST (#3033).

Article Title: Helianthus Annuus L. ameliorates atherosclerosis-induced myocardial infarction via inhibiting inflammation and oxidative stress
Article Snippet: P-p65 (Ser536) , Rabbit , CST, America, #3033 , 1:1000.

Image Search Results

The mRNA expression of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2 , and Caspase 3 in E.tenella host cells.

Journal: Poultry Science

Article Title: Pathogenic mechanism of Eimeria tenella Et MIC2 promotes Eimeria tenella invasion and inhibits host cell apoptosis through binding to the ITGAV receptor

doi: 10.1016/j.psj.2026.106922

Figure Lengend Snippet: The mRNA expression of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2 , and Caspase 3 in E.tenella host cells.

Article Snippet: p-p65 Rabbit Ab , Bioss , bs-0982R , 1: 1500.

Techniques: Expressing

The protein activity changes of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2, and Caspase 3 in E.tenella host cells.

Journal: Poultry Science

Article Title: Pathogenic mechanism of Eimeria tenella Et MIC2 promotes Eimeria tenella invasion and inhibits host cell apoptosis through binding to the ITGAV receptor

doi: 10.1016/j.psj.2026.106922

Figure Lengend Snippet: The protein activity changes of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2, and Caspase 3 in E.tenella host cells.

Article Snippet: p-p65 Rabbit Ab , Bioss , bs-0982R , 1: 1500.

Techniques: Activity Assay

Journal: Oncology Letters

Article Title: Schisandrin B suppresses cholangiocarcinoma by targeting the ROS/p38 MAPK/NF-κB axis

doi: 10.3892/ol.2026.15551

Figure Lengend Snippet: Sch B inhibits NF-κB signaling pathway expression. mRNA expression levels of (A) IL-6, (B) IL-8 (C) and TNF-α were measured in CCA cells treated with different concentrations of Sch B (0, 40, 80, 160 µmol/l). Statistical analysis was performed using Welch's ANOVA followed by Dunnett's T3 post hoc test. (D) NF-κB expression in CCA cells was evaluated using a double luciferase assay with different concentrations of Sch B (0, 10, 20, 40, 80, 160 µmol/l). (E) Hoechst immunofluorescence staining of p65 expression in CCA cells. (F) CCA cell activity was assessed after treatment with Sch B and Bay 11–7082, a targeted NF-κB inhibitor. Statistical analysis was performed using ANOVA and Dunnett's post hoc test. *P<0.05, **P<0.01, ***P<0.001. Sch B, Schisandrin B; CCA, cholangiocarcinoma.

Article Snippet: p-p65 NF-κB (Ser536) , 3033 , 1:1,000 , Cell Signaling Technology, Inc..

Techniques: Expressing, Luciferase, Immunofluorescence, Staining, Activity Assay

LPS inhibited the expression of NLRP12 and promoted the activation of the NF-κB signalling pathway in PDLSCs. (A) The expression level of NLRP12 in PDLSCs after LPS treatment was detected by immunofluorescence staining (scale bar = 50 μm). The qRT-PCR (B) and WB (C) analysis revealed significantly reduced expression of NLRP12 in PDLSCs after treatment with 10 µg/mL LPS. (D) WB analysis demonstrated that the expression of p-p65 and p-IκBα was significantly elevated relative to GAPDH in PDLSCs treated with 10 µg/mL LPS. Data were presented as mean ± SD ( n = 3). *** P < .001, **** P < .0001.

Journal: International Dental Journal

Article Title: NLRP12 Alleviated Periodontal Destruction via Suppressing Nuclear Factor Kappa-B Signalling Pathway

doi: 10.1016/j.identj.2026.109417

Figure Lengend Snippet: LPS inhibited the expression of NLRP12 and promoted the activation of the NF-κB signalling pathway in PDLSCs. (A) The expression level of NLRP12 in PDLSCs after LPS treatment was detected by immunofluorescence staining (scale bar = 50 μm). The qRT-PCR (B) and WB (C) analysis revealed significantly reduced expression of NLRP12 in PDLSCs after treatment with 10 µg/mL LPS. (D) WB analysis demonstrated that the expression of p-p65 and p-IκBα was significantly elevated relative to GAPDH in PDLSCs treated with 10 µg/mL LPS. Data were presented as mean ± SD ( n = 3). *** P < .001, **** P < .0001.

Article Snippet: After blocking with rapid sealing fluid for 30 minutes, the membranes were incubated with primary antibodies, including COL1 (#12256; CST), RUNX2 (#8486; CST), NLRP12 (#DF14960; Affinity Biosciences), phospho-p65 (p-p65) (#3033; CST), p65 (#8242; CST), p-IκBα (#2859; CST), IκBα (#4814; CST), GAPDH (#60004; Proteintech) overnight at 4°C.

Techniques: Expressing, Activation Assay, Immunofluorescence, Staining, Quantitative RT-PCR

Overexpression of NLRP12 alleviated the inflammatory responses and osteogenic differentiation inhibition of PDLSCs by suppressing the NF-κB pathway. (A) WB results showing the changes of protein expression levels of p-p65, p65, p-IκBα, and IκBα in PDLSCs after NLRP12 overexpression. (B) WB results showing the changes of protein expression levels of p-p65 and p65 in PDLSCs overexpressing NLRP12 after PMA treatment. (C)The qRT-PCR results demonstrating the transcriptional expression levels of IL-6, IL-8 , and IL-10 in PDLSCs overexpressing NLRP12 after PMA treatment. (D)WB results demonstrating alterations in the protein expression levels of COL1 and RUNX2 in PDLSCs overexpressing NLRP12 after PMA treatment. (E) Representative pictures showing ALP staining (scale bar = 500 μm) (F) Representative pictures showing alizarin red staining (scale bar = 500 μm). oeNC: PDLSCs transfected via negative control lentiviral. oeNLRP12: PDLSCs transfected via lentiviral with overexpression- NLRP12 . oeNC + LPS: PDLSCs transfected via negative control lentiviral and subsequently cultured under 10 µg/mL LPS. oeNLRP12 + LPS: PDLSCs transfected via lentiviral with overexpression- NLRP12 and subsequently cultured under 10 µg/mL LPS. Data were presented as mean ± SD ( n = 3). ns, no significant difference, * P < .05, ** P < .01, *** P < .001, **** P < .0001.

Journal: International Dental Journal

Article Title: NLRP12 Alleviated Periodontal Destruction via Suppressing Nuclear Factor Kappa-B Signalling Pathway

doi: 10.1016/j.identj.2026.109417

Figure Lengend Snippet: Overexpression of NLRP12 alleviated the inflammatory responses and osteogenic differentiation inhibition of PDLSCs by suppressing the NF-κB pathway. (A) WB results showing the changes of protein expression levels of p-p65, p65, p-IκBα, and IκBα in PDLSCs after NLRP12 overexpression. (B) WB results showing the changes of protein expression levels of p-p65 and p65 in PDLSCs overexpressing NLRP12 after PMA treatment. (C)The qRT-PCR results demonstrating the transcriptional expression levels of IL-6, IL-8 , and IL-10 in PDLSCs overexpressing NLRP12 after PMA treatment. (D)WB results demonstrating alterations in the protein expression levels of COL1 and RUNX2 in PDLSCs overexpressing NLRP12 after PMA treatment. (E) Representative pictures showing ALP staining (scale bar = 500 μm) (F) Representative pictures showing alizarin red staining (scale bar = 500 μm). oeNC: PDLSCs transfected via negative control lentiviral. oeNLRP12: PDLSCs transfected via lentiviral with overexpression- NLRP12 . oeNC + LPS: PDLSCs transfected via negative control lentiviral and subsequently cultured under 10 µg/mL LPS. oeNLRP12 + LPS: PDLSCs transfected via lentiviral with overexpression- NLRP12 and subsequently cultured under 10 µg/mL LPS. Data were presented as mean ± SD ( n = 3). ns, no significant difference, * P < .05, ** P < .01, *** P < .001, **** P < .0001.

Techniques: Over Expression, Inhibition, Expressing, Quantitative RT-PCR, Staining, Transfection, Negative Control, Cell Culture

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p p65 nf κb ser536 (Cell Signaling Technology Inc)

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1) Product Images from "Schisandrin B suppresses cholangiocarcinoma by targeting the ROS/p38 MAPK/NF-κB axis"

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