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anti p ikk 2697t  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc anti p ikk 2697t
    Anti P Ikk 2697t, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1246 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p+ikk/Phospho-IKKalpha%2Fbeta+(Ser176%2F180)+Rabbit+mAb/pm41866004-71-1-9
    Average 96 stars, based on 1246 article reviews
    anti p ikk 2697t - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    other:

    Article Title: Selective inhibition of long isoforms of phosphodiesterase 4D mitigates liver fibrosis in mouse models
    Article Snippet: Primary antibodies were used at 1:1,000 dilution, including COL1A1 (#84336, Cell signaling); ACTA2 (#A2547, Sigma-Aldrich); COL1A1 (#84336, Cell signaling); p-SMAD2 (#3108, Cell signaling); p-SMAD3 (#ab52903, abcam); SMAD2/3 (#8685, Cell signaling); SMAD4 (#46535, Cell signaling); LAMIN (#13435, Cell signaling); p-ERK (#4370, Cell signaling); ERK (#4696, Cell signaling); p-IKK (#2697, Cell signaling); IKK (#11930, Cell signaling); p-NF-κB p65 S536 (#3033, Cell signaling); NF-κB P65 (#8242, Cell signaling); p-AKT (#4060, Cell signaling); AKT (#4691, Cell signaling); p-FOXO1 S256 (#9461, Cell signaling); p-FOXO3a S253 (#13129, Cell signaling); FOXO1 (#2880, Cell signaling); p18 INK4C (#2896, Cell signaling); p21 Waf1/Cip1 (#2947, Cell signaling); CDK4 (#12790, Cell signaling); CDK6 (#3136, Cell signaling); PARP (#9542, Cell signaling); CASPASE3 (#14220, Cell signaling); Integrin a5 (#ab150361, abcam); p-FAK Y397 (#8556, Cell signaling); p-FAK Y925 (#3284, Cell signaling); FAK (#13009, Cell signaling); FLAG (#F1804, Sigma-Aldrich); a-tubulin (sc-8035, Santa Cruz).

    Article Title: Apelin promotes RANKL-mediated osteoclastogenesis by activating MAPK and NF-κB pathways
    Article Snippet: Antibodies for p-IKK (cat. no. 2697S) were from Cell Signaling Technology, Inc., antibodies for p-IκB (cat. no. sc-8404) were obtained from Santa Cruz Biotechnology, Inc. and antibodies targeting p-p65 (cat. no. AP0124) were obtained from ABclonal Biotech Co., Ltd.

    Article Title: Selective inhibition of long isoforms of phosphodiesterase 4D mitigates liver fibrosis in mouse models
    Article Snippet: COL1A1 (#84336, Cell signaling); ACTA2 (#A2547, Sigma-Aldrich); COL1A1 (#84336, Cell signaling); p-SMAD2 (#3108, Cell signaling); p-SMAD3 (#ab52903, abcam); SMAD2/3 (#8685, Cell signaling); SMAD4 (#46535, Cell signaling); LAMIN (#13435, Cell signaling); p-ERK (#4370, Cell signaling); ERK (#4696, Cell signaling); p-IKK (#2697, Cell signaling); IKK (#11930, Cell signaling); p-NF-κB p65 S536 (#3033, Cell signaling); NF-κB P65 (#8242, Cell signaling); p-AKT (#4060, Cell signaling); AKT (#4691, Cell signaling); p-FOXO1 S256 (#9461, Cell signaling); p-FOXO3a S253 (#13129, Cell signaling); FOXO1 (#2880, Cell signaling); p18 INK4C (#2896, Cell signaling); p21 Waf1/Cip1 (#2947, Cell signaling); CDK4 (#12790, Cell signaling); CDK6 (#3136, Cell signaling); PARP (#9542, Cell signaling); CASPASE3 (#14220, Cell signaling); Integrin a5 (#ab150361, abcam); p-FAK Y397 (#8556, Cell signaling); p-FAK Y925 (#3284, Cell signaling); FAK (#13009, Cell signaling); FLAG (#F1804, Sigma-Aldrich); a-tubulin (sc-8035, Santa Cruz).

    Article Title: Apelin promotes RANKL‑mediated osteoclastogenesis by activating MAPK and NF‑κB pathways.
    Article Snippet: The JnK inhibitor SP600125 was purchased from enzo life Sciences, inc. whereas the p38 inhibitor SB203580 and nF‐κB inhibitor pyrrolidinedithiocarbamate ammonium (PdTc) were obtained from MilliporeSigma. antibodies against iKK (cat. no. GTX52348), iκB (cat. no. GTX110521), p65 (cat. no. GTX102090) and β‐actin (1:10,000; cat. no. GT5512) were purchased from GeneTex international corporation. antibodies for p‐iKK (cat. no. 2697S) were from cell Signaling Technology, inc., antibodies for p‐iκB (cat. no. sc‐8404) were obtained from Santa cruz Biotechnology, inc. and antibodies targeting p‐p65 (cat. no. aP0124) were obtained from aBclonal Biotech co., ltd.

    Western Blot:

    Article Title: PDPN+ cancer‐associated fibroblasts enhance gastric cancer angiogenesis via AKT/NF‐κB activation and the CCL2‐ACKR1 axis
    Article Snippet: .. Western blot antibodies include monoclonal mouse antiβ-actin (1:5000 dilution, Cat# AF7018, Affinity), PI3K (Cat# 4257, CST), P-PI3K (Cat# 4228, CST), AKT (Cat# 4685, CST), P-AKT (Cat# 4060, CST), IKKa (Cat# 11930, CST), IKKb (Cat# 8943, CST), p-IKK (Cat# 2697, CST), pP65 (Cat# 3033, CST), P65 (Cat# 8242, CST), IκBa (Cat# 4814, CST), p-IκBa (Cat# 2859, CST), GAPDH (Cat# 5174, CST), PDPN (Cat# sc-376695, Santa Cruz) at 1:1000 dilution, and secondary antibody-goat anti-Rabbit and Mouse (Cat# M21003, Abmart). .. Other antibodies include CD31 (Cat# ab81289, Abcam), CCL2 neutralizing antibody (Cat# MAB679, R&D), humanCCL2 (Cat# 300-04-5, PeproTech).

    Article Title: PDPN+ cancer‐associated fibroblasts enhance gastric cancer angiogenesis via AKT/NF‐κB activation and the CCL2‐ACKR1 axis
    Article Snippet: .. Western blot antibodies include monoclonal mouse anti‐β‐actin (1:5000 dilution, Cat# AF7018, Affinity), PI3K (Cat# 4257, CST), P‐PI3K (Cat# 4228, CST), AKT (Cat# 4685, CST), P‐AKT (Cat# 4060, CST), IKKa (Cat# 11930, CST), IKKb (Cat# 8943, CST), p‐IKK (Cat# 2697, CST), p‐P65 (Cat# 3033, CST), P65 (Cat# 8242, CST), IκBa (Cat# 4814, CST), p‐IκBa (Cat# 2859, CST), GAPDH (Cat# 5174, CST), PDPN (Cat# sc‐376695, Santa Cruz) at 1:1000 dilution, and secondary antibody‐goat anti‐Rabbit and Mouse (Cat# M21003, Abmart). .. Other antibodies include CD31 (Cat# ab81289, Abcam), CCL2 neutralizing antibody (Cat# MAB679, R&D), human CCL2 (Cat# 300‐04‐5, PeproTech).

    Article Title: Hypoxia-preconditioned cardiomyocyte-derived extracellular vesicles alleviate myocardial ischemic injury by reprogramming macrophage polarization via the Fgl2/NF-κB pathway.
    Article Snippet: Protein detection was performed using an enhanced chemiluminescence (ECL) system, and results were analyzed using image system software (Protein Simple, USA). .. Primary antibodies used for Western blot included Fgl2 (Proteintech, 11827–1-AP), TLR4 (Proteintech, 66350–1-Ig), iNOS (Proteintech, 22226–1-AP), COX2 (Proteintech, 12375–1-AP), p-IKK (CST #2697), IKK (CST #8943), p-IκB (Proteintech, 82349–1-RR), IκB (Proteintech, 10268–1-AP), p-NF-κB (Proteintech, 82335–1-RR), NF-κB (Proteintech, 10745–1-AP), p-MAPK (Proteintech, 28796–1-AP), MAPK (Proteintech, 14064–1-AP), Bax (Proteintech, 50599–2-Ig), Bcl2 (Proteintech, 26593–1-AP), TNF-α (Proteintech, 17590–1-AP), IL-1β (Abcam, 254360), IL-6 (Proteintech, 21865–1-AP), IL-10 (Proteintech, 60269–1- Ig), Arg-1 (Proteintech, 16001–1-AP), APOA1 (Proteintech, 14427–1- AP), β-actin (HUABIO, EM21002), and GAPDH (Proteintech, 60004–1- Ig). .. The phagocytic capacity of RAW264.7 macrophages was assessed using the VybrantTM Phagocytosis Assay Kit (V-6694, Molecular Probes, USA).

    Incubation:

    Article Title: CircFRRS1 drives neuroinflammation through the miR-27a-3p/TLR4 pathway after deep hypothermic circulatory arrest
    Article Snippet: .. After the primary antibody protocol was completed, mMembranes were then washed in TBST and incubated with secondary antibody at room temperature for 1 h. The primary and secondary antibodies used in this experiment were as follows: primary antibodies: TLR4 (1:1,000; GB11519, Servicebio), Myd88 (1:1,000; GB111554 , Servicebio), p-IKK (1:1,000; CST#2697, Cell Signaling Technology), IKK (1:1,000; WL01900, Wanleibio), p-IκB (1:1,000; CST #2859, Cell Signaling Technology), IκB (1:1,000; CST#4812, Cell Signaling Technology), p-P65(1:500; CST#3033, Cell Signaling Technology), P65 (1:1,000; CST#3034, Cell Signaling Technology) and NLRP3 (1:1,000; GB114320 , Servicebio); secondary antibodies: HRP conjugated Goat Anti-Rabbit IgG (H+L) (GB23303, Servicebio). .. Bound proteins were detected using Amersham Imager 800 (Cytiva, Inc.) and quantified by ImageJ software (v1.54). β-Actin was used as an internal control for protein inputs.



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    C28/I2 cells were exposed to H₂O₂ (100 μM, 2 h) followed by treatment with AA-enhanced WJSC-conditioned medium or exosomes. Cell viability, exosome uptake, NF-κB signaling proteins, cartilage-associated markers, and intracellular ROS levels were analyzed. (A) AA-enhanced conditioned medium at concentrations of 1%, 3%, 5%, 7%, and 9% for 24 hours significantly promoted C28/I2 cell proliferation compared to the control group. (B) After 2 hours of oxidative stress with H₂O₂, treatment with AA-enhanced conditioned medium restored cell viability in a dose-dependent manner. (C) Similarly, treatment with increasing concentrations of AA-enhanced WJSCs exosomes after H₂O₂ exposure enhanced cell viability. (D) Fluorescence microscopy confirmed cellular uptake of PKH67-labeled exosomes, with F-actin filaments stained in red (Scale bar = 20 μm). (E) Immunoblot analysis showed decreased expression of inflammation markers <t>(p-IKKα/β,</t> p-NF-κB, IκBα) and OA marker MMP13, with increased COL2A1 at higher concentrations of AA-enhanced conditioned medium (5%, 7%, 9%). (F) Similarly, AA-enhanced WJSCs exosomes (80 μg/mL) modulated inflammatory and OA markers. (G) mRNA expression of ADAMTS14, ADAMTS15, TNF-α, and IL-17A was normalized to β-actin using the 2-∆∆Ct method. (H) ROS generation was assessed by DCFDA staining. Fluorescence microscopy showed reduced ROS levels in cells treated with AA-enhanced exosomes (80 μg/mL) compared to the H₂O₂ group (Scale bar = 40 μm). (I) Quantification confirmed significant reduction in ROS levels, emphasizing the antioxidant effects of AA- conditioned vesicles. Data are presented as mean ± SD (n = 3), * p < 0.05, ** p < 0.01, *** p < 0.001, ****p < 0.0001 vs. untreated control group; # p < 0.05, ## p < 0.01, ### p < 0.001, #### p < 0.0001 vs. H₂O₂ treated group.
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    Image Search Results


    C28/I2 cells were exposed to H₂O₂ (100 μM, 2 h) followed by treatment with AA-enhanced WJSC-conditioned medium or exosomes. Cell viability, exosome uptake, NF-κB signaling proteins, cartilage-associated markers, and intracellular ROS levels were analyzed. (A) AA-enhanced conditioned medium at concentrations of 1%, 3%, 5%, 7%, and 9% for 24 hours significantly promoted C28/I2 cell proliferation compared to the control group. (B) After 2 hours of oxidative stress with H₂O₂, treatment with AA-enhanced conditioned medium restored cell viability in a dose-dependent manner. (C) Similarly, treatment with increasing concentrations of AA-enhanced WJSCs exosomes after H₂O₂ exposure enhanced cell viability. (D) Fluorescence microscopy confirmed cellular uptake of PKH67-labeled exosomes, with F-actin filaments stained in red (Scale bar = 20 μm). (E) Immunoblot analysis showed decreased expression of inflammation markers (p-IKKα/β, p-NF-κB, IκBα) and OA marker MMP13, with increased COL2A1 at higher concentrations of AA-enhanced conditioned medium (5%, 7%, 9%). (F) Similarly, AA-enhanced WJSCs exosomes (80 μg/mL) modulated inflammatory and OA markers. (G) mRNA expression of ADAMTS14, ADAMTS15, TNF-α, and IL-17A was normalized to β-actin using the 2-∆∆Ct method. (H) ROS generation was assessed by DCFDA staining. Fluorescence microscopy showed reduced ROS levels in cells treated with AA-enhanced exosomes (80 μg/mL) compared to the H₂O₂ group (Scale bar = 40 μm). (I) Quantification confirmed significant reduction in ROS levels, emphasizing the antioxidant effects of AA- conditioned vesicles. Data are presented as mean ± SD (n = 3), * p < 0.05, ** p < 0.01, *** p < 0.001, ****p < 0.0001 vs. untreated control group; # p < 0.05, ## p < 0.01, ### p < 0.001, #### p < 0.0001 vs. H₂O₂ treated group.

    Journal: International Journal of Medical Sciences

    Article Title: Artemisia argyi -enhanced Mesenchymal Stem Cell Exosomes Alleviates Inflammation in C28/I2 Chondrocytes by inhibiting NF-κB

    doi: 10.7150/ijms.126119

    Figure Lengend Snippet: C28/I2 cells were exposed to H₂O₂ (100 μM, 2 h) followed by treatment with AA-enhanced WJSC-conditioned medium or exosomes. Cell viability, exosome uptake, NF-κB signaling proteins, cartilage-associated markers, and intracellular ROS levels were analyzed. (A) AA-enhanced conditioned medium at concentrations of 1%, 3%, 5%, 7%, and 9% for 24 hours significantly promoted C28/I2 cell proliferation compared to the control group. (B) After 2 hours of oxidative stress with H₂O₂, treatment with AA-enhanced conditioned medium restored cell viability in a dose-dependent manner. (C) Similarly, treatment with increasing concentrations of AA-enhanced WJSCs exosomes after H₂O₂ exposure enhanced cell viability. (D) Fluorescence microscopy confirmed cellular uptake of PKH67-labeled exosomes, with F-actin filaments stained in red (Scale bar = 20 μm). (E) Immunoblot analysis showed decreased expression of inflammation markers (p-IKKα/β, p-NF-κB, IκBα) and OA marker MMP13, with increased COL2A1 at higher concentrations of AA-enhanced conditioned medium (5%, 7%, 9%). (F) Similarly, AA-enhanced WJSCs exosomes (80 μg/mL) modulated inflammatory and OA markers. (G) mRNA expression of ADAMTS14, ADAMTS15, TNF-α, and IL-17A was normalized to β-actin using the 2-∆∆Ct method. (H) ROS generation was assessed by DCFDA staining. Fluorescence microscopy showed reduced ROS levels in cells treated with AA-enhanced exosomes (80 μg/mL) compared to the H₂O₂ group (Scale bar = 40 μm). (I) Quantification confirmed significant reduction in ROS levels, emphasizing the antioxidant effects of AA- conditioned vesicles. Data are presented as mean ± SD (n = 3), * p < 0.05, ** p < 0.01, *** p < 0.001, ****p < 0.0001 vs. untreated control group; # p < 0.05, ## p < 0.01, ### p < 0.001, #### p < 0.0001 vs. H₂O₂ treated group.

    Article Snippet: The following antibodies were used in the current study: CD9 (#13174; Cell signaling technology, Danvers, MA, USA), CD63(Merck Millipore; Burlington, MA, USA), CD81(sc-166028; Santa Cruz Biotechnology, Dallas, TX, USA), Calnexin (#2679, Cell signaling), β-actin(sc-47778, Santa Cruz), p-IKKα/β (bs-3237R; Bioss Antibodies, Woburn, MA, USA), p-NF-κB p-p65 (#3033, Cell signaling), NF-κB p65(#8242, Cell signaling), p-IκB-α (#2859, Cell signaling), IκB-α (sc-1643, Santa Cruz), COL2A1 (GB11021; Servicebio, Wuhan, Hubei, China), MMP-13 (GTX100665; GeneTex, Irvine, CA, USA), Nanog (#4903, Cell Signaling), KLF4 (#4038, Cell signaling), CXCR4 (60042-1-Ig; Proteintech, San Diego, CA, USA), CXCR7 (bs-4897R, Bioss), CD44 (#3570, Cell signaling), CD90 (sc-53456, Santa Cruz).

    Techniques: Control, Fluorescence, Microscopy, Labeling, Staining, Western Blot, Expressing, Marker

    Verification of AA-enhanced exosomes reducing H₂O₂-induced inflammation in C28/I2 cells and supporting cartilage homeostasis via inhibition of the NF-κB pathway using an NF-κB activator. C28/I2 cells were pretreated with H 2 O 2 for 2 hours and then co-treated with standard WJSCs exosomes or AA-enhanced WJSCs exosomes (80 μg/mL) with NF-κB activator (5μM) for 22 hours. (A) Western blot analysis reveals expression levels of key inflammation-related proteins, including p-IKKα/β, p-NF-κB, and IκBα, as well as OA markers MMP13 and COL2A1. (B) Translocation of p65 was determined using a NF-κB p65 antibody and an Alexa Fluor 488-conjugated anti-rabbit IgG antibody. Nuclei were counterstained with DAPI. Scale bar = 40 μm.

    Journal: International Journal of Medical Sciences

    Article Title: Artemisia argyi -enhanced Mesenchymal Stem Cell Exosomes Alleviates Inflammation in C28/I2 Chondrocytes by inhibiting NF-κB

    doi: 10.7150/ijms.126119

    Figure Lengend Snippet: Verification of AA-enhanced exosomes reducing H₂O₂-induced inflammation in C28/I2 cells and supporting cartilage homeostasis via inhibition of the NF-κB pathway using an NF-κB activator. C28/I2 cells were pretreated with H 2 O 2 for 2 hours and then co-treated with standard WJSCs exosomes or AA-enhanced WJSCs exosomes (80 μg/mL) with NF-κB activator (5μM) for 22 hours. (A) Western blot analysis reveals expression levels of key inflammation-related proteins, including p-IKKα/β, p-NF-κB, and IκBα, as well as OA markers MMP13 and COL2A1. (B) Translocation of p65 was determined using a NF-κB p65 antibody and an Alexa Fluor 488-conjugated anti-rabbit IgG antibody. Nuclei were counterstained with DAPI. Scale bar = 40 μm.

    Article Snippet: The following antibodies were used in the current study: CD9 (#13174; Cell signaling technology, Danvers, MA, USA), CD63(Merck Millipore; Burlington, MA, USA), CD81(sc-166028; Santa Cruz Biotechnology, Dallas, TX, USA), Calnexin (#2679, Cell signaling), β-actin(sc-47778, Santa Cruz), p-IKKα/β (bs-3237R; Bioss Antibodies, Woburn, MA, USA), p-NF-κB p-p65 (#3033, Cell signaling), NF-κB p65(#8242, Cell signaling), p-IκB-α (#2859, Cell signaling), IκB-α (sc-1643, Santa Cruz), COL2A1 (GB11021; Servicebio, Wuhan, Hubei, China), MMP-13 (GTX100665; GeneTex, Irvine, CA, USA), Nanog (#4903, Cell Signaling), KLF4 (#4038, Cell signaling), CXCR4 (60042-1-Ig; Proteintech, San Diego, CA, USA), CXCR7 (bs-4897R, Bioss), CD44 (#3570, Cell signaling), CD90 (sc-53456, Santa Cruz).

    Techniques: Inhibition, Western Blot, Expressing, Translocation Assay