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antinfκb  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc antinfκb
    Antinfκb, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 7404 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antinfκb/product/Cell Signaling Technology Inc
    Average 99 stars, based on 7404 article reviews
    antinfκb - by Bioz Stars, 2026-03
    99/100 stars

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    Cell Signaling Technology Inc antinfκb p65 igg
    FIGURE 1 Schematic diagrams of signal transduction in the canonical Wnt/β-catenin and canonical TNF-α-NFκB signaling pathways. (A) (Left panel) In the absence of a Wnt stimulus, β-catenin is phosphorylated by the destruction complex targeting it for poly-ubiquitination and subsequent proteasome-mediated proteolysis. Low cytoplasmic levels of β-catenin permit repression of LEF/TCF-dependent transcription by Groucho/TLE. (Right panel) Binding of Wnt ligands to the Frizzled/LRP5/6 receptor complex promotes recruitment of Disheveled and Axin, resulting in disassembly of the β-catenin destruction complex. Cytoplasmic accumulation of β-catenin allows for its nuclear translocation, where β-catenin displaces Groucho/TLE from LEF/TCF, enabling transcriptional regulation. (B) Binding of the TNF-α ligand to the TNF receptor recruits, phosphorylates and activates the IKK complex via oligomerisation of a series of adaptor proteins. In turn, the activated IKK complex phosphorylates IκBα, resulting in poly-ubiquitination of IκBα and its rapid proteasomal degradation. The unbound NFκB heterodimer complex, where p50 and <t>p65</t> are members of NFκB family, translocates to the nucleus and regulates transcription of target genes involved inflammation. APC, adenomatous polyposis coli; GSK-3β, glycogen synthase kinase-3β; IκBα, inhibitor of κB-α; IKK, IκB kinase; LEF, lymphoid enhancer-building factor; LRP5/6, lipoprotein receptor-related protein 5/6; NFκB, nuclear factor kappa-light-chain-enhancer of activated B cells; P, phosphorylation; TCF, T-cell factor; TLE, transducin-like enhancer of split; TNF-α, tumor necrosis factor-α; TNFR, tumor necrosis factor receptor.
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    FIGURE 1 Schematic diagrams of signal transduction in the canonical Wnt/β-catenin and canonical TNF-α-NFκB signaling pathways. (A) (Left panel) In the absence of a Wnt stimulus, β-catenin is phosphorylated by the destruction complex targeting it for poly-ubiquitination and subsequent proteasome-mediated proteolysis. Low cytoplasmic levels of β-catenin permit repression of LEF/TCF-dependent transcription by Groucho/TLE. (Right panel) Binding of Wnt ligands to the Frizzled/LRP5/6 receptor complex promotes recruitment of Disheveled and Axin, resulting in disassembly of the β-catenin destruction complex. Cytoplasmic accumulation of β-catenin allows for its nuclear translocation, where β-catenin displaces Groucho/TLE from LEF/TCF, enabling transcriptional regulation. (B) Binding of the TNF-α ligand to the TNF receptor recruits, phosphorylates and activates the IKK complex via oligomerisation of a series of adaptor proteins. In turn, the activated IKK complex phosphorylates IκBα, resulting in poly-ubiquitination of IκBα and its rapid proteasomal degradation. The unbound NFκB heterodimer complex, where p50 and p65 are members of NFκB family, translocates to the nucleus and regulates transcription of target genes involved inflammation. APC, adenomatous polyposis coli; GSK-3β, glycogen synthase kinase-3β; IκBα, inhibitor of κB-α; IKK, IκB kinase; LEF, lymphoid enhancer-building factor; LRP5/6, lipoprotein receptor-related protein 5/6; NFκB, nuclear factor kappa-light-chain-enhancer of activated B cells; P, phosphorylation; TCF, T-cell factor; TLE, transducin-like enhancer of split; TNF-α, tumor necrosis factor-α; TNFR, tumor necrosis factor receptor.

    Journal: Frontiers in cardiovascular medicine

    Article Title: Pro-inflammatory role of Wnt/β-catenin signaling in endothelial dysfunction.

    doi: 10.3389/fcvm.2022.1059124

    Figure Lengend Snippet: FIGURE 1 Schematic diagrams of signal transduction in the canonical Wnt/β-catenin and canonical TNF-α-NFκB signaling pathways. (A) (Left panel) In the absence of a Wnt stimulus, β-catenin is phosphorylated by the destruction complex targeting it for poly-ubiquitination and subsequent proteasome-mediated proteolysis. Low cytoplasmic levels of β-catenin permit repression of LEF/TCF-dependent transcription by Groucho/TLE. (Right panel) Binding of Wnt ligands to the Frizzled/LRP5/6 receptor complex promotes recruitment of Disheveled and Axin, resulting in disassembly of the β-catenin destruction complex. Cytoplasmic accumulation of β-catenin allows for its nuclear translocation, where β-catenin displaces Groucho/TLE from LEF/TCF, enabling transcriptional regulation. (B) Binding of the TNF-α ligand to the TNF receptor recruits, phosphorylates and activates the IKK complex via oligomerisation of a series of adaptor proteins. In turn, the activated IKK complex phosphorylates IκBα, resulting in poly-ubiquitination of IκBα and its rapid proteasomal degradation. The unbound NFκB heterodimer complex, where p50 and p65 are members of NFκB family, translocates to the nucleus and regulates transcription of target genes involved inflammation. APC, adenomatous polyposis coli; GSK-3β, glycogen synthase kinase-3β; IκBα, inhibitor of κB-α; IKK, IκB kinase; LEF, lymphoid enhancer-building factor; LRP5/6, lipoprotein receptor-related protein 5/6; NFκB, nuclear factor kappa-light-chain-enhancer of activated B cells; P, phosphorylation; TCF, T-cell factor; TLE, transducin-like enhancer of split; TNF-α, tumor necrosis factor-α; TNFR, tumor necrosis factor receptor.

    Article Snippet: Primary antibodies included anti-ADAMTS13 IgG (Abcam; ab177940), anti-ICAM-1 IgG (Abcam; ab53013), anti-IκBα IgG (Cell Signaling Technology; 4814), anti-integrin αv IgG (Cell Signaling Technology; 4711), anti-integrin β3 IgG (Cell Signaling Technology; 13166), antiNFκB p65 IgG (Cell Signaling Technology; 8242), anti-VCAM-1 IgG (Abcam; ab134047), and anti-von Willebrand factor IgG (Cell Signaling; 65707S).

    Techniques: Transduction, Protein-Protein interactions, Ubiquitin Proteomics, Binding Assay, Translocation Assay, Phospho-proteomics