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factor κ b kinase subunit β ikkβ  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc factor κ b kinase subunit β ikkβ
    Factor κ B Kinase Subunit β Ikkβ, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 161 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/factor+%CE%BA+b+kinase+subunit+%CE%B2+ikk%CE%B2/IKKbeta+(L570)+Antibody/pm36345807-52-31-41
    Average 95 stars, based on 161 article reviews
    factor κ b kinase subunit β ikkβ - by Bioz Stars, 2026-10
    95/100 stars

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    other:

    Article Title: Over expression of ubiquitin-conjugating enzyme E2O in bone marrow mesenchymal stromal cells partially attenuates acute myeloid leukaemia progression.
    Article Snippet: © 2022 British Society for Haematology and John Wiley & Sons Ltd. Chen Tian, Zehui Chen and Lina Wang cofirst authors.. Department of Haematology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China Department of Haematology, Hotan District People's Hospital, Hotan, China State Key Laboratory of Experimental Haematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Haematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China Department of Haematopathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA



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    Figure 3. Effects of PD1 on inflammatory gene expression in Con A‑induced hepatitis. Livers were removed and RNA was extracted using TRIzol. Quantification of mRNA expression levels of (A) TNF‑α, (B) NF‑κB p65, (C) IL‑6, (D) <t>IKKβ,</t> (E) HMGB1, (F) CX3CL1, (G) IFN‑γ, (H) IκBα, (I) CX3CR1, (J) caspase‑1 and (K) IL‑1β in Con A‑induced liver tissue. The bars indicate the mean ± standard error of the mean (n=10). #P<0.05, ##P<0.01 vs. control group; *P<0.05, **P<0.01 vs. Con A (30 mg/kg). PD1, protectin D1; Con A, concanavalin A; HPD1, 20 µg/kg PD1 pretreatment group; LPD1, 10 µg/kg PD1 pretreatment group; TNF‑α, tumor necrosis factor‑α; NF‑κB p65, nuclear factor κ‑light‑chain‑enhancer of activated B cells p65 subunit; IL, interleukin; IKKβ, inhibitor of nuclear factor κ‑B kinase subunit β; HMGB1, high mobility group B1; CX3CL1, chemokine (C‑X3‑C motif) ligand 1; IFN‑γ, interferon‑γ; IκBα, nuclear factor of κ light polypeptide gene enhancer in B‑cells inhibitor, α; CX3CR1, chemokine (C‑X3‑C motif) receptor 1; mRNA, messenger RNA.
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    Figure 3. Effects of PD1 on inflammatory gene expression in Con A‑induced hepatitis. Livers were removed and RNA was extracted using TRIzol. Quantification of mRNA expression levels of (A) TNF‑α, (B) NF‑κB p65, (C) IL‑6, (D) IKKβ, (E) HMGB1, (F) CX3CL1, (G) IFN‑γ, (H) IκBα, (I) CX3CR1, (J) caspase‑1 and (K) IL‑1β in Con A‑induced liver tissue. The bars indicate the mean ± standard error of the mean (n=10). #P<0.05, ##P<0.01 vs. control group; *P<0.05, **P<0.01 vs. Con A (30 mg/kg). PD1, protectin D1; Con A, concanavalin A; HPD1, 20 µg/kg PD1 pretreatment group; LPD1, 10 µg/kg PD1 pretreatment group; TNF‑α, tumor necrosis factor‑α; NF‑κB p65, nuclear factor κ‑light‑chain‑enhancer of activated B cells p65 subunit; IL, interleukin; IKKβ, inhibitor of nuclear factor κ‑B kinase subunit β; HMGB1, high mobility group B1; CX3CL1, chemokine (C‑X3‑C motif) ligand 1; IFN‑γ, interferon‑γ; IκBα, nuclear factor of κ light polypeptide gene enhancer in B‑cells inhibitor, α; CX3CR1, chemokine (C‑X3‑C motif) receptor 1; mRNA, messenger RNA.

    Journal: Molecular medicine reports

    Article Title: Protectin D1 reduces concanavalin A-induced liver injury by inhibiting NF-κB-mediated CX3CL1/CX3CR1 axis and NLR family, pyrin domain containing 3 inflammasome activation.

    doi: 10.3892/mmr.2016.4980

    Figure Lengend Snippet: Figure 3. Effects of PD1 on inflammatory gene expression in Con A‑induced hepatitis. Livers were removed and RNA was extracted using TRIzol. Quantification of mRNA expression levels of (A) TNF‑α, (B) NF‑κB p65, (C) IL‑6, (D) IKKβ, (E) HMGB1, (F) CX3CL1, (G) IFN‑γ, (H) IκBα, (I) CX3CR1, (J) caspase‑1 and (K) IL‑1β in Con A‑induced liver tissue. The bars indicate the mean ± standard error of the mean (n=10). #P<0.05, ##P<0.01 vs. control group; *P<0.05, **P<0.01 vs. Con A (30 mg/kg). PD1, protectin D1; Con A, concanavalin A; HPD1, 20 µg/kg PD1 pretreatment group; LPD1, 10 µg/kg PD1 pretreatment group; TNF‑α, tumor necrosis factor‑α; NF‑κB p65, nuclear factor κ‑light‑chain‑enhancer of activated B cells p65 subunit; IL, interleukin; IKKβ, inhibitor of nuclear factor κ‑B kinase subunit β; HMGB1, high mobility group B1; CX3CL1, chemokine (C‑X3‑C motif) ligand 1; IFN‑γ, interferon‑γ; IκBα, nuclear factor of κ light polypeptide gene enhancer in B‑cells inhibitor, α; CX3CR1, chemokine (C‑X3‑C motif) receptor 1; mRNA, messenger RNA.

    Article Snippet: Immunoblotting was conducted using the following primary polyclonal rabbitantibodies: Rabbit anti-GAPDH (dilution, 1:1,000; cat. no. 5174), NF-κB (dilution, 1:1,000; cat. no. 8242), phosphorylated-NF-κB (dilution, 1:1,000; cat. no. 4887), TLR4 (dilution, 1:1,000; cat. no. 14358), nuclear factor of κ light polypeptide gene enhancer in B-cells inhibitor, α (IκBα) (dilution, 1:1,000; cat. no. 4814), inhibitor of nuclear factor κ-B kinase subunit beta (IKKβ) (dilution, 1:1,000; cat. no. 8943), myeloid differentiation primary response gene 88 (MyD88) (dilution, 1:2,000; cat. no. 4283), NLRP3 (dilution, 1:1,000; cat. no. 13158), IL-1β (dilution, 1:1,000; cat. no. 12426), caspase-1 (dilution, 1:1,000; cat. no. 3866) (Cell Signaling Technology, Inc., Danvers, MA, USA), CX3CR1 (cat. no. ab8021) and CX3CL1 (dilution, 1:1,000; cat. no. ab25088) (Abcam, Cambridge, MA, USA).

    Techniques: Gene Expression, Expressing, Control

    Figure 5. PD1 inhibits NF‑κB‑stimulated CX3CL1/CX3CR1‑dependent inflammatory pathway activation and generation of the inflammasome. Western blot analysis for NF‑κB and CX3CL1/CX3CR1 activity was used to demonstrate the effect of PD1 on Con A‑induced liver injury and the underlying mechanisms. (A and B) Bands and quantification of TLR4, p‑NF‑κB, IκBα, IKKβ and MyD88 protein. (C and D) Bands and quantification of CX3CL1 and CX3CR1 protein. (E) Bands and quantification of NLRP3 and caspase‑1 protein. The bars indicate means ± standard error of the mean (n=10). ##P<0.01 vs. control group; *P<0.05 vs. Con A (30 mg/kg). PD1, protectin D1; Con A, concanavalin A; HPD1, 20 µg/kg PD1 pretreatment group; LPD1, 10 µg/kg PD1 pretreatment group; TLR4, Toll‑like receptor 4; NF‑κB, nuclear factor κ‑light‑chain‑enhancer of activated B cells; p‑NF‑κB, phosphorylated NF‑κB; IκBα, nuclear factor of κ light polypeptide gene enhancer in B‑cells inhibitor, α; IKKβ, inhibitor of nuclear factor κ‑B kinase subunit β; MyD88, myeloid differentiation primary response gene 88; CX3CL1, chemokine (C‑X3‑C motif) ligand 1; CX3CR1, chemokine (C‑X3‑C motif) receptor 1; NLRP3, NLR family, pyrin domain containing 3; IL‑1β, interleukin‑1β.

    Journal: Molecular medicine reports

    Article Title: Protectin D1 reduces concanavalin A-induced liver injury by inhibiting NF-κB-mediated CX3CL1/CX3CR1 axis and NLR family, pyrin domain containing 3 inflammasome activation.

    doi: 10.3892/mmr.2016.4980

    Figure Lengend Snippet: Figure 5. PD1 inhibits NF‑κB‑stimulated CX3CL1/CX3CR1‑dependent inflammatory pathway activation and generation of the inflammasome. Western blot analysis for NF‑κB and CX3CL1/CX3CR1 activity was used to demonstrate the effect of PD1 on Con A‑induced liver injury and the underlying mechanisms. (A and B) Bands and quantification of TLR4, p‑NF‑κB, IκBα, IKKβ and MyD88 protein. (C and D) Bands and quantification of CX3CL1 and CX3CR1 protein. (E) Bands and quantification of NLRP3 and caspase‑1 protein. The bars indicate means ± standard error of the mean (n=10). ##P<0.01 vs. control group; *P<0.05 vs. Con A (30 mg/kg). PD1, protectin D1; Con A, concanavalin A; HPD1, 20 µg/kg PD1 pretreatment group; LPD1, 10 µg/kg PD1 pretreatment group; TLR4, Toll‑like receptor 4; NF‑κB, nuclear factor κ‑light‑chain‑enhancer of activated B cells; p‑NF‑κB, phosphorylated NF‑κB; IκBα, nuclear factor of κ light polypeptide gene enhancer in B‑cells inhibitor, α; IKKβ, inhibitor of nuclear factor κ‑B kinase subunit β; MyD88, myeloid differentiation primary response gene 88; CX3CL1, chemokine (C‑X3‑C motif) ligand 1; CX3CR1, chemokine (C‑X3‑C motif) receptor 1; NLRP3, NLR family, pyrin domain containing 3; IL‑1β, interleukin‑1β.

    Article Snippet: Immunoblotting was conducted using the following primary polyclonal rabbitantibodies: Rabbit anti-GAPDH (dilution, 1:1,000; cat. no. 5174), NF-κB (dilution, 1:1,000; cat. no. 8242), phosphorylated-NF-κB (dilution, 1:1,000; cat. no. 4887), TLR4 (dilution, 1:1,000; cat. no. 14358), nuclear factor of κ light polypeptide gene enhancer in B-cells inhibitor, α (IκBα) (dilution, 1:1,000; cat. no. 4814), inhibitor of nuclear factor κ-B kinase subunit beta (IKKβ) (dilution, 1:1,000; cat. no. 8943), myeloid differentiation primary response gene 88 (MyD88) (dilution, 1:2,000; cat. no. 4283), NLRP3 (dilution, 1:1,000; cat. no. 13158), IL-1β (dilution, 1:1,000; cat. no. 12426), caspase-1 (dilution, 1:1,000; cat. no. 3866) (Cell Signaling Technology, Inc., Danvers, MA, USA), CX3CR1 (cat. no. ab8021) and CX3CL1 (dilution, 1:1,000; cat. no. ab25088) (Abcam, Cambridge, MA, USA).

    Techniques: Activation Assay, Western Blot, Activity Assay, Control