Phospho-IKK alpha/ beta (Ser180/Ser181) Antibody - #AF3013

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产品: 磷酸化 IKK alpha/ beta (Ser180/Ser181) 抗体
货号: AF3013
描述: Rabbit polyclonal antibody to Phospho-IKK alpha/ beta (Ser180/Ser181)
应用: WB IHC IF/ICC
文献验证: WB
反应: Human, Mouse, Rat
预测: Pig, Zebrafish, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
蛋白号: O15111 | O14920
RRID: AB_2834452

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产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human, Mouse, Rat
克隆:
Polyclonal
特异性:
Phospho-IKK alpha/ beta (Ser180/Ser181) Antibody detects endogenous levels of IKK alpha/ beta only when phosphorylated at Serine 180/181.
RRID:
AB_2834452
引用格式: Affinity Biosciences Cat# AF3013, RRID:AB_2834452.
偶联:
Unconjugated.
纯化:
The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho-peptide and non-phospho-peptide affinity columns.
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

chuk; CHUK1; Conserved Helix Loop Helix Ubiquitous Kinase; Conserved helix loop ubiquitous kinase; Conserved helix-loop-helix ubiquitous kinase; I Kappa B Kinase 1; I Kappa B Kinase Alpha; I-kappa-B kinase 1; I-kappa-B kinase alpha; IkappaB kinase; IkB kinase alpha subunit; IkBKA; IKK 1; IKK A; IKK a kinase; IKK-A; IKK-alpha; IKK1; IKKA; IKKA_HUMAN; Inhibitor Of Kappa Light Polypeptide Gene Enhancer In B Cells; Inhibitor Of Nuclear Factor Kappa B Kinase Alpha Subunit; Inhibitor of nuclear factor kappa-B kinase subunit alpha; NFKBIKA; Nuclear Factor Kappa B Inhibitor Kinase Alpha; Nuclear factor NF kappa B inhibitor kinase alpha; Nuclear factor NF-kappa-B inhibitor kinase alpha; Nuclear factor NFkappaB inhibitor kinase alpha; Nuclear Factor Of Kappa Light Chain Gene Enhancer In B Cells Inhibitor; TCF-16; TCF16; Transcription factor 16; I kappa B kinase 2; I kappa B kinase beta; I-kappa-B kinase 2; I-kappa-B-kinase beta; IkBKB; IKK beta; IKK-B; IKK-beta; IKK2; IKKB; IKKB_HUMAN; IMD15; Inhibitor of kappa light polypeptide gene enhancer in B cells, kinase beta; Inhibitor of nuclear factor kappa-B kinase subunit beta; NFKBIKB; Nuclear factor NF-kappa-B inhibitor kinase beta;

抗原和靶标

免疫原:

A synthesized peptide derived from human IKK- alpha/ beta around the phosphorylation site of Ser180/181.

基因/基因ID:
CHUK(1147) | IKBKB(3551)
描述:
IKK-beta a kinase of the IKK family. Phosphorylates inhibitors of NF-kappa-B thus leading to the dissociation of the inhibitor/NF-kappa-B complex and ultimately the degradation of the inhibitor. Preferentially found as a heterodimer with IKK-alpha but also as an homodimer.

研究领域

· Cellular Processes > Cell growth and death > Apoptosis.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Ras signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > NF-kappa B signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > FoxO signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > mTOR signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > TNF signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Antifolate resistance.

· Human Diseases > Endocrine and metabolic diseases > Type II diabetes mellitus.

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Infectious diseases: Bacterial > Epithelial cell signaling in Helicobacter pylori infection.

· Human Diseases > Infectious diseases: Bacterial > Shigellosis.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Viral > Hepatitis C.

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Measles.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > MicroRNAs in cancer.

· Human Diseases > Cancers: Specific types > Pancreatic cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Prostate cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Chronic myeloid leukemia.   (View pathway)

· Human Diseases > Cancers: Specific types > Acute myeloid leukemia.   (View pathway)

· Human Diseases > Cancers: Specific types > Small cell lung cancer.   (View pathway)

· Organismal Systems > Immune system > Chemokine signaling pathway.   (View pathway)

· Organismal Systems > Development > Osteoclast differentiation.   (View pathway)

· Organismal Systems > Immune system > Toll-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > RIG-I-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Cytosolic DNA-sensing pathway.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Th1 and Th2 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > Th17 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > T cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > B cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Nervous system > Neurotrophin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Insulin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Adipocytokine signaling pathway.

文献引用

1). Exosome-based bone-targeting drug delivery alleviates impaired osteoblastic bone formation and bone loss in inflammatory bowel diseases. Cell reports. Medicine, 2023 (PubMed: 36603578) [IF=11.7]

Application: WB    Species: Mouse    Sample: BMSCs

Figure 5 TNF-α promoted β-catenin degradation and inhibited osteogenic gene expression (A) Co-immunoprecipitation of BMSCs treated by vehicle or recombinant TNF-α. (B) Immunoblotting of downstream molecules of the Wnt and NF-κB signaling pathways in BMSCs after vehicle or recombinant TNF-α treatment. (C) Luciferase reporter assay. BMSC was transfected with β-catenin expression plasmid with TOPFlash reporter. Firefly luciferase activities were measured. (D) Immunoblotting of β-catenin and the presence of ubiquitin. (E) Cycloheximide chasing assay of β-catenin in BMSCs after being treated by vehicle or recombinant TNF-α for 24 h. (F) Immunoblotting of β-catenin in the cytoplasm and nucleus of BMSCs, which were treated by vehicle or recombinant TNF-α for 24 h. (G and H) Chromatin immunoprecipitation (ChIP) assays on the promoter regions of the Runx2 and Osterix genes were performed in BMSCs treated by vehicle or recombinant TNF-α for 24 h. n = 3. Data are represented as mean ± SD (error bars) from biological replicates. ns, not significant, ∗∗∗∗p < 0.0001, by paired Student’s t test.
2). Arsenic retention in erythrocytes and excessive erythrophagocytosis is related to low selenium status by impaired redox homeostasis. Redox Biology, 2022 (PubMed: 35500533) [IF=10.7]
3). A Novel pH-Responsive Baicalein@Chitosan Hydrogel for the Topical Treatment of Herpes Simplex Virus Type 1 Skin Infections: Therapeutic Potential and Mechanisms. Advanced healthcare materials, 2025 (PubMed: 40109148) [IF=10.0]
4). Hyperphosphorylated tau mediates neuronal death by inducing necroptosis and inflammation in Alzheimer’s disease. Journal of Neuroinflammation, 2022 (PubMed: 35971179) [IF=9.3]

Application: WB    Species: Mouse    Sample: HT22 cells

Fig. 4NF-κB is required for hyperphosphorylated tau-mediated cytokine induction. A HT22 cells were transfected with vector or TauP301S following treatment with DMSO or Nec-1 (30 μM) for 48 h, and the lysates were analyzed by western blotting using indicated antibodies. B Representative confocal images (left) and quantification (right) of p65 in HT22 cells transfected with vector or TauP301S following treatment with DMSO or Nec-1 (30 μM) for 48 h. Scale bars, 10 μm. C mRNA was extracted from HT22 cells transfected with vector or TauP301S following treatment with DMSO or TPCA1 (4 μM) and quantified to determine levels of indicated cytokines by qPCR. D Effect of NF-κB inhibitor on the chemotaxis of pTau-induced cytokines on BV2 cells was analyzed by transwell assays, Scale bars, 100 μm. E, F, I HT22 cells were transfected with vector or TauP301S following treatment with DMSO or TPCA1 (4 μM) or TPCA1 (4 μM) + Nec-1 (30 μM) for 48 h; E cell death was measured measuring LDH levels; F levels of the indicated cytokines were analyzed using qPCR; I lysates were analyzed by western blotting using indicated antibodies. G, J HT22 cells were transfected with vector or TauP301S following treatment with DMSO or QNZ (5 μM) or QNZ (5 μM) + Nec-1 (30 μM) for 48 h. G Cell death was evaluated by measuring LDH levels; J lysates were analyzed by western blotting using indicated antibodies. H mRNA was extracted from HT22 cells transfected with vector or TauP301S following treatment with DMSO or SP600125 (5 μM), PH797804 (5 μM), or C176 (2 μM), followed by quantification to determine levels of the indicated cytokines by qPCR. Data are presented as the mean ± standard error of the mean (SEM) of three experiments, statistical analysis was performed using two-tailed unpaired t test in E, G and one-way ANOVA with Dunnett’s multiple comparisons test in C, F. K NC HT22, RIPK1-KO HT22, RIPK3-KO HT22, and MLKL-KO HT22 cells were transfected with vector or TauP301S, and lysates were analyzed by western blotting using indicated antibodies. L Representative confocal images (left) and quantification (right) of p65 in NC HT22, RIPK1-KO HT22, RIPK3-KO HT22, and MLKL-KO HT22 cells transfected with vector or TauP301S. Scale bars, 10 μm. Data are presented as the mean ± standard error of the mean (SEM) of three experiments, and statistical analysis was performed using two-tailed unpaired t test in B, L
5). The matrix protein of Newcastle disease virus inhibits inflammatory response through IRAK4/TRAF6/TAK1/NF-κB signaling pathway. International Journal of Biological Macromolecules, 2022 (PubMed: 35872314) [IF=7.7]
6). Lactate facilitated mitochondrial fission-derived ROS to promote pulmonary fibrosis via ERK/DRP-1 signaling. Journal of translational medicine, 2024 (PubMed: 38773615) [IF=7.4]

Application: WB    Species: Mouse    Sample:

Fig. 5 Lactate promoted nuclear translocation of P65 through ROS and contributed to the development of pulmonary fibrosis. A Western blotting was performed for expressions determination of p65 in total fraction, cytoplasm fraction and nucleus fraction of MRC5. B p65 nuclear translocation assessed by immunofluorescence staining in HMCC97H cells with control group, lactate group, lactate + MT group and lactate + DPI group. C phosphorylation of NK-κB signaling components in MRC5 with control group, lactate group, lactate + MT group was determined by Immunoblotting. D, E COL1A1 and α-SMA was tested by Western blotting through SH-P65. *p 
7). Macrophage SCAP Contributes to Metaflammation and Lean NAFLD by Activating STING-NF-κB Signaling Pathway. Cellular and molecular gastroenterology and hepatology, 2022 (PubMed: 35367665) [IF=7.1]

Application: WB    Species: Mouse    Sample: liver tissue

Figure 11 Macrophage SCAP deletion alleviates inflammatory response in liver tissue of PD-fed mice via inhibition of STING–NF-κB signaling. (A) Protein levels of P65 and P-P65 in total liver tissues, P65 in liver nuclear and cytosol (n = 6). (B) Protein levels of IKKα, IKKβ, P-IKKα/β, IκBα, and P-IκBα in liver tissues (n = 6). (C) Immunofluorescence staining of F4/80 and P65 in liver tissues (n = 3). (D) Schematic diagram of mechanisms by which STING activates NF-κB signaling. (E) Protein levels of STING, P-TBK1, and TBK1 in liver tissues (n = 6). (F) Immunohistochemical staining of STING in liver tissues (n = 6). (G) Immunofluorescence staining of F4/80 and STING in liver tissues (n = 3). Data are expressed as mean ± SD. ∗P < .05; ∗∗P < .01; ∗∗∗P < .0001; ns, nonsignificant (2-tailed unpaired t test in bar graphs).
8). Chemical composition and anti-inflammatory activity of water extract from black cocoa tea (Camellia ptilophylla). Food Research International, 2022 (PubMed: 36192963) [IF=7.0]
9). Isolation and identification of immunomodulatory peptides from the protein hydrolysate of tuna trimmings (Thunnas albacares). LWT, 2022 [IF=6.0]
10). Bmp8a deletion leads to obesity through regulation of lipid metabolism and adipocyte differentiation. Communications Biology, 2023 (PubMed: 37553521) [IF=5.9]

Application: WB    Species: Mouse    Sample: 3T3-L1 cells

Fig. 7 The interaction of NF-ĸB and PPARγ mediates the effect of Bmp8a on adipogenesis. a, c After induction of adipogenic differentiation, the downregulated (a) and upregulated (c) KEGG pathway in overexpression zebrafish bmp8a 3T3-L1 cells. b, d After induction of adipogenic differentiation, the downregulated (b) and upregulated (d) KEGG pathway in overexpression mouse Bmp8a 3T3-L1 cells. e, f Immunoblot analysis and quantification of p-IKKα/β and p-p65 in Mock, LV-ZsGreen1, and LV-bmp8a 3T3-L1 cells (n = 3). g, h Immunoblot analysis and quantification of p-IKKα/β and p-p65 in Mock, LV-ZsGreen1, and LV-Bmp8a 3T3-L1cells. Protein expression levels were quantified by ImageJ software and normalized to total protein (n = 3). i Co-immunoprecipitation and immunoblot analysis of co-transfected with PPARγ and p65 (n = 3). j Schematic drawing of predicted PPRE site in Fabp4 promoter region. k Schematic drawing of WT and PPRE site mutation Luc-report plasmids. l, m Quantification of the activity of Fabp4-promoter (l) and Fabp4-promoter-ΔPPRE (m) luciferase reporters in mouse HEK293T cells transfected with Vector, pCMV-Pparγ, or co-transfected pCMV-Pparγ and pCMV-p65, respectively. Renilla luciferase was used as the internal control (n = 3). Data were from three independent experiments and were analyzed by One-way ANOVA and were presented as mean ± SD (ns not significant, **p 
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