IKK-beta Antibody - #AF6009

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Product: IKK-beta Antibody
Catalog: AF6009
Description: Rabbit polyclonal antibody to IKK-beta
Application: WB IHC IF/ICC
Cited expt.: WB
Reactivity: Human, Mouse, Rat, Monkey
Prediction: Pig, Zebrafish, Bovine, Horse, Rabbit, Dog, Xenopus
Mol.Wt.: 86kDa; 87kD(Calculated).
Uniprot: O14920
RRID: AB_2834943

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MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
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: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat,Monkey
Prediction:
Pig(100%), Zebrafish(100%), Bovine(100%), Horse(100%), Rabbit(100%), Dog(100%), Xenopus(100%)
Clonality:
Polyclonal
Specificity:
IKK-beta Antibody detects endogenous levels of total IKK-beta.
RRID:
AB_2834943
Cite Format: Affinity Biosciences Cat# AF6009, RRID:AB_2834943.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
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.
Alias:

Fold/Unfold

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;

Immunogens

Immunogen:

A synthesized peptide derived from human IKK-beta, corresponding to a region within the internal amino acids.

Uniprot:

O14920(IKKB_HUMAN) >>Visit HPA database.

Gene(ID):
IKBKB(3551)
Expression:
O14920 IKKB_HUMAN:

Highly expressed in heart, placenta, skeletal muscle, kidney, pancreas, spleen, thymus, prostate, testis and peripheral blood.

Description:
IKK-beta is 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.
Sequence:
MSWSPSLTTQTCGAWEMKERLGTGGFGNVIRWHNQETGEQIAIKQCRQELSPRNRERWCLEIQIMRRLTHPNVVAARDVPEGMQNLAPNDLPLLAMEYCQGGDLRKYLNQFENCCGLREGAILTLLSDIASALRYLHENRIIHRDLKPENIVLQQGEQRLIHKIIDLGYAKELDQGSLCTSFVGTLQYLAPELLEQQKYTVTVDYWSFGTLAFECITGFRPFLPNWQPVQWHSKVRQKSEVDIVVSEDLNGTVKFSSSLPYPNNLNSVLAERLEKWLQLMLMWHPRQRGTDPTYGPNGCFKALDDILNLKLVHILNMVTGTIHTYPVTEDESLQSLKARIQQDTGIPEEDQELLQEAGLALIPDKPATQCISDGKLNEGHTLDMDLVFLFDNSKITYETQISPRPQPESVSCILQEPKRNLAFFQLRKVWGQVWHSIQTLKEDCNRLQQGQRAAMMNLLRNNSCLSKMKNSMASMSQQLKAKLDFFKTSIQIDLEKYSEQTEFGITSDKLLLAWREMEQAVELCGRENEVKLLVERMMALQTDIVDLQRSPMGRKQGGTLDDLEEQARELYRRLREKPRDQRTEGDSQEMVRLLLQAIQSFEKKVRVIYTQLSKTVVCKQKALELLPKVEEVVSLMNEDEKTVVRLQEKRQKELWNLLKIACSKVRGPVSGSPDSMNASRLSQPGQLMSQPSTASNSLPEPAKKSEELVAEAHNLCTLLENAIQDTVREQDQSFTALDWSWLQTEEEEHSCLEQAS

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Dog
100
Xenopus
100
Zebrafish
100
Rabbit
100
Sheep
69
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

Research Backgrounds

Function:

Serine kinase that plays an essential role in the NF-kappa-B signaling pathway which is activated by multiple stimuli such as inflammatory cytokines, bacterial or viral products, DNA damages or other cellular stresses. Acts as part of the canonical IKK complex in the conventional pathway of NF-kappa-B activation. Phosphorylates inhibitors of NF-kappa-B on 2 critical serine residues. These modifications allow polyubiquitination of the inhibitors and subsequent degradation by the proteasome. In turn, free NF-kappa-B is translocated into the nucleus and activates the transcription of hundreds of genes involved in immune response, growth control, or protection against apoptosis. In addition to the NF-kappa-B inhibitors, phosphorylates several other components of the signaling pathway including NEMO/IKBKG, NF-kappa-B subunits RELA and NFKB1, as well as IKK-related kinases TBK1 and IKBKE. IKK-related kinase phosphorylations may prevent the overproduction of inflammatory mediators since they exert a negative regulation on canonical IKKs. Phosphorylates FOXO3, mediating the TNF-dependent inactivation of this pro-apoptotic transcription factor. Also phosphorylates other substrates including NCOA3, BCL10 and IRS1. Within the nucleus, acts as an adapter protein for NFKBIA degradation in UV-induced NF-kappa-B activation. Phosphorylates RIPK1 at 'Ser-25' which represses its kinase activity and consequently prevents TNF-mediated RIPK1-dependent cell death (By similarity).

PTMs:

Upon cytokine stimulation, phosphorylated on Ser-177 and Ser-181 by MEKK1 and/or MAP3K14/NIK as well as TBK1 and PRKCZ; which enhances activity. Once activated, autophosphorylates on the C-terminal serine cluster; which decreases activity and prevents prolonged activation of the inflammatory response. Phosphorylated by the IKK-related kinases TBK1 and IKBKE, which is associated with reduced CHUK/IKKA and IKBKB activity and NF-kappa-B-dependent gene transcription. Dephosphorylated at Ser-177 and Ser-181 by PPM1A and PPM1B.

(Microbial infection) Acetylation of Thr-180 by Yersinia yopJ prevents phosphorylation and activation, thus blocking the I-kappa-B pathway.

Ubiquitinated. Monoubiquitination involves TRIM21 that leads to inhibition of Tax-induced NF-kappa-B signaling. According to 'Ser-163' does not serve as a monoubiquitination site. According to ubiquitination on 'Ser-163' modulates phosphorylation on C-terminal serine residues.

(Microbial infection) Monoubiquitination by TRIM21 is disrupted by Yersinia yopJ.

Hydroxylated by PHD1/EGLN2, loss of hydroxylation under hypoxic conditions results in activation of NF-kappa-B.

Subcellular Location:

Cytoplasm. Nucleus. Membrane raft.
Note: Colocalized with DPP4 in membrane rafts.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Highly expressed in heart, placenta, skeletal muscle, kidney, pancreas, spleen, thymus, prostate, testis and peripheral blood.

Family&Domains:

The kinase domain is located in the N-terminal region. The leucine zipper is important to allow homo- and hetero-dimerization. At the C-terminal region is located the region responsible for the interaction with NEMO/IKBKG.

Belongs to the protein kinase superfamily. Ser/Thr protein kinase family. I-kappa-B kinase subfamily.

Research Fields

· 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 > 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.

References

1). 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
2). Overproduction of Gastrointestinal 5-HT Promotes Colitis-Associated Colorectal Cancer Progression via Enhancing NLRP3 Inflammasome Activation. Cancer Immunology Research, 2021 (PubMed: 34285037) [IF=8.1]
3). 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]
4). Anti-Inflammatory Effects of Huangqin Decoction on Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice Through Regulation of the Gut Microbiota and Suppression of the Ras-PI3K-Akt-HIF-1α and NF-κB Pathways. Frontiers in Pharmacology, 2020 (PubMed: 32038240) [IF=5.6]

Application: WB    Species: mouse    Sample: colorectal

FIGURE 7 | Effects of Huangqin decoction (HQD) on colonic expression levels of nuclear factor-kappa B (NF-kB) pathway proteins assessed by Western blot in dextran sulfate sodium (DSS)-induced colitis mice (A).
5). Nr2e1 deficiency aggravates insulin resistance and chronic inflammation of visceral adipose tissues in a diet-induced obese mice model. LIFE SCIENCES, 2021 (PubMed: 33915130) [IF=5.2]

Application: WB    Species: mice    Sample: adipose tissues

Fig. 5. Nr2e1 deficiency exacerbated inflammation in EAT. Comparison of the epididymal fat weight (A). The ratio of epididymal fat weight to the total body weight (B). The mRNA expression of F4/80 (C). The mRNA and protein expressions of IL-6, IL-1β, TNF-α and MCP-1 (E, F). The protein levels of p-IKKβ/IKKβ, p-P65/P65 (G, H). The data are expressed as means ± SEM. *P < 0.05, **P < 0.01. ns: not significant.
6). Qinlian hongqu decoction ameliorates hyperlipidemia via the IRE1-α/IKKB-β/NF-κb signaling pathway: Network pharmacology and experimental validation. Journal of Ethnopharmacology, 2024 (PubMed: 37406747) [IF=4.8]
7). Antidepressant-like effects of helicid on a chronic unpredictable mild stress-induced depression rat model: Inhibiting the IKK/IκBα/NF-κB pathway through NCALD to reduce inflammation. International Immunopharmacology, 2021 (PubMed: 33578182) [IF=4.8]

Application: WB    Species: rat    Sample: hippocampus

Fig. 10. The effects of the IKK/IκBα/NF-κB signaling pathway in the hippocampus after AAV-siNCALD. (A) Representative NCALD, IKKβ, p-IKKβ, IкBα, p- IкBα, NF-кB, β-actin, and Lamin B western blot bands. (B), (C), (D), (E), (F), (G), (H) The relative ratios of the grayscale values of NCALD, IKKβ, p-IKKβ, IкBα, pIкBα, and NF-кB to the corresponding β-actin or Lamin B, n = 4. ###P < 0.001, CUMS + saline vs. sham; *P < 0.05; **P < 0.01; ***P < 0.001, CUMS + saline vs. CUMS + AAV-siNCALD. All data are shown as the mean ± SEM.
8). Mechanism of Astragalus mongholicus Bunge ameliorating cerebral ischemia-reperfusion injury: Based on network pharmacology analysis and experimental verification. Journal of ethnopharmacology, 2024 (PubMed: 38588987) [IF=4.8]
9). Caveolin-1 aggravates neurological deficits by activating neuroinflammation following experimental intracerebral hemorrhage in rats. Experimental Neurology, 2023 (PubMed: 37598879) [IF=4.6]
10). CTRP1 attenuates cerebral ischemia/reperfusion injury via the PERK signaling pathway. Frontiers in Cell and Developmental Biology, 2021 (PubMed: 34422821) [IF=4.6]

Application: WB    Species: Rat    Sample: cortex

FIGURE 5 CTRP1 inhibited ERS via PERK signal pathway in the cortex of MCAO/R-treated rats. (A) Western blot analyzed the expression of PERK, p-PERK, GRP78, ATF6, ATF4, IRE1α, p-IRE1α. n = 4 per group. (B) CTRP1 affected the interaction between PERK and GRP78 after CIRI. n = 3 per group. ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05 vs. sham group, ####p < 0.0001, ###p < 0.001, ## p < 0.01, #p < 0.05 vs. MCAO/R + LV-NC group.
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