IKK alpha Antibody (YA348)
(Synonyms: IKKA, TCF16, CHUK, Inhibitor of nuclear factor kappa-B kinase subunit alpha, I-kappa-B kinase alpha, IKK-A, IKK-alpha, IkBKA, IkappaB kinase, Conserved helix-loop-helix ubiquitous kinase, I-kappa-B kinase 1, Nuclear factor NF-kappa-B inhibitor kinase alpha, Transcription factor 16, IKK-1, IKK1, NFKBIKA, TCF-16)
Based on 1 Customer Validation
IKK alpha Antibody (YA348) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to IKK alpha.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, ICC/IF, IHC-P, FC, IP
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Reactivity :
Human, Mouse
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Formulation:
Supplied in 1*TBS (pH7.4), 0.05% BSA and 40% Glycerol. Preservative: 0.05% Sodium Azide.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
Predicted band size
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Observed band size
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|---|---|---|
| Dilution Ratio | 85 kDa | 85 kDa |
Product Details
IKK alpha Antibody (YA348) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to IKK alpha.
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Host Rabbit
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Clonality Recombinant,Monoclonal
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Species ReactivityHuman, Mouse
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Observed Molecular WeightObserved band size: 85 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 85 kDa
Synthetic peptide within N-terminal human IKK alpha.
Endogenous
Protein A affinity purified.
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in 1*TBS (pH7.4), 0.05% BSA and 40% Glycerol. Preservative: 0.05% Sodium Azide.
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Verification Images
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Western blot analysis of extracts from RAW264.7(lane 2(20μg) or lane 3(40μg)) and C6(lane 4(20μg) or lane 5(40μg)), using IKK alpha (HY-P80413) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% BSA in TBST for 2 hour at room temperature. The primary antibody (HY-P80413, 1/1000) and Loading control antibody (GAPDH, HY-P80954, 1/3000) was used in 5% BSA in TBST at 4°C overnight. Goat Anti-Rabbit/Mouse IgG-HRP Secondary Antibody (HY-P8001/HY-P8004, 1/10,000) was used for 1 hour at room temperature. -
Western blot analysis was performed on protein extracts (25 μg) from RAW264.7 (lane 2), HeLa (lane 3), HCT 116 (lane 4), A549 (lane 5) and HepG2 (lane 6) using IKK alpha antibody. Proteins were transferred onto a 0.45 μm PVDF membrane using the Trans-Blot® Turbo™ system for 13 min. The membrane was then blocked with 5% nonfat milk in TBST (HY-K1025) for 1 h at room temperature. The primary antibody (1:1000) and loading control antibody GAPDH Antibody (HRP) (HY-P80954A) (1:5000) were diluted in 5% nonfat milk in TBST and incubated with the membrane overnight at 4°C. After washing, the membrane of primary antibody was incubated with HRP-conjugated goat anti-rabbit/mouse IgG secondary antibody (HY-P8001/HY-P8004) (1:5000) diluted in 5% nonfat milk in TBST for 1 h at room temperature. Protein bands were visualized using an Ultra High Sensitivity ECL detection kit (HY-K1005). -
Flow cytometric analysis of 1X106 HepG2 cells labeling IKK alpha Antibody (HY-P80413, red). Cells were fixed with 4% paraformaldehyde and permeabilised with 90% methanol. Then stained with the primary antibody at 1/100 dilution for an hour at 4℃. AF488-conjugated Goat Anti-Rabbit IgG H&L (HY-P8002) was used as the secondary antibody at 1/1,000 dilution for 30 minutes at 4℃. Rabbit IgG Isotype Control (HY-P80879, blue) was used as the isotype control, cells without incubation with primary antibody were used as the unlabeled control (black).
Background
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Function
IKK alpha 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 a part of the canonical IKK complex in the conventional pathway of NF-kappa-B activation and phosphorylates inhibitors of NF-kappa-B on 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. Negatively regulates the pathway by phosphorylating the scaffold protein TAXBP1 and thus promoting the assembly of the A20/TNFAIP3 ubiquitin-editing complex (composed of A20/TNFAIP3, TAX1BP1, and the E3 ligases ITCH and RNF11). Therefore, CHUK plays a key role in the negative feedback of NF-kappa-B canonical signaling to limit inflammatory gene activation. As part of the non-canonical pathway of NF-kappa-B activation, the MAP3K14-activated CHUK/IKKA homodimer phosphorylates NFKB2/p100 associated with RelB, inducing its proteolytic processing to NFKB2/p52 and the formation of NF-kappa-B RelB-p52 complexes. In turn, these complexes regulate genes encoding molecules involved in B-cell survival and lymphoid organogenesis. Also participates in the negative feedback of the non-canonical NF-kappa-B signaling pathway by phosphorylating and destabilizing MAP3K14/NIK. Within the nucleus, phosphorylates CREBBP and consequently increases both its transcriptional and histone acetyltransferase activities. Modulates chromatin accessibility at NF-kappa-B-responsive promoters by phosphorylating histones H3 at 'Ser-10' that are subsequently acetylated at 'Lys-14' by CREBBP. Additionally, phosphorylates the CREBBP-interacting protein NCOA3. Also phosphorylates FOXO3 and may regulate this pro-apoptotic transcription factor. Phosphorylates RIPK1 at 'Ser-25' which represses its kinase activity and consequently prevents TNF-mediated RIPK1-dependent cell death. Phosphorylates AMBRA1 following mitophagy induction, promoting AMBRA1 interaction with ATG8 family proteins and its mitophagic activity[1][2][3][4][5][6][7][8][9][10][11].
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Subcellular Localization
Cytoplasm; Nucleus
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Expression
Tissue_specificity:Broad expression -
Subunit
Component of the I-kappa-B-kinase (IKK) core complex consisting of CHUK, IKBKB and IKBKG; probably four alpha/CHUK-beta/IKBKB dimers are associated with four gamma/IKBKG subunits (PubMed:32935379).
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SwissProt ID
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Synonyms
IKKA, TCF16, CHUK, Inhibitor of nuclear factor kappa-B kinase subunit alpha, I-kappa-B kinase alpha, IKK-A, IKK-alpha, IkBKA, IkappaB kinase, Conserved helix-loop-helix ubiquitous kinase, I-kappa-B kinase 1, Nuclear factor NF-kappa-B inhibitor kinase alpha, Transcription factor 16, IKK-1, IKK1, NFKBIKA, TCF-16
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Research Field
Signal Transduction
Documentation
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Data Sheet (264 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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User Guide for Antibodies (1077 KB)
[1]. Solt LA, et al. The IkappaB kinase complex: master regulator of NF-kappaB signaling. Immunol Res. 2008;42(1-3):3-18. [Content Brief]
[2]. Régnier CH, et al. Identification and characterization of an IkappaB kinase. Cell. 1997 Jul 25;90(2):373-83. [Content Brief]
[3]. DiDonato JA, et al. A cytokine-responsive IkappaB kinase that activates the transcription factor NF-kappaB. Nature. 1997 Aug 7;388(6642):548-54. [Content Brief]
[4]. Mercurio F, et al. IKK-1 and IKK-2: cytokine-activated IkappaB kinases essential for NF-kappaB activation. Science. 1997 Oct 31;278(5339):860-6. [Content Brief]
[5]. Liu Y, et al. TRIM56 positively regulates TNFα-induced NF-κB signaling by enhancing the ubiquitination of TAK1. Int J Biol Macromol. 2022 Oct 31;219:571-578. [Content Brief]
[6]. Shembade N, et al. The kinase IKKα inhibits activation of the transcription factor NF-κB by phosphorylating the regulatory molecule TAX1BP1. Nat Immunol. 2011 Jul 17;12(9):834-43. [Content Brief]
[7]. Razani B, et al. Negative feedback in noncanonical NF-kappaB signaling modulates NIK stability through IKKalpha-mediated phosphorylation. Sci Signal. 2010 May 25;3(123):ra41. [Content Brief]
[8]. Huang WC, et al. Phosphorylation of CBP by IKKalpha promotes cell growth by switching the binding preference of CBP from p53 to NF-kappaB. Mol Cell. 2007 Apr 13;26(1):75-87. [Content Brief]
[9]. Yamamoto Y, et al. Histone H3 phosphorylation by IKK-alpha is critical for cytokine-induced gene expression. Nature. 2003 Jun 5;423(6940):655-9. [Content Brief]
[10]. Hu MC, et al. IkappaB kinase promotes tumorigenesis through inhibition of forkhead FOXO3a. Cell. 2004 Apr 16;117(2):225-37. [Content Brief]
[11]. Di Rita A, et al. HUWE1 E3 ligase promotes PINK1/PARKIN-independent mitophagy by regulating AMBRA1 activation via IKKα. Nat Commun. 2018 Sep 14;9(1):3755. [Content Brief]
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