Alexa Fluor® 647 Anti-IKK beta antibody [EPR6043],Abcam,AB310104

Patented technology Our RabMAb ® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb ® patents . How are conjugated primary antibodies validated? This conjugated primary antibody is released using a quantitative quality control method that evaluates binding affinity post-conjugation and efficiency of antibody labeling. For suitable applications and species reactivity, please refer to the unconjugated version of this clone. What are the advantages of a recombinant monoclonal antibody? This product is a recombinant monoclonal antibody, which offers several advantages including: - High batch-to-batch consistency and reproducibility - Improved sensitivity and specificity - Long-term security of supply - Animal-free batch production For more information, read more on recombinant antibodies .

Host

Rabbit

Reactivity

Human, Mouse

Application

Target Binding Affinity, IHC-P, Antibody Labelling

Conjugate

Alexa Fluor® 647

Platform ID

BAB312116992

Abcam

Headquarters

Discovery Drive Cambridge Biomedical Campus Cambridge CB2 0AX UK

Contact

Tel: +44 (0)1223 696000
Fax: +44 (0)1223 215 215

Product Specifications
Scientific Background

Specifications

NameAlexa Fluor® 647 Anti-IKK beta antibody [EPR6043]
Cat. No.AB310104
HostRabbit
IsotypeIgG
ReactivityHuman, Mouse
ConjugationAlexa Fluor® 647
ApplicationTarget Binding Affinity, IHC-P, Antibody Labelling
ClonalityMonoclonal
Clone NumberEPR6043
ImmunogenThe exact immunogen used to generate this antibody is proprietary information.
PurityAffinity purification Protein A
Appearance/FormLiquid
ShippingBlue Ice
FormulationpH: 7.4 Preservative: 0.02% Sodium azide Constituents: PBS, 30% Glycerol (glycerin, glycerine), 1% BSA
Storage-20°C
Regulatory StatusResearch Use Only

Scientific Background

Target data 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 (PubMed : 20434986, PubMed : 20797629, PubMed : 21138416, PubMed : 30337470, PubMed : 9346484). Acts as a part of the canonical IKK complex in the conventional pathway of NF-kappa-B activation (PubMed : 9346484). Phosphorylates inhibitors of NF-kappa-B on 2 critical serine residues (PubMed : 20434986, PubMed : 20797629, PubMed : 21138416, PubMed : 9346484). These modifications allow polyubiquitination of the inhibitors and subsequent degradation by the proteasome (PubMed : 20434986, PubMed : 20797629, PubMed : 21138416, PubMed : 9346484). 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 (PubMed : 20434986, PubMed : 20797629, PubMed : 21138416, PubMed : 9346484). 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 (PubMed : 11297557, PubMed : 14673179, PubMed : 20410276, PubMed : 21138416). IKK-related kinase phosphorylations may prevent the overproduction of inflammatory mediators since they exert a negative regulation on canonical IKKs (PubMed : 11297557, PubMed : 20410276, PubMed : 21138416). Phosphorylates FOXO3, mediating the TNF-dependent inactivation of this pro-apoptotic transcription factor (PubMed : 15084260). Also phosphorylates other substrates including NAA10, NCOA3, BCL10 and IRS1 (PubMed : 17213322, PubMed : 19716809). Phosphorylates RIPK1 at 'Ser-25' which represses its kinase activity and consequently prevents TNF-mediated RIPK1-dependent cell death (By similarity). Phosphorylates the C-terminus of IRF5, stimulating IRF5 homodimerization and translocation into the nucleus (PubMed : 25326418). Following bacterial lipopolysaccharide (LPS)-induced TLR4 endocytosis, phosphorylates STAT1 at 'Thr-749' which restricts interferon signaling and anti-inflammatory responses and promotes innate inflammatory responses (PubMed : 38621137). IKBKB-mediated phosphorylation of STAT1 at 'Thr-749' promotes binding of STAT1 to the ARID5A promoter, resulting in transcriptional activation of ARID5A and subsequent ARID5A-mediated stabilization of IL6 (PubMed : 32209697). It also promotes binding of STAT1 to the IL12B promoter and activation of IL12B transcription (PubMed : 32209697). See full target information IKBKB

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