Alexa Fluor® 568 Anti-IKK beta 抗体 [EPR6043]

ターゲットの情報

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).