Anti-phospho-CHUK (pThr23) antibody produced in rabbit
affinity isolated antibody
別名:
Anti-IKBKA antibody produced in rabbit, Anti-IKK-alpha antibody produced in rabbit, Anti-IKK1 antibody produced in rabbit, Anti-IKKA antibody produced in rabbit, Anti-conserved helix-loop-helix ubiquitous kinase antibody produced in rabbit
Peptide sequence around phosphorylation site of threonine 23 (L-G-T(p)-G-G), according to the protein CHUK.
特徴および利点
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ターゲットの説明
Acts as part of the IKK complex in the conventional pathway of NF-kappa-B activation and 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. 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. Also phosphorylates NCOA3. Phosphorylates 'Ser-10' of histone H3 at NF-kappa-B-regulated promoters during inflammatory responses triggered by cytokines.
物理的形状
PBS（0.02％ アジ化ナトリウム、50％ グリセロール含有）
免責事項
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Cell death and differentiation, 23(9), 1471-1482 (2016-04-09)
Radioresistance is a major obstacle in successful clinical cancer radiotherapy, and the underlying mechanisms are not clear. Here we show that IKKα-mediated miR-196a biogenesis via interaction with Drosha regulates the sensitivity of nasopharyngeal carcinoma (NPC) cells to radiotherapy. Phosphorylation of
Prostaglandin E2 (PGE2) promotes colorectal tumor formation and progression by unknown mechanisms. We sought to identify microRNAs (miRNAs) that might mediate the effects of PGE2 on colorectal cancer (CRC) development. We incubated LS174T colorectal cancer cells with PGE2 or without
Cholangiocyte proliferation and ductular reaction contribute to the onset and progression of liver diseases. Little is known about the role of the transcription factor nuclear factor-κB (NF-κB) in this process. We investigated the activities of the RELB proto-oncogene NF-κB subunit
