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Cat. Number
070226511249084
Chemical Name
IKKα Monoclonal Antibody (Clone 14A231)
References
Synonyms
  • CHUK
  • IKK1
  • TCF16
  • IKBKA
Formulation 100 µg of protein G-purified IgG in 200 µl PBS, containing 0.0.5% BSA and 0.05% sodium azide
Stability 1 year
Storage -20°C
Shipping Wet ice in continental US; may vary elsewhere
Specificity
Human IKKα +
Monkey IKKα +
Mouse IKKα +
Size Global Purchasing
1 ea  

Description

Antigen: his-tagged full-length recombinant human IKKα · Clone designation: 14A231 · Host: mouse · Isotype: IgG1κ · Application(s): FC (intracellular), IHC (paraffin-embedded sections), IP, and WB · Nuclear Factor-κB (NF-κB) is sequestered in the cytoplasm by the IκB family of inhibitory proteins that mask the nuclear localization signal of NF-κB, thereby preventing translocation of NF-κB to the nucleus. External stimuli such as tumor necrosis factor or other cytokines result in phosphorylation and degradation of IκB, releasing NF-κB dimers. NF-κB dimers subsequently translocate to the nucleu and activates target genes. Synthesis of IκBα is autoregulated. IκB proteins are phosphorylated by IκB kinase complex consisting of at least three proteins, IKK1/α, IKK2/β, and IKK3/γ. In vitro, IKK1/α and IKK2/β can form homo- and heterodimers that can phosphorylate IκBs at the regulatory serine residues directly. IKK1/α and IKK2/β are phosphorylated by NF-κB-inducing kinase (NIK) and MAP kinase kinase-1 (MEKK-1), respectively.1 Targeted disruption of IKK1/α gene in mice results in skin and limb abnormalities and death of newborns.2,3

1 Delhase, M., Hayakawa, M., Chen, Y., et al. Positive and negative regulation of IκB kinase activity through IKKβ subunit phophorylation. Science 284 309-313 (1999).

2 Takeda, K., Takeuchi, O., Tsujimura, T., et al. Limb and skin abnormalities in mice lacking IKKa. Science 284(5412) 313-316 (1999 Jun 9 1999).

3 Hu, Y., Baud, V., Delhase, M., et al. Abnormal morphogenesis but intact IKK activation in mice lacking the IKKa subunit of IkB kinase. Science 284(5412) 316-320 (1999 Apr 9 1999).

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