IKK Gma Pure 54/IKKGma/NEMO 50ug

In most cells, NF-κB is sequestered in an inactive cytoplasmic form via interactions with the inhibitory proteins IκBα, IκBβ, and IκBε. Cell

stimulation induces the release, activation, and nuclear translocation of NF-κB. Release of NF-κB results from the phosphorylation and

subsequent proteolytic degradation of the IκB proteins. Two cytokine-inducible IκB kinases (IKKα and IKKβ) phosphorylate and target the

IκB proteins for degradation by the ubiquitin pathway. These kinases are components of a 700-900 kDa multisubunit complex that also

contains NF-κB/RelA, IκBα, MEKK1, NIK, IKAP, and IKKγ/NEMO (NF-κB essential modulator). IKKγ contains two coiled-coil domains

and a leucine zipper which allow it to form dimers and trimers that interact directly with IKKβ. IKKγ, essential for IKKα/IKKβ activation of

NF-κB, is located functionally and physically upstream of these subunits. In addition, IKKγ enables the HTLV-1 Tax oncoprotein to interact

with IKKβ, resulting in constitutive activation of NF-κB and maintenance of cellular transformation. Thus, IKKγ is an essential element of the

IκB complex and an adaptor that mediates stable formation of Tax-IKK complexes.

1.Since applications vary, each investigator should titrate the reagent to obtain optimal results.

2.Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.