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IkB alpha, Activated, Recombinant, Human, 6-His-tag (NF-kappa-B Inhibitor alpha, I-kappa-B-alpha, IkB-alpha, IkappaBalpha, Major Histocompatibility Complex Enhancer-binding Protein MAD3, NFKBIA, IKBA, MAD3, NFKBI)

Cat no: 029513

IkB alpha, Activated, Recombinant, Human, 6-His-tag (NF-kappa-B Inhibitor alpha, I-kappa-B-alpha, IkB-alpha, IkappaBalpha, Major Histocompatibility Complex Enhancer-binding Protein MAD3, NFKBIA, IKBA, MAD3, NFKBI)

Ikba is a cellular protein that inhibits the transcription factor NF-kB. NF-kB plays a central role in cellular stress and inflammatory responses by controlling cytokine-inducible gene expression and lymphocyte stimulation by antigens. In non-stimulated cells NF-kB is sequestered in the cytoplasm via the inhibitory protein Ikba, which obscures the nuclear localization signal of NF-kB and also blocks its ability to bind DNA. In response to various stimuli, including viral infection, ultraviolet radiation and inflammatory cytokines, Ikba is phosphorylated by the protein kinase complex IKK, which triggers its rapid degradation by ubiquitin mediated proteolysis. The liberated NF-kB then translocates to the nucleus and activates the expression of target genes. Mutations in the gene for Ikba result in the functional impairment of NF-kB which causes a decreased production of proinflammatory cytokines and certain interferons, rendering patients susceptible to infection.\n\nSource: \nRecombinant corresponding to full length human IkBa, fused to 6His-tag at N-terminal c-Myc, expressed by baculovirus in Sf21 insect cells.\n\nMolecular Weight: \n~41kD\n\nStorage and Stability:\nAliquot to avoid repeated freezing and thawing and store at -70 degrees C. Aliquots are stable for 6 months. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

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SPECIFICATIONS

Catalog Number

029513

Size

10ug

Reactivities

Hum

Form

Supplied as a liquid in 25mM MOPS pH7.5, 5mM MgCl2, 0.01% Tween 20, 1mM ATP.

Purity

~62% (SDS-PAGE, Coomassie blue staining)

References

1. Ferreiro D.U. and Komives E. A. Molecular Mechanisms of System Control of NF-kB Signaling by IkBa. Biochemistry, 49: 1560-1567, 2010. 2. Scherer D. C. et al., Signal-Induced Degradation of IkBa Requires Site-Specific Ubiquitination. PNAS. 92:11259-11263, 1995. 3. Jungnickel B. et al., Clonal Deleterious Mutations in the IkBa Gene in the Malignant Cells in Hodgkin's Lymphoma. J Exp Med., 191: 395-402, 2000. 4. Strack P. et al., SCFb-TRCP and Phosphorylation Dependent Ubiquitination of IkBa Catalysed by Ubc3 and Ubc4. Oncogene, 19: 3529-3536, 2000. 5. Winston J. T. et al., The SCFb-TRCP-Ubiquitin Ligase Complex Associates Specifically with Phosphorylated Destruction Motifs in IkBa and b-catenin and Stimulates IkBa Ubiquitination in vitro. Genes Dev, 13: 270- 283, 1999.

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