|Other Names||NF-kappa-B essential modulator, NEMO, FIP-3, IkB kinase-associated protein 1, IKKAP1, Inhibitor of nuclear factor kappa-B kinase subunit gamma, I-kappa-B kinase subunit gamma, IKK-gamma, IKKG, IkB kinase subunit gamma, NF-kappa-B essential modifier, IKBKG, FIP3, NEMO|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP8110d was selected from the N-term region of human IKK gamma. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Regulatory subunit of the IKK core complex which 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. Its binding to scaffolding polyubiquitin seems to play a role in IKK activation by multiple signaling receptor pathways. However, the specific type of polyubiquitin recognized upon cell stimulation (either 'Lys-63'- linked or linear polyubiquitin) and its functional importance is reported conflictingly. Also considered to be a mediator for TAX activation of NF-kappa-B. Could be implicated in NF-kappa-B- mediated protection from cytokine toxicity. Essential for viral activation of IRF3. Involved in TLR3- and IFIH1-mediated antiviral innate response; this function requires 'Lys-27'-linked polyubiquitination.|
|Cellular Location||Cytoplasm. Nucleus. Note=Sumoylated NEMO accumulates in the nucleus in response to genotoxic stress|
|Tissue Location||Heart, brain, placenta, lung, liver, skeletal muscle, kidney and pancreas|
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IKK gamma is a regulatory subunit part of the IKK-signalosome complex activation. It is also considered to be a mediator for TAX activation of NF-kappa-B. This protein could be implicated in NF-kappa-B-mediated protection from cytokine toxicity. Defects in IKBKG are the cause of anhidrotic ectodermal dysplasia with immunodeficiency (EDA-ID). EDA-ID is a X-linked recessive disorder characterized by absence of sweat glands, sparse scalp hair, rare conical teeth and immunological abnormalities resulting in severe infectious diseases. Defects in IKBKG are the cause of familial incontinentia pigmenti type II (IP2), an X-linked dominant disease causing death in male fetuses. In heterozygous female, it is characterized by disturbance of skin pigmentation sometimes associated with a variety of malformations of the eye, nails, teeth, skeleton, heart, and central nervous system.
Orange, J.S., et al., J. Allergy Clin. Immunol. 114(3):650-656 (2004).Stilo, R., et al., J. Biol. Chem. 279(33):34323-34331 (2004).Nishikomori, R., et al., Blood 103(12):4565-4572 (2004).Orange, J.S., et al., J. Allergy Clin. Immunol. 113(4):725-733 (2004).Yang, F., et al., J. Immunol. 172(4):2446-2452 (2004).
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