IKBKG, Polyclonal Antibody

For Research Use Only. Not for use in diagnostic procedures.

Polyclonal

Rabbit

Affinity Purified

Liquid. Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.

For short term use, store at 2-8 degree C up to 1 week. For long term storage, store at -20 degree C in small aliquots to prevent freeze-thaw cycles.

Small volumes of anti-IKBKG antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

This is a rabbit polyclonal antibody against IKBKG. It was validated on Western Blot using a cell lysate as a positive control.

Target Description: IKBKG is the 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. IKBKG also considered to be a mediator for TAX activation of NF-kappa-B. IKBKG could be implicated in NF-kappa-B-mediated protection from cytokine toxicity.Familial incontinentia pigmenti (IP) is a genodermatosis that segregates as an X-linked dominant disorder and is usually lethal prenatally in males (The International Incontinentia Pigmenti Consortium, 2000 [PubMed 10839543]). In affected females it causes highly variable abnormalities of the skin, hair, nails, teeth, eyes, and central nervous system. The prominent skin signs occur in 4 classic cutaneous stages: perinatal inflammatory vesicles, verrucous patches, a distinctive pattern of hyperpigmentation, and dermal scarring. Cells expressing the mutated X chromosome are eliminated selectively around the time of birth, so females with IP exhibit extremely skewed X-inactivation. Familial incontinentia pigmenti is caused by mutations in the NEMO gene and is here referred to as IP2, or 'classical' incontinentia pigmenti. Sporadic incontinentia pigmenti, the so-called IP1, which maps to Xp11, is categorized as hypomelanosis of Ito (MIM 300337).[supplied by OMIM]. Sequence Note: removed 1 base from the 5' end that did not align to the reference genome assembly. Publication Note: This RefSeq record includes a subset of the publications that are available for this gene. Please see the Entrez Gene record to access additional publications. PRIMARYREFSEQ_SPAN PRIMARY_IDENTIFIER PRIMARY_SPAN COMP 1-2120 AF261086.1 2-2121

Polyclonal; Transcription Factor; Lymphocyte Signaling; Transcription Regulation; Cell Biology; Disease Related; Transcription Factors;

Western Blot (WB)

WB Suggested Anti-IKBKG Antibody Titration: 0.2-1 ug/ml
ELISA Titer: 1:62500
Positive Control: Human Spleen

48kDa

inhibitor of nuclear factor kappa B kinase regulatory subunit gamma

NF-kappa-B essential modulator

NF-kappa-B essential modulator

FIP3; NEMO; NEMO; IKKAP1; I-kappa-B kinase subunit gamma; IKK-gamma; IKKG  [Similar Products]

NEMO_HUMAN

This gene encodes the regulatory subunit of the inhibitor of kappaB kinase (IKK) complex, which activates NF-kappaB resulting in activation of genes involved in inflammation, immunity, cell survival, and other pathways. Mutations in this gene result in incontinentia pigmenti, hypohidrotic ectodermal dysplasia, and several other types of immunodeficiencies. A pseudogene highly similar to this locus is located in an adjacent region of the X chromosome. [provided by RefSeq, Mar 2016]

IKKG: a regulatory subunit of the IKK-signalosome complex. Interacts preferentially with IKK-beta but also able to interact with IKK-alpha, IKAP, TAX, RIP and MAP3K14/NIK. Defects are the cause of familial incontinentia pigmenti type II (IP2).

Protein type: Protein kinase, regulatory subunit; Adaptor/scaffold

Chromosomal Location of Human Ortholog: Xq28

Cellular Component: spindle pole; cytoplasm; intracellular; IkappaB kinase complex; nucleus; cytosol; ubiquitin ligase complex

Molecular Function: protein domain specific binding; signal transducer activity; peroxisome proliferator activated receptor binding; protein binding; protein homodimerization activity; protein heterodimerization activity; metal ion binding; ubiquitin protein ligase binding

Biological Process: I-kappaB kinase/NF-kappaB cascade; establishment of vesicle localization; viral reproduction; activation of MAPK activity; apoptosis; stress-activated MAPK cascade; toll-like receptor 3 signaling pathway; T cell receptor signaling pathway; activation of NF-kappaB transcription factor; toll-like receptor 10 signaling pathway; toll-like receptor 5 signaling pathway; B cell homeostasis; positive regulation of interferon type I production; JNK cascade; inflammatory response; toll-like receptor 4 signaling pathway; positive regulation of I-kappaB kinase/NF-kappaB cascade; transcription, DNA-dependent; MyD88-independent toll-like receptor signaling pathway; response to virus; activation of NF-kappaB-inducing kinase; toll-like receptor 2 signaling pathway; MyD88-dependent toll-like receptor signaling pathway; toll-like receptor signaling pathway; innate immune response; positive regulation of transcription from RNA polymerase II promoter; immune response; toll-like receptor 9 signaling pathway; response to DNA damage stimulus

Disease: Invasive Pneumococcal Disease, Recurrent Isolated, 2; Ectodermal Dysplasia, Hypohidrotic, With Immune Deficiency; Immunodeficiency Without Anhidrotic Ectodermal Dysplasia; Immunodeficiency 33; Incontinentia Pigmenti; Ectodermal Dysplasia, Anhidrotic, With Immunodeficiency, Osteopetrosis, And Lymphedema

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