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I0505

Sigma-Aldrich

Anti-IκBα antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Synonym(s):

Anti-AUTSX3, Anti-MRX16, Anti-MRX79, Anti-MRXS13, Anti-MRXSL, Anti-PPMX, Anti-RS, Anti-RTS, Anti-RTT

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About This Item

MDL number:
MFCD01092370
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

200

conjugate

unconjugated

antibody form

IgG fraction of antiserum

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 36 kDa

species reactivity

mouse, human, rat

technique(s)

microarray: suitable
western blot: 1:2,000 using a whole extract of human epidermal carcinoma A431 cells
western blot: 1:2,000 using a whole extract of human epitheloid carcinoma HeLa cells

UniProt accession no.

P25963

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... NFKBIA(4792)
mouse ... Nfkbia(18035)
rat ... Nfkbia(25493)

General description

The gene NFKBIA (nuclear factor of κ light polypeptide gene enhancer B-cells inhibitor-α) encodes the α member of the NF-κ-B inhibitor family IκB, which also consists of IκBβ and IκBε. NFKBIA is also referred to as IκBα. It is the strongest inhibitor of nuclear NF-κB activity among these members. Specific phosphorylation of the inhibitor IκBα at Ser32 and Ser36, its ubiubiquitination and subsequent proteolytic degradation is necessary for the activation of NF-κ-B. It is localized to the cytosol, where it retains NF-κB. Polymorphism in this gene is linked to recurrent acute rejections in liver transplant recipients. Mutations in this gene have been linked to autosomal dominant anhidrotic ectodermal dysplasia and T cell immunodeficiency. The gene NFKBIA is mapped to human chromosome 14q13.

Immunogen

synthetic peptide corresponding to the C-terminus of human IκBα (amino acids 297-317 with N-terminally added lysine) conjugated to KLH.

Application

Anti-IκBα antibody produced in rabbit has been used in western blotting.

Biochem/physiol Actions

Specific phosphorylation of the inhibitor IκBα at Ser32 and Ser36, its ubiquitination and subsequent proteolytic degradation is necessary for the activation of NF-κ-B. Polymorphism in this gene is linked to recurrent acute rejections in liver transplant recipients. Mutations in this gene have been linked to autosomal dominant anhidrotic ectodermal dysplasia and T cell immunodeficiency.

Physical form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Description
Pricing

Storage Class Code

10 - Combustible liquids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Micah N Zuhl et al.
Journal of applied physiology (Bethesda, Md. : 1985), 116(2), 183-191 (2013-11-29)
The objectives of this study are threefold: 1) to assess whether 7 days of oral glutamine (GLN) supplementation reduces exercise-induced intestinal permeability; 2) whether supplementation prevents the proinflammatory response; and 3) whether these changes are associated with upregulation of the
K Kramer et al.
Tissue antigens, 84(4), 370-377 (2014-08-13)
The nuclear factor of kappa light polypeptide gene enhancer B-cells inhibitor-alpha (NFKBIA) gene encodes a member of the nuclear factor-kappa-B inhibitor family. Polymorphisms in this gene might be associated with a susceptibility to acute rejection episodes following liver transplantation, as
Pavel I Makarevich et al.
PloS one, 13(5), e0197566-e0197566 (2018-05-23)
Since development of plasmid gene therapy for therapeutic angiogenesis by J. Isner this approach was an attractive option for ischemic diseases affecting large cohorts of patients. However, first placebo-controlled clinical trials showed its limited efficacy questioning further advance to practice.
Gilles Courtois et al.
The Journal of clinical investigation, 112(7), 1108-1115 (2003-10-03)
X-linked anhidrotic ectodermal dysplasia with immunodeficiency (XL-EDA-ID) is caused by hypomorphic mutations in the gene encoding NEMO/IKKgamma, the regulatory subunit of the IkappaB kinase (IKK) complex. IKK normally phosphorylates the IkappaB-inhibitors of NF-kappaB at specific serine residues, thereby promoting their
Feng Chen et al.
Hepatology (Baltimore, Md.), 53(4), 1294-1305 (2011-04-12)
Mechanisms of brain edema in acute liver failure (ALF) are not completely understood. We recently demonstrated that matrix metalloproteinase 9 (MMP-9) induces significant alterations to occludin in brain endothelial cells in vitro and in brains of mice with experimental ALF
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