I0505
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
Pricing and availability is not currently available.
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biological source
rabbit
Quality Level
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.
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
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The effects of acute oral glutamine supplementation on exercise-induced gastrointestinal permeability and heat shock protein expression in peripheral blood mononuclear cells
Zuhl M, et al.
Cell Stress & Chaperones, 20(1), 85-93 (2015)
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
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
Z J Chen et al.
Cell, 84(6), 853-862 (1996-03-22)
Signal-induced activation of the transcription factor NF-kappaB requires specific phosphorylation of the inhibitor IkappaBalpha and its subsequent proteolytic degradation. Phosphorylation of serine residues 32 and 36 targets IkappaBalpha to the ubiquitin (Ub)-proteasome pathway. Here we report the identification of a
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.
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