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I0505

Sigma-Aldrich

Anti-IκBα antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Sinonimo/i:

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

Numero MDL:
Codice UNSPSC:
12352203
NACRES:
NA.41

Origine biologica

rabbit

Coniugato

unconjugated

Forma dell’anticorpo

IgG fraction of antiserum

Tipo di anticorpo

primary antibodies

Clone

polyclonal

Forma fisica

buffered aqueous solution

PM

antigen 36 kDa

Reattività contro le specie

mouse, human, rat

tecniche

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

N° accesso UniProt

Condizioni di spedizione

dry ice

Temperatura di conservazione

−20°C

modifica post-traduzionali bersaglio

unmodified

Informazioni sul gene

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

Descrizione generale

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.

Immunogeno

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

Applicazioni

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

Azioni biochim/fisiol

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.

Stato fisico

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

Esclusione di responsabilità

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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Raccomandato

N° Catalogo
Descrizione
Determinazione del prezzo

Codice della classe di stoccaggio

10 - Combustible liquids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


Certificati d'analisi (COA)

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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)
Marianna Romzova et al.
Human immunology, 67(9), 706-713 (2006-09-28)
Nuclear factor kappa B (NFkappaB) is an important transcription factor that together with its inhibitor (IkappaB) participates in the activation of genes involved in immune responses. We examined the CA repeat polymorphism of the NFKB1 gene (encoding for NFkappaB) and
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
A polymorphism of the NFKBIA gene is associated with Crohn's disease patients lacking a predisposing allele of the CARD15 gene
Klein W, et al.
International Journal of Colorectal Disease, 19(2), 153-156 (2004)
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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