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I0505

Sigma-Aldrich

Anti-IκBα antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Synonyme(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

Numéro MDL:
MFCD01092370
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Conjugué

unconjugated

Forme d'anticorps

IgG fraction of antiserum

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen 36 kDa

Espèces réactives

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

Numéro d'accès UniProt

P25963

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

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

Description générale

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.

Immunogène

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.

Actions biochimiques/physiologiques

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.

Forme physique

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

Clause de non-responsabilité

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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Réf. du produit
Description
Tarif

Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

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
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)
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
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.
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
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