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Key Documents

SAB4501989

Sigma-Aldrich

Anti-NF-κB p105 antibody produced in rabbit

affinity isolated antibody

Synonyme(s) :

DNA-binding factor KBF1, EBP-1, NF-κ-B1 p84/NF-κ-B1 p98, NFKB1, NFkB-p50

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen 105 kDa

Espèces réactives

rat, mouse, human

Concentration

~1 mg/mL

Technique(s)

ELISA: 1:20000
immunohistochemistry: 1:50-1:100
western blot: 1:500-1:1000

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

wet ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... NFKB1(4790)

Catégories apparentées

Description générale

Anti-NF-κB p105 Antibody detects endogenous levels of total NF-κB p105 protein.
The gene NFκB1 (nuclear factor κ B subunit 1) is mapped to human chromosome 4q24. It codes for NF-κB p105/p50 isoforms.

Immunogène

The antiserum was produced against synthesized peptide derived from human NF-kappaB p105/p50.

Immunogen Range: 304-353

Actions biochimiques/physiologiques

NF-κB (nuclear factor κ B subunit) is an important transcription factor that regulates the process of apoptosis, immune response and cell-growth control genes. It is associated with a number of human disorders including inflammatory diseases and cancers. NF-κB signaling cascade is known to be stimulated by many genotoxic stresses and also DNA damage. NF-κB is involved in bone metabolism. Downregulation of NF-κB mediates GPER (G-protein coupled estrogen receptor) specific agonist G-1 induced EMT (epithelial mesenchymal transition) suppression. Thereby, it prevents the motility of triple-negative breast cancer cells in vitro.

Caractéristiques et avantages

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Forme physique

Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

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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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

nwg

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

Luca Bisanti et al.
Animals : an open access journal from MDPI, 14(15) (2024-08-10)
The close phylogenetic relationship between ascidians (Tunicata) and vertebrates makes them a powerful model for studying the innate immune system. To better understand the nature and dynamics of immune responses and the mechanisms through which bacterial infections are detected and
L Bisanti et al.
Scientific reports, 14(1), 8495-8495 (2024-04-12)
A worldwide increase in the prevalence of coral diseases and mortality has been linked to ocean warming due to changes in coral-associated bacterial communities, pathogen virulence, and immune system function. In the Mediterranean basin, the worrying upward temperature trend has
Amir S Karban et al.
Human molecular genetics, 13(1), 35-45 (2003-11-14)
Nuclear Factor-kappaB (NF-kappaB) is a major transcription regulator of immune response, apoptosis and cell-growth control genes, and is upregulated in inflammatory bowel disease (IBD), both ulcerative colitis (UC) and Crohn's disease. The NFKB1 gene encodes the NF-kappaB p105/p50 isoforms. Genome-wide
Zhuo-Jia Chen et al.
Molecular oncology, 10(6), 775-788 (2016-02-05)
The targeted therapy for triple-negative breast cancer (TNBC) is a great challenge due to our poor understanding on its molecular etiology. In the present study, our clinical data showed that the expression of G-protein coupled estrogen receptor (GPER) is negatively
F Ahmad et al.
Cell death & disease, 7, e2213-e2213 (2016-05-07)
Given the involvement of telomerase activation and dysregulated metabolism in glioma progression, the connection between these two critical players was investigated. Pharmacological inhibition of human Telomerase reverse transcriptase (hTERT) by Costunolide induced glioma cell apoptosis in a reactive oxygen species

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