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SAB4501991

Sigma-Aldrich

Anti-NF-κB p105 antibody produced in rabbit

affinity isolated antibody

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Synonym(s):
DNA-binding factor KBF1, EBP-1, NF-κ-B1 p84/NF-κ-B1 p98, NFKB1, NFkB-p50
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 105 kDa

species reactivity

human

concentration

~1 mg/mL

technique(s)

ELISA: 1:10000
immunofluorescence: 1:100-1:500
immunohistochemistry: 1:50-1:100
western blot: 1:500-1:1000

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... NFKB1(4790)

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This Item
SAB4501990SAB1305889SAB4501993
conjugate

unconjugated

conjugate

unconjugated

conjugate

-

conjugate

unconjugated

Quality Level

100

Quality Level

100

Quality Level

100

Quality Level

100

biological source

rabbit

biological source

rabbit

biological source

rabbit

biological source

rabbit

species reactivity

human

species reactivity

human

species reactivity

human

species reactivity

rat, human, mouse

storage temp.

−20°C

storage temp.

−20°C

storage temp.

−20°C

storage temp.

−20°C

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General description

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.

Immunogen

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

Immunogen Range: 874-923

Biochem/physiol Actions

NF-κB (nuclear factor κ B subunit 1) 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.

Features and Benefits

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.

Physical form

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

Storage Class

10 - Combustible liquids

wgk_germany

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable


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Kai Fu et al.
eLife, 5, 1-12 (2016-12-21)
Previously we reported that Src-associated-substrate-during-mitosis-of-68kDa (Sam68/KHDRBS1) is pivotal for DNA damage-stimulated NF-κB transactivation of anti-apoptotic genes (Fu et al., 2016). Here we show that Sam68 is critical for genotoxic stress-induced NF-κB activation in the γ-irradiated colon and animal and that
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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