Merck

SAB4501989

Sigma-Aldrich

Anti-NF-κB p105 antibody produced in rabbit

affinity isolated antibody

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

生物来源

rabbit

质量水平

偶联物

unconjugated

抗体形式

affinity isolated antibody

antibody product type

primary antibodies

克隆

polyclonal

形式

buffered aqueous solution

分子量

antigen 105 kDa

species reactivity

rat, mouse, human

浓度

~1 mg/mL

technique(s)

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

NCBI登记号

UniProt登记号

运输

wet ice

储存温度

−20°C

target post-translational modification

unmodified

Gene Information

human ... NFKB1(4790)

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此商品
SAB4501990SAB4501991SAB4501993
conjugate

unconjugated

conjugate

unconjugated

conjugate

unconjugated

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody form

affinity isolated antibody

antibody form

affinity isolated antibody

antibody form

affinity isolated antibody

clone

polyclonal

clone

polyclonal

clone

polyclonal

clone

polyclonal

form

buffered aqueous solution

form

buffered aqueous solution

form

buffered aqueous solution

form

buffered aqueous solution

mol wt

antigen 105 kDa

mol wt

antigen 105 kDa

mol wt

antigen 105 kDa

mol wt

antigen 96 kDa

一般描述

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.

免疫原

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

Immunogen Range: 304-353

生化/生理作用

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.

特点和优势

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.

外形

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

免责声明

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.

储存分类代码

10 - Combustible liquids

WGK

nwg

闪点(F)

Not applicable

闪点(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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