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Merck

SAB4501989

Sigma-Aldrich

Anti-NF-κB p105 antibody produced in rabbit

affinity isolated antibody

別名:

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

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About This Item

UNSPSCコード:
12352203
NACRES:
NA.41

由来生物

rabbit

結合体

unconjugated

抗体製品の状態

affinity isolated antibody

抗体製品タイプ

primary antibodies

クローン

polyclonal

形状

buffered aqueous solution

分子量

antigen 105 kDa

化学種の反応性

rat, mouse, human

濃度

~1 mg/mL

テクニック

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

NCBIアクセッション番号

UniProtアクセッション番号

輸送温度

wet ice

保管温度

−20°C

ターゲットの翻訳後修飾

unmodified

遺伝子情報

human ... NFKB1(4790)

関連するカテゴリー

詳細

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

生物化学的/生理学的作用

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.

特徴および利点

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.

物理的形状

ウサギIgGのPBS溶液(Mg2+およびCa2+を含まず)、pH 7.4、150 mM NaCl、0.02% アジ化ナトリウム、50% グリセロール

免責事項

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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保管分類コード

10 - Combustible liquids

WGK

nwg

引火点(°F)

Not applicable

引火点(℃)

Not applicable


試験成績書(COA)

製品のロット番号・バッチ番号を入力して、試験成績書(COA) を検索できます。ロット番号・バッチ番号は、製品ラベルに「Lot」または「Batch」に続いて記載されています。

以前この製品を購入いただいたことがある場合

文書ライブラリで、最近購入した製品の文書を検索できます。

文書ライブラリにアクセスする

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
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
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

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