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Merck
CN

05-535

Anti-IKKβ Antibody, clone 10AG2

clone 10AG2, Upstate®, from mouse

Synonym(s):

I-kappa-B kinase 2, I-kappa-B-kinase beta, Nuclear factor NF-kappa-B inhibitor kinase beta, inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase beta, inhibitor of nuclear factor kappa B kinase beta subunit

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702

Key Documents

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Product Name

Anti-IKKβ Antibody, clone 10AG2, clone 10AG2, Upstate®, from mouse

biological source

mouse

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

10AG2, monoclonal

species reactivity

rat, human, mouse

manufacturer/tradename

Upstate®

technique(s)

western blot: suitable

isotype

IgG1

NCBI accession no.

NM_001556

UniProt accession no.

O14920

shipped in

dry ice

target post-translational modification

unmodified

Quality Level

100

Gene Information

mouse ... Ikbkb(16150)

Analysis Note

Control
Positive Antigen Control: Catalog #12-303, Jurkat cell lysate.
Routinely evaluated by western blot on human Jurkat RIPA cell lysate, human A431, HeLa nuclear extract, mouse 3T3/A31 or rat PC-12 RIPA cell lysates.

Western Blot Analysis:
0.5-2 µg/mL of this lot detected IKK/IKK2 in human HeLa cell lysate. A previous lot was tested in human Jurkat RIPA cell lysate, A431, extract, mouse 3T3/A31 and rat PC-12 RIPA cell lysates.

Application

Anti-IKKβ Antibody, clone 10AG2 detects level of IKKβ & has been published & validated for use in WB.

Biochem/physiol Actions

Other species not tested.
This antibody recognizes IKKβ/IKK2, Mr 87 kDa.

General description

87 kDa
IKK beta (I-Kappa-B kinase-beta) is a member of the IKK complex which is composed of IKK alpha, IKK beta, IKK gamma and IKAP. Phosphorylation of I-Kappa-B on a serine residue by the IKK complex frees NF-kB from I-Kappa-B and marks it for degradation via ubiquination. IKK beta has been shown to activate NF-kB and phosphorylate IKB alpha and beta. Phosphorylation of 2 sites at the activation loop of IKK beta is essential for activation of IKK by TNF and IL1. Once activated, IKK beta autophosphorylates which in turn decreases IKK activity and prevents prolonged activation of the inflammatory response. Additionally, IKK beta activity can also be regulated by MEKK-1.

Immunogen

His-tagged, full length human IKKβ/IKK2. Clone: 10AG2.

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Physical form

Format: Purified
Purified mouse monoclonal IgG1 in buffer containing PBS and 0.05% sodium azide. Frozen solution.

Legal Information

UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany

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Storage Class

12 - Non Combustible Liquids

wgk

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Serine phosphorylation of insulin receptor substrate 1 by inhibitor kappa B kinase complex.
Gao, Z; Hwang, D; Bataille, F; Lefevre, M; York, D; Quon, MJ; Ye, J
The Journal of Biological Chemistry null
Siddharth Bakshi et al.
The Biochemical journal, 474(7), 1163-1174 (2017-02-06)
The double-stranded RNA mimetic poly(I:C) and lipopolysaccharide (LPS) activate Toll-like receptors 3 (TLR3) and TLR4, respectively, triggering the activation of TANK (TRAF family member-associated NF-κB activator)-binding kinase 1 (TBK1) complexes, the phosphorylation of interferon regulatory factor 3 (IRF3) and transcription
zVAD-induced necroptosis in L929 cells depends on autocrine production of TNF? mediated by the PKC-MAPKs-AP-1 pathway.
Wu, YT; Tan, HL; Huang, Q; Sun, XJ; Zhu, X; Shen, HM
Cell Death and Differentiation null
Crystal structure of inhibitor of ?B kinase ?.
Xu, G; Lo, YC; Li, Q; Napolitano, G; Wu, X; Jiang, X; Dreano, M; Karin, M; Wu, H
Nature null
Daniela S Bassères et al.
Genes & cancer, 5(1-2), 41-55 (2014-06-24)
Activating mutations in KRAS are prevalent in cancer, but therapies targeted to oncogenic RAS have been ineffective to date. These results argue that targeting downstream effectors of RAS will be an alternative route for blocking RAS-driven oncogenic pathways. We and
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