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IKB beta antibody

Cat. No. GTX27547

Host

 Rabbit

Clonality

 Polyclonal

Isotype

 IgG

Application

 WB, ELISA

Reactivity

 Human, Mouse, Rat
Package
50 μl ($399)
See all IKB beta products

APPLICATION

Application Note

*Optimal dilutions/concentrations should be determined by the researcher.
Application Recommended Dilution
WB 1:500 - 1:3000
ELISA 1:5000 - 1:25000
Not tested in other applications.

Calculated MW

38 kDa. ( Note )

Positive Control

A control peptide is available, GTX27548

PROPERTIES

Form

Liquid

Buffer

Serum

Preservative

0.01% Sodium azide

Storage

Store as concentrated solution. Centrifuge briefly prior to opening vial. For short-term storage (1-2 weeks), store at 4ºC. For long-term storage, aliquot and store at -20ºC or below. Avoid multiple freeze-thaw cycles.

Antigen Species

Human

Immunogen

IkBb peptide corresponding to a region near the C-terminus of the human protein conjugated to Keyhole Limpet Hemocyanin (KLH).

Purification

Antiserum
This product was prepared from monospecific antiserum by delipidation and defibrination.

Conjugation

Unconjugated

Note

For laboratory research use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.

Purchasers shall not, and agree not to enable third parties to, analyze, copy, reverse engineer or otherwise attempt to determine the structure or sequence of the product.

TARGET

Synonyms

NFKB inhibitor beta , IKBB , TRIP9

Cellular Localization

Cytoplasm,Nucleus

Background

Three major forms of IkB-like molecules have been identified and each is characterized by multiple copies of ankyrin repeats. IkB-alpha and IkB-beta appear to be the major regulatory forms of IkB in most cells. These proteins interact with p65 or c-Rel containing forms of NFkB and block nuclear import by masking the nuclear localization sequences of NFkB. The activation of NFkB involves the inducible phosphorylation and subsequent degradation of IkB. Immunoblotting easily detects the hyper-phosphorylated forms of IkB-alpha, but not phosphorylated IkB-beta. Interestingly, IkB-alpha and IkB-beta mediate different NFkB responses. IkB-alpha appears to control more transient activation of NFkB in response to an inducer, while IkB-beta controls a persistent response. Bcl-3 interacts with p50 and p52 containing forms of NFkB, but rather than being an inhibitor it appears to function to stimulate transcription. The degradation of IkB is confirmed by immunoblotting.

Database

Research Area

REFERENCE

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REVIEW

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SDS
Sodium Azide.pdf
Package List Price ($)
$ 399