Phospho-IkappaB alpha (Ser32) (14D4) Rabbit Monoclonal Antibody (BSA and Azide Free)#71278,Cell Signaling Technology (CST),71278

Phospho-IkappaB alpha (Ser32) (14D4) Rabbit Monoclonal Antibody (BSA and Azide Free) detects endogenous levels of IκBα only when phosphorylated at Ser32.

Host

Rabbit

Reactivity

Human, Mouse, Rat, Monkey

Platform ID

BAB622435554

Cell Signaling Technology (CST)

Headquarters

3 Trask Lane Danvers, MA 01923

Contact

Tel: 877-616-2355,978-867-2388
Fax: 877-616-2355

Product Specifications
Scientific Background
Synonyms

Specifications

NamePhospho-IkappaB alpha (Ser32) (14D4) Rabbit Monoclonal Antibody (BSA and Azide Free)#71278
Cat. No.71278
Accession NumberP25963
Gene ID (Entrez)25963, 4792
HostRabbit
SensitivityEndogenous
ReactivityHuman, Mouse, Rat, Monkey
Molecular Weight40
ImmunogenIgG
FormulationThis product is the carrier free version of product #2859. All data were generated using the same antibody clone in the standard formulation which contains BSA and glycerol.This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, pleasecontact us. Optimal dilutions/concentrations should be determined by the end user.BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity.
StorageStore at -20°C.This product will freeze at -20°C so it is recommended to aliquot into single-use vials to avoid multiple freeze/thaw cycles.A slight precipitate may be present and can be dissolved by gently vortexing. This will not interfere with antibody performance.
Regulatory StatusResearch Use Only

Scientific Background

The NF-κB/Rel transcription factors are present in the cytosol in an inactive state complexed with the inhibitory IκB proteins (1-3). Activation occurs via phosphorylation of IκBα at Ser32 and Ser36 followed by proteasome-mediated degradation that results in the release and nuclear translocation of active NF-κB (3-7). IκBα phosphorylation and resulting Rel-dependent transcription are activated by a highly diverse group of extracellular signals including inflammatory cytokines, growth factors, and chemokines. Kinases that phosphorylate IκB at these activating sites have been identified (8).Baeuerle, P.A. and Baltimore, D. (1988)Science242, 540-6.Beg, A.A. and Baldwin, A.S. (1993)Genes Dev7, 2064-70.Finco, T.S. et al. (1994)Proc Natl Acad Sci USA91, 11884-8.Brown, K. et al. (1995)Science267, 1485-8.Brockman, J.A. et al. (1995)Mol Cell Biol15, 2809-18.Traenckner, E.B. et al. (1995)EMBO J14, 2876-83.Chen, Z.J. et al. (1996)Cell84, 853-62.Karin, M. and Ben-Neriah, Y. (2000)Annu Rev Immunol18, 621-63.Alternate NamesEDAID2; I-kappa-B-alpha; IkappaBalpha; IkB-alpha; IKBA; MAD-3; MAD3; Major histocompatibility complex enhancer-binding protein MAD3; NF-kappa-B inhibitor alpha; NFKB inhibitor alpha; NFKBI; NFKBIA; nuclear factor of kappa light chain gene enhancer in B-cells; nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha

Synonyms

EDAID2; I-kappa-B-alpha; IkappaBalpha; IkB-alpha; IKBA; MAD-3; MAD3; Major histocompatibility complex enhancer-binding protein MAD3; NF-kappa-B inhibitor alpha; NFKB inhibitor alpha; NFKBI; NFKBIA; nuclear factor of kappa light chain gene enhancer in B-cells; nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha

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