This gene encodes a member of the NF-kappa-B inhibitor family, which contain multiple ankrin repeat domains. The encoded protein interacts with REL dimers to inhibit NF-kappa-B/REL complexes which are involved in inflammatory responses. The encoded protein moves between the Cytoplasm and the nucleus via a nuclear localization signal and CRM1-mediated nuclear export. Mutations in this gene have been found in ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant disease. [provided by RefSeq, Aug 2011]
Catalog No
A1053
Reactivity
Human, Mouse, Rat, Monkey
Applications
WB, IHC-p, IF(paraffin section), ELISA
Modification
Phospho Specific
Source
Polyclonal Rabbit
Dilution
Western Blot: 1/500 - 1/2000. Immunohistochemistry: 1/100 - 1/300. ELISA: 1/5000. Not yet tested in other applications.
Purification
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Concentration
1 mg/ml
Storage and Stability
-20°C/1 year
Other Name
NFKBIA; IKBA; MAD3; NFKBI; NF-kappa-B inhibitor alpha; I-kappa-B-alpha; IkB-alpha; IkappaBalpha; Major histocompatibility complex enhancer-binding protein MAD3
Molecular Weight (Da)
35609
Gene Name
NFKBIA
Protein Name
NF-kappa-B inhibitor alpha
Human Gene ID
4792
Human Swiss Prot No.
P25963
Immunogen
The antiserum was produced against synthesized peptide derived from human IkappaB-alpha around the phosphorylation site of Tyr305. AA range:268-317
Specificity
Phospho-IκB-α (Y305) Polyclonal Antibody detects endogenous levels of IκB-α protein only when phosphorylated at Y305.
Formulation
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Western blot analysis of lysates from COS7 cells treated with nocodazole 1ug/ml 16h, using IkappaB-alpha (Phospho-Tyr305) Antibody. The lane on the right is blocked with the phospho peptide.
Immunohistochemistry analysis of paraffin-embedded human lymph node, using IkappaB-alpha (Phospho-Tyr305) Antibody. The picture on the right is blocked with the phospho peptide.