免 疫 原：Recombinant human IKB alpha Protein
抗原表位：1-77/314
SWISS：P25963
Gene ID ：4792
Human Gene ID：4792

Three major forms of IKB like molecules have been identified and each is characterised 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 cRel containing forms of NFkB and block nuclear import by masking the nuclear localisation sequences of NFkB. The activation of NFkB involves the inducible phosphorylation and subsequent degradation of IKB. Immunoblotting easily detects the hyperphosphorylated 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. Bcl3 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.
Function：Inhibits the activity of dimeric NF-kappa-B/REL complexes by trapping REL dimers in the cytoplasm through masking of their nuclear localization signals. On cellular stimulation by immune and proinflammatory responses, becomes phosphorylated promoting ubiq
Subunit：Interacts with RELA; the interaction requires the nuclear import signal. Interacts with NKIRAS1 and NKIRAS2. Part of a 70-90 kDa complex at least consisting of CHUK, IKBKB, NFKBIA, RELA, IKBKAP and MAP3K14. Interacts with HBV protein X. Interacts with RWD
Subcellular Location：Cytoplasm. Nucleus.
Tissue Specificity：Highly expressed in lymph node, thymus followed by liver, brain, muscle, kidney, gastrointestinal and reproductive tract.
Post-translational modifications：Phosphorylated; disables inhibition of NF-kappa-B DNA-binding activity.
Phosphorylation at positions 32 and 36 is prerequisite to recognition by UBE2D3 leading to polyubiquitination and subsequent degradation.
Sumoylated; sumoylation requires the
DISEASE：Defects in NFKBIA are the cause of ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant (ADEDAID) [MIM:612132]. Ectodermal dysplasia defines a heterogeneous group of disorders due to abnormal development of two or more ectoderma
Similarity：Belongs to the NF-kappa-B inhibitor family.
Contains 5 ANK repeats.
Important Note：This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.