The antiserum was produced against synthesized peptide derived from human IkappaB-alpha around the phosphorylation site of Ser32/Ser36. AA range:15-64

This antibody detects endogenous levels of IκB-α only when phosphorylated at Ser32 or Ser36.and dually phosphorylated at two sites.The name of modified sites may be influenced by many factors, such as species (the modified site was not originally found in human samples) and the change of protein sequence (the previous protein sequence is incomplete, and the protein sequence may be prolonged with the development of protein sequencing technology). When naming, we will use the "numbers" in historical reference to keep the sites consistent with the reports. The antibody binds to the following modification sequence (lowercase letters are modification sites):RHDsGLDsM

NFKBIA IKBA MAD3 NFKBI

NF-kappa-B inhibitor alpha

NFKBIA ;
IKBA ;
MAD3 ;
NFKBI ;
NF-kappa-B inhibitor alpha ;
I-kappa-B-alpha ;
IkB-alpha ;
IkappaBalpha ;
Major histocompatibility complex enhancer-binding protein MAD3

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],

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 ectodermal structures. ADEDAID is an ectodermal dysplasia associated with decreased production of pro-inflammatory cytokines and certain interferons, rendering patients susceptible to infection.,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 ubiquitination and degradation, enabling the dimeric RELA to tranlocate to the nucleus and activate transcription.,induction:Induced in adherent monocytes.,online information:NFKBIA mutation db,PTM:Phosphorylated; disables inhibition of NF-kappa-B DNA-binding activity.,PTM:Sumoylated; sumoylation requires the presence of the nuclear import signal.,PTM:Ubiquitinated; subsequent to stimulus-dependent phosphorylation on serines.,similarity:Belongs to the NF-kappa-B inhibitor family.,similarity:Contains 5 ANK repeats.,subcellular location:Shuttles between the nucleus and the cytoplasm by a nuclear localization signal (NLS) and a CRM1-dependent nuclear export.,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 RWDD3; the interaction enhances sumoylation.,

Cytoplasm. Nucleus. Shuttles between the nucleus and the cytoplasm by a nuclear localization signal (NLS) and a CRM1-dependent nuclear export. .

Brain,Kidney,Lymph node,Monocyte,

>>cAMP signaling pathway ;
>>Chemokine signaling pathway ;
>>NF-kappa B signaling pathway ;
>>Apoptosis ;
>>Osteoclast differentiation ;
>>Toll-like receptor signaling pathway ;
>>NOD-like receptor signaling pathway ;
>>RIG-I-like receptor signaling pathway ;
>>Cytosolic DNA-sensing pathway ;
>>C-type lectin receptor signaling pathway ;
>>IL-17 signaling pathway ;
>>Th1 and Th2 cell differentiation ;
>>Th17 cell differentiation ;
>>T cell receptor signaling pathway ;
>>B cell receptor signaling pathway ;
>>TNF signaling pathway ;
>>Neurotrophin signaling pathway ;
>>Adipocytokine signaling pathway ;
>>Relaxin signaling pathway ;
>>Insulin resistance ;
>>Alcoholic liver disease ;
>>Epithelial cell signaling in Helicobacter pylori infection ;
>>Pathogenic Escherichia coli infection ;
>>Shigellosis ;
>>Salmonella infection ;
>>Legionellosis ;
>>Yersinia infection ;
>>Leishmaniasis ;
>>Chagas disease ;
>>Toxoplasmosis ;
>>Hepatitis C ;
>>Hepatitis B ;
>>Measles ;
>>Human cytomegalovirus infection ;
>>Influenza A ;
>>Human T-cell leukemia virus 1 infection ;
>>Kaposi sarcoma-associated herpesvirus infection ;
>>Herpes simplex virus 1 infection ;
>>Epstein-Barr virus infection ;
>>Human immunodeficiency virus 1 infection ;
>>Coronavirus disease - COVID-19 ;
>>Pathways in cancer ;
>>Viral carcinogenesis ;
>>Chemical carcinogenesis - reactive oxygen species ;
>>Prostate cancer ;
>>Chronic myeloid leukemia ;
>>Small cell lung cancer ;
>>PD-L1 expression and PD-1 checkpoint pathway in cancer ;
>>Lipid and atherosclerosis