产品名称
IκB α (2A5) Mouse Monoclonal Antibody
别名
NF-kappa-B inhibitor alpha (I-kappa-B-alpha) (IkB-alpha) (IkappaBalpha) (Major histocompatibility complex enhancer-binding protein MAD3)
基因名称
NFKBIA IKBA MAD3 NFKBI
蛋白名称
NF-kappa-B inhibitor alpha
存储缓冲液
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.44% New type preservative N.
Human Gene Link
https://www.uniprot.org/uniprot/4792
Human Swissprot No.
P25963
Human Swissprot Link
https://www.uniprot.org/uniprotkb/P25963/entry
Mouse Gene Link
https://www.uniprot.org/uniprot/18035
Mouse Swissprot No.
Q9Z1E3
Mouse Swissprot Link
https://www.uniprot.org/uniprotkb/Q9Z1E3
Rat Gene Link
https://www.uniprot.org/uniprot/25493
Rat Swissprot Link
https://www.uniprot.org/uniprotkb/Q63746
免疫原
Synthesized peptide derived from human IκB α
特异性
This antibody detects endogenous levels of IκB α at Human, Mouse,Rat
稀释度
IHC-p1:50-200 ,WB 1:1000-2000
背景介绍
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],
组织表达
Brain,Kidney,Lymph node,Monocyte,
细胞定位
Cytoplasm. Nucleus. Shuttles between the nucleus and the cytoplasm by a nuclear localization signal (NLS) and a CRM1-dependent nuclear export. .
功能
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.,
纯化
The antibody was affinity-purified from mouse ascites by affinity-chromatography using specific immunogen.
