|别 名||NFKBIA; Inhibitor of KB alpha; I kappa B alpha; I(Kappa)B(alpha); IkappaBalpha; IKBA; IKBalpha; MAD 3; MAD3; Major histocompatibility complex enhancer binding protein MAD3; NF kappa B 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; IKBA_HUMAN.|
|研究领域||肿瘤 免疫学 信号转导 转录调节因子 激酶和磷酸酶|
|交叉反应||Human, Mouse, Rat,|
|产品应用||WB=1:500-2000 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 Flow-Cyt=1μg/Test IF=1:100-500 （石蜡切片需做抗原修复）
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
|分 子 量||36kDa|
|性 状||Lyophilized or Liquid|
|免 疫 原||KLH conjugated synthetic peptide derived from human IKB alpha:1-120/314|
|纯化方法||affinity purified by Protein A|
|储 存 液||0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.|
|保存条件||Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.|
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.
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 translocate to the nucleus and activate transcription.
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. Interacts (when phosphorylated at the 2 serine residues in the destruction motif D-S-G-X(2,3,4)-S) with BTRC. Associates with the SCF(BTRC) complex, composed of SKP1, CUL1 and BTRC; the association is mediated via interaction with BTRC. Part of a SCF(BTRC)-like complex lacking CUL1, which is associated with RELA; RELA interacts directly with NFKBIA. Interacts with PRMT2. Interacts with PRKACA in platelets; this interaction is disrupted by thrombin and collagen. Interacts with HIF1AN.
Highly expressed in lymph node, thymus followed by liver, brain, muscle, kidney, gastrointestinal and reproductive tract.
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 presence of the nuclear import signal.
Monoubiquitinated at Lys-21 and/or Lys-22 by UBE2D3. Ubiquitin chain elongation is then performed by CDC34 in cooperation with the SCF(FBXW11) E3 ligase complex, building ubiquitin chains from the UBE2D3-primed NFKBIA-linked ubiquitin. The resulting polyubiquitination leads to protein degradation. Also ubiquitinated by SCF(BTRC) following stimulus-dependent phosphorylation at Ser-32 and Ser-36.
Deubiquitinated by porcine reproductive and respiratory syndrome virus Nsp2 protein, which thereby interferes with NFKBIA degradation and impairs subsequent NF-kappa-B activation.
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.
Belongs to the NF-kappa-B inhibitor family.
Contains 5 ANK repeats.
Entrez Gene: 18035 Mouse
Omim: 164008 Human
SwissProt: P25963 Human
SwissProt: Q9Z1E3 Mouse
Unigene: 81328 Human
Unigene: 170515 Mouse
Unigene: 12550 Rat
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
|Alexa Fluor 350 标记|
|Alexa Fluor 488 标记|
|Alexa Fluor 555 标记|
|Alexa Fluor 594 标记|
|Alexa Fluor 647 标记|