英文名称IKB alpha
中文名称核因子κB抑制蛋白α抗体
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. IκB-α,
JournalPMIDIFApplicationACS Nano (2015)2638970912.8810WBThe Journal of Headache and Pain (2016)271501052.8000WBJournal of Ethnopharmacology (2013)244323692.7550WBLife Sciences (2016)266564672.7020WBEuropean journal of pharmacology (2010)204707702.5920WBInternational Immunopharmacology (2016)266441682.4720WBJournal of Surgical Research (2015)261527932.1210WBCardiovascular Toxicology (2015)261380961.7210WB
说 明 书50ul 100ul 200ul
研究领域肿瘤 **学 信号转导 转录调节因子 激酶和磷酸酶
抗体来源Rabbit
克隆类型Polyclonal
IKB alpha抗体交叉反应 Human, Mouse, Rat,
产品应用WB=1:500-2000 ELISA=1:500-1000 IHC-P=1:400-800 IHC-F=1:400-800 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
细胞定位细胞核 细胞浆
性 状Lyophilized or Liquid
浓 度1mg/1ml
免 疫 原KLH conjugated synthetic peptide derived from human IKB alpha
亚 型IgG
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.
PubMedPubMed
产品介绍background:
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 ubiquitination and degradation, enabling the dimeric RELA to translocate to the nucleus and activate transcription.
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. 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.
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 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.
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.
Similarity:
Belongs to the NF-kappa-B inhibitor family.
Contains 5 ANK repeats.
SWISS:
Q9Z1E3
Gene ID:
4792