Phospho-NFKBIA (Tyr42)磷酸化IKB α抗体

本公司经销Phospho-NFKBIA （Tyr42），磷酸化IKB α抗体，克隆类型为polyclonal，宿主来源是Rabbit，Phospho-NFKBIA （Tyr42）磷酸化IKB α抗体可应用于WB、elisa、IP、IF、IHC等实验，欢迎垂询订购！

货号：BY-5514R
英文名称：Anti-Phospho-NFKBIA （Tyr42）
中文名称：磷酸化IKB α抗体
其他名称：名phospho-NFKBIA（Tyr42）; NFKBIA（phospho Y42）; IKB-alpha（Phospho-Tyr42）; IKB alpha; 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.
抗体来源：Rabbit
克隆类型：polyclonal
蛋白分子量：predicted molecular weight: 35kDa
纯化方法：affinity purified by Protein A
交叉反应：hu, mo, pig, shp, cow, Rb
产品介绍：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].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. Note=Shuttles between the nucleus ａnd the cytoplasm by a nuclear localization signal （NLS） ａnd a CRM1-dependent nuclear export.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.