ARG65808

anti-TNFAIP3 / A20 antibody

anti-TNFAIP3 / A20 antibody for ICC/IF,IHC-Formalin-fixed paraffin-embedded sections,Western blot and Human,Mouse,Rat

publication_link 参考文献1

概述

产品描述 Rabbit Polyclonal antibody recognizes TNFAIP3 / A20
反应物种 Hu, Ms, Rat
应用 ICC/IF, IHC-P, WB
宿主 Rabbit
克隆 Polyclonal
同位型 IgG
靶点名称 TNFAIP3 / A20
抗原物种 Human
抗原 KLH-conjugated synthetic peptide around the center region of Human A20.
偶联标记 Un-conjugated
別名 A20; OTUD7C; EC 6.3.2.-; Zinc finger protein A20; Tumor necrosis factor alpha-induced protein 3; Putative DNA-binding protein A20; TNFA1P2; OTU domain-containing protein 7C; TNF alpha-induced protein 3; EC 3.4.19.12

应用说明

应用建议
应用 推荐稀释比
ICC/IF1:100 - 1:500
IHC-P1:100 - 1:200
WB1:500 - 1:1000
应用说明 IHC-P: Antigen Retrieval: Boil tissue sections in Sodium citrate buffer (pH 6.0)
* The dilutions indicate recommended starting dilutions and the optimal dilutions or concentrations should be determined by the scientist.

属性

形式 Liquid
纯化 Affinity purification with immunogen.
缓冲液 Liquid (pH 7.3), 0.42% Potassium phosphate, 0.87% NaCl, 0.01% Sodium azide and 30% Glycerol.
抗菌剂 0.01% Sodium azide
稳定剂 30% Glycerol
存放说明 For continuous use, store undiluted antibody at 2-8°C for up to a week. For long-term storage, aliquot and store at -20°C. Storage in frost free freezers is not recommended. Avoid repeated freeze/thaw cycles. Suggest spin the vial prior to opening. The antibody solution should be gently mixed before use.
注意事项 For laboratory research only, not for drug, diagnostic or other use.

生物信息

数据库连接

GeneID: 21929 Mouse TNFAIP3

GeneID: 7128 Human TNFAIP3

Swiss-port # P21580 Human Tumor necrosis factor alpha-induced protein 3

Swiss-port # Q60769 Mouse Tumor necrosis factor alpha-induced protein 3

基因名称 TNFAIP3
全名 tumor necrosis factor, alpha-induced protein 3
背景介绍 This gene was identified as a gene whose expression is rapidly induced by the tumor necrosis factor (TNF). The protein encoded by this gene is a zinc finger protein and ubiqitin-editing enzyme, and has been shown to inhibit NF-kappa B activation as well as TNF-mediated apoptosis. The encoded protein, which has both ubiquitin ligase and deubiquitinase activities, is involved in the cytokine-mediated immune and inflammatory responses. Several transcript variants encoding the same protein have been found for this gene. [provided by RefSeq, Jul 2012]
生物功能 Ubiquitin-editing enzyme that contains both ubiquitin ligase and deubiquitinase activities. Involved in immune and inflammatory responses signaled by cytokines, such as TNF-alpha and IL-1 beta, or pathogens via Toll-like receptors (TLRs) through terminating NF-kappa-B activity. Essential component of a ubiquitin-editing protein complex, comprising also RNF11, ITCH and TAX1BP1, that ensures the transient nature of inflammatory signaling pathways. In cooperation with TAX1BP1 promotes disassembly of E2-E3 ubiquitin protein ligase complexes in IL-1R and TNFR-1 pathways; affected are at least E3 ligases TRAF6, TRAF2 and BIRC2, and E2 ubiquitin-conjugating enzymes UBE2N and UBE2D3. In cooperation with TAX1BP1 promotes ubiquitination of UBE2N and proteasomal degradation of UBE2N and UBE2D3. Upon TNF stimulation, deubiquitinates 'Lys-63'-polyubiquitin chains on RIPK1 and catalyzes the formation of 'Lys-48'-polyubiquitin chains. This leads to RIPK1 proteasomal degradation and consequently termination of the TNF- or LPS-mediated activation of NF-kappa-B. Deubiquitinates TRAF6 probably acting on 'Lys-63'-linked polyubiquitin. Upon T-cell receptor (TCR)-mediated T-cell activation, deubiquitinates 'Lys-63'-polyubiquitin chains on MALT1 thereby mediating disassociation of the CBM (CARD11:BCL10:MALT1) and IKK complexes and preventing sustained IKK activation. Deubiquitinates NEMO/IKBKG; the function is facilitated by TNIP1 and leads to inhibition of NF-kappa-B activation. Upon stimulation by bacterial peptidoglycans, probably deubiquitinates RIPK2. Can also inhibit I-kappa-B-kinase (IKK) through a non-catalytic mechanism which involves polyubiquitin; polyubiquitin promotes association with IKBKG and prevents IKK MAP3K7-mediated phosphorylation. Targets TRAF2 for lysosomal degradation. In vitro able to deubiquitinate 'Lys-11'-, 'Lys-48'- and 'Lys-63' polyubiquitin chains. Inhibitor of programmed cell death. Has a role in the function of the lymphoid system. Required for LPS-induced production of proinflammatory cytokines and IFN beta in LPS-tolerized macrophages. [UniProt]
预测分子量 90 kDa
翻译后修饰 Proteolytically cleaved by MALT1 upon TCR stimulation; disrupts NF-kappa-B inhibitory function and results in increased IL-2 production. It is proposed that only a fraction of TNFAIP3 colocalized with TCR and CBM complex is cleaved, leaving the main TNFAIP3 pool intact.

检测图片 (3) Click the Picture to Zoom In

  • ARG65808 anti-TNFAIP3 / A20 antibody ICC/IF image

    Immunofluorescence: Formalin-fixed HeLa cells were permeabilized with 0.1% Triton X-100 in TBS for 5-10 min and blocked with 3% BSA-PBS for 30 min at RT. Cells were stained with ARG65808 anti-TNFAIP3 / A20 antibody in 3% BSA-PBS and incubated overnight at 4°C in a humidified chamber. Cells were washed with PBST and incubated with a DyLight 594-conjugated secondary antibody (red) in PBS at RT in the dark. DAPI was used to stain the cell nuclei (blue).

  • ARG65808 anti-TNFAIP3 / A20 antibody IHC-P image

    Immunohistochemistry: Formalin-fixed and paraffin-embedded Human lung cancer. Antigen retrieval: Boil tissue sections in Sodium citrate buffer (pH 6.0). The section was then incubated with ARG65808 anti-TNFAIP3 / A20 antibody at RT and detected using an HRP conjugated compact polymer system. DAB was used as the chromogen. The section was then counterstained with haematoxylin and mounted with DPX.

  • ARG65808 anti-TNFAIP3 / A20 antibody WB image

    Western blot: HeLa, Daudi and RAW264.7 whole cell lysates stained with ARG65808 anti-TNFAIP3 / A20 antibody.

文献引用

Decrease of miR-19b-3p in Brain Microvascular Endothelial Cells Attenuates Meningitic Escherichia coli-Induced Neuroinflammation via TNFAIP3-Mediated NF-κB Inhibition.

WB / Human

Amjad Nouman et al.
Pathogens.,  (2019)

publication_link

 

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