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Description
A20/TNFAIP3 Recombinant Rabbit mAb (S-2578-5)Product Specification Host Rabbit Antigen A20 TNFAIP3 Synonyms Tumor necrosis factor alpha induced protein 3; TNF alpha induced protein 3; OTU domain containing protein 7C; Putative DNA binding protein A20; Zinc finger protein A20; OTUD7C Immunogen Synthetic Peptide Location Cytoplasm, Nucleus, Lysosome Accession P21580 Clone Number S 2578 5 Antibody Type Recombinant mAb Isotype IgG Application WB Reactivity Hu Positive Sample Jurkat, HeLa, U 87 MG,
Product Specification
| Host | Rabbit |
| Antigen | A20/TNFAIP3 |
| Synonyms | Tumor necrosis factor alpha-induced protein 3; TNF alpha-induced protein 3; OTU domain-containing protein 7C; Putative DNA-binding protein A20; Zinc finger protein A20; OTUD7C |
| Immunogen | Synthetic Peptide |
| Location | Cytoplasm, Nucleus, Lysosome |
| Accession | P21580 |
| Clone Number | S-2578-5 |
| Antibody Type | Recombinant mAb |
| Isotype | IgG |
| Application | WB |
| Reactivity | Hu |
| Positive Sample | Jurkat, HeLa, U-87 MG, MDA-MB-231 |
| Purification | Protein A |
| Concentration | 0.5 mg/ml |
| Conjugation | Unconjugated |
| Physical Appearance | Liquid |
| Storage Buffer | PBS, 40% Glycerol, 0.05% BSA, 0.03% Proclin 300 |
| Stability & Storage | 12 months from date of receipt / reconstitution, -20 °C as supplied |
Dilution
| application | dilution | species |
| WB | 1:1000 | Hu |
Background
A20/TNFAIP3 is a 790-residue cytoplasmic zinc-finger deubiquitinase and E3 ubiquitin ligase whose dual enzymatic activities act as a pivotal negative feedback brake on NF-κB, IRF3, RIPK1 and NLRP3 inflammasome signaling by cleaving K63-linked polyubiquitin chains from adaptor proteins such as TRAF6, NEMO and RIPK2 while simultaneously assembling K48-linked ubiquitin onto these same targets to promote their proteasomal degradation, thereby preventing excessive inflammatory cytokine, type-I interferon and cell death responses; its expression is rapidly up-regulated by NF-κB itself and by type-I interferons, creating an autoregulatory loop that is indispensable for immune homeostasis, because germline loss-of-function variants cause auto-inflammatory or autoimmune disorders in humans—such as haploinsufficiency leading to Behçet-like disease, psoriasis or systemic lupus erythematosus—whereas somatic inactivation is frequently observed in B-cell lymphomas, promoting malignant survival, making A20/TNFAIP3 both a critical rheostat of innate immunity and a tumor suppressor whose manipulation is a promising therapeutic target in chronic inflammation and cancer.
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