WB result of A20/TNFAIP3 Recombinant Rabbit mAb
Primary antibody: A20/TNFAIP3 Recombinant Rabbit mAb at 1/1000 dilution
Lane 1: MCF7 whole cell lysate 20 µg
Lane 2: T-47D whole cell lysate 20 µg
Lane 3: Jurkat whole cell lysate 20 µg
Lane 4: HeLa whole cell lysate 20 µg
Lane 5: U-87 MG whole cell lysate 20 µg
Lane 6: MDA-MB-231 whole cell lysate 20 µg
Low expression control: MCF7 whole cell lysate; T-47D whole cell lysate
Secondary antibody: Goat Anti-rabbit IgG, (H+L), HRP conjugated at 1/10000 dilution
Predicted MW: 90 kDa
Observed MW: 90 kDa
Product Details
Product Details
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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Western Blot
