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Description
TNF-R1 Recombinant Rabbit mAb (S-4713)Product Specification Host Rabbit Antigen TNF RI Synonyms Tumor necrosis factor receptor superfamily member 1A; Tumor necrosis factor receptor 1 (TNF R1); Tumor necrosis factor receptor type I (TNF RI; TNFR I); p55; p60; CD120a; TNFAR; TNFR1; TNFRSF1A Location Secreted, Cell membrane Accession P19438 Clone Number S 4713 Antibody Type Recombinant mAb Isotype IgG Application WB Reactivity Ms, Rt Positive Sample L929, NIH 3T3 Purification Protein A
Product Specification
| Host | Rabbit |
| Antigen | TNF-RI |
| Synonyms | Tumor necrosis factor receptor superfamily member 1A; Tumor necrosis factor receptor 1 (TNF-R1); Tumor necrosis factor receptor type I (TNF-RI; TNFR-I); p55; p60; CD120a; TNFAR; TNFR1; TNFRSF1A |
| Location | Secreted, Cell membrane |
| Accession | P19438 |
| Clone Number | S-4713 |
| Antibody Type | Recombinant mAb |
| Isotype | IgG |
| Application | WB |
| Reactivity | Ms, Rt |
| Positive Sample | L929, NIH/3T3 |
| 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, Ms |
Background
TNF RI (TNFRSF1A/CD120a) is a 55 kDa type I transmembrane receptor of the TNF superfamily whose extracellular cysteine-rich domain avidly binds TNF-α and TNF-β/lymphotoxin-α; upon ligation it triggers caspase-8-mediated apoptosis, activates NF-κB, acid sphingomyelinase and antiviral programs, and is essential for germinal-center formation and defense against intracellular pathogens like Listeria. Stored in the Golgi and mobilized to the cell surface by pro-inflammatory stimuli, TNF RI is stabilized by TNF-α within lipid rafts, cleaved by ADAM-17/TACE and constitutively released as a 28–34 kDa soluble ectodomain that buffers excess TNF-α and helps resolve inflammation, whereas raft exclusion drives receptor internalization and apoptosis; mutations in TNF RI underlie the autoinflammatory TRAPS syndrome.
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