Anti-Tumor Necrosis Factor Receptor antibody [H398] (STJ16100922)
SPECIFICATIONS
ClonalityMonoclonal
HostMouse
ConjugationUnconjugated
IsotypeIgG2a
General Information
| Short Description | Mouse monoclonal anti-Tumor Necrosis Factor Receptor for use in IHC-F, FC, ELISA, IP and WB in Human and Rat samples. Datasheet included with dilution recommendations, and related reagents. |
| Applications | IHC-F/FC/ELISA/IP/WB |
| Host | Mouse |
| Reactivity | Human/Rat |
| Note | STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS. |
Product Properties
| Clonality | Monoclonal |
| Clone ID | H398 |
| Isotype | IgG2a |
| Conjugation | Unconjugated |
| Concentration | 100 Mu g/mL |
| Formulation | PBS with 0.1% BSA and 0.02% sodium azide |
| Storage Instruction | Store at 2-8°C for up to 1-year, upon receipt. |
Target Information
Additional Info
| Background | The monoclonal antibody H398 recognizes the extracellular part of the Tumor Necrosis Factor Receptor type I (TNF-RI) of the membrane-bound as well as the soluble receptor. TNF-RI (~55-60 kDa) is present on most cell types and is considered to play a prominent role in cell stimulation by TNF-alpha. TNF-alpha activates inflammatory responses, induces apoptosis, regulates cellular proliferation, and may even promote cancer progression. The effects of TNF-alpha are mediated by TNF-RI and TNF-RII, which have both distinct and overlapping downstream signaling cascades. Induction of cytotoxicity and other functions are mediated largely via TNF-RI. TNF-RI is equally well activated by both the 17 kDa soluble and 26 kDa membrane-bound form, whereas TNF-RII is efficiently activated only by the membrane bound form of TNF-alpha. TNF-RI signaling is initiated when trimeric TNF-alpha binds TNF-RI receptors. Subsequent TNF-RI trimerization promotes the recruitment of a proximal signaling complex composed of TNF Receptor Associated protein with a Death Domain (TRADD) , Receptor Interacting Protein (RIP) , cellular Inhibitor of Apoptosis Protein 1 (cIAP1) , TNF Receptor Associated Factor 2 (TRAF2) , and likely TRAF5. Studies with TNF-RI-deficient mice indicate that TNF-RI mediates most of the proliferation, pro-inflammatory, and apoptosis-activating pathways. |
Information sourced from Uniprot.org