Anticorps Recombinant de lapin anti-TNFR2/CD120b
TNFR2/CD120b Recombinant Antibody for
Hôte / Isotype
Lapin / IgG
Réactivité testée
Humain
Applications
Conjugaison
Non conjugué
CloneNo.
230328B3
N° de cat : 98010-1-PBS
Synonymes
Galerie de données de validation
Informations sur le produit
98010-1-PBS cible TNFR2/CD120b dans les applications de et montre une réactivité avec des échantillons Humain
| Réactivité | Humain |
| Hôte / Isotype | Lapin / IgG |
| Clonalité | Recombinant |
| Type | Anticorps |
| Immunogène | TNFR2/CD120b Protéine recombinante Eg0086 |
| Nom complet | tumor necrosis factor receptor superfamily, member 1B |
| Masse moléculaire calculée | 48 kDa |
| Numéro d’acquisition GenBank | BC052977 |
| Symbole du gène | TNFR2 |
| Identification du gène (NCBI) | 7133 |
| Conjugaison | Non conjugué |
| Forme | Liquide |
| Méthode de purification | Purification par protéine A |
| Tampon de stockage | PBS only |
| Conditions de stockage | Store at -80°C. Stable for one year after shipment. |
Informations générales
Tumor necrosis factor-alpha (TNFA/TNFSF2) is a multifunctional cytokine that plays a key role in regulating inflammation, immune functions, host defense, and apoptosis (PMID: 16407280). TNFA signals through two distinct cell surface receptors, TNFR1 (TNFRSF1A, CD120a, p55) and TNFR2 (TNFRSF1B, CD120b, p75). TNFR1 is widely expressed, whereas TNFR2 exhibits more restricted expression, being found on CD4 and CD8 T lymphocytes, endothelial cells, microglia, oligodendrocytes, neuron subtypes, cardiac myocytes, thymocytes and human mesenchymal stem cells (PMID: 20489699; 22374304). In contrast to TNFR1, TNFR2 does not have a death domain. TNFR2 only signals for antiapoptotic reactions. However, recent evidence indicates that TNFR2 also signals to induce TRAF2 degradation (PMID: 22374304). Various defects in the TNFR2 pathway, due to polymorphisms in the TNFR2 gene, upregulated expression of TNFR2 and TNFR2 shedding, have been implicated in the pathology of several autoimmune disorders (PMID: 20489699).
