Anti-Mouse CD357 (GITR) NALE(TM) Purified (Clone: DTA-1)

Anti-Mouse CD357 (GITR) NALE(TM) Purified (Clone: DTA-1)
Item number Size Datasheet Manual SDS Delivery time Quantity Price
ABE-43-1076-100 100 µg -

3 - 11 business days*

443.00€
 
The DTA-1 monoclonal antibody specifically reacts with Mouse Glucocorticoid-Induced TNFR-related... more
Product information "Anti-Mouse CD357 (GITR) NALE(TM) Purified (Clone: DTA-1)"
The DTA-1 monoclonal antibody specifically reacts with Mouse Glucocorticoid-Induced TNFR-related protein, also known as GITR and TNFRSF18, a 66-70 kDa homodimer glycoprotein, detected in the T cells treated with glucocorticoid dexamethasone. GITR is also expressed in naive mice by CD25+/CD4+/CD8a- thymocytes and on CD25+/CD4+/CD45RB-low splenocytes. Low levels were detected in splenic CD25+/CD4+/CD45RB-low T cells, B cells, dendritic cells and macrophages. A GITR ligand was detected on dendritic cells, macrophages and B cells. The DTA-1 antibody stimulates GITR and abrogates suppression by T regulatory cells (Treg), without affecting their proliferation. DTA-1 administration or the removal of GITR-expressing cells led to organ specific autoimmune disease. Protein function: Receptor for TNFSF18. Seems to be involved in interactions between activated T-lymphocytes and endothelial cells and in the regulation of T-cell receptor-mediated cell death. Mediated NF-kappa-B activation via the TRAF2/NIK pathway. [The UniProt Consortium]
Keywords: Anti-Gitr, Anti-CD357, Anti-Tnfrsf18, Anti-Glucocorticoid-induced TNFR-related protein, Anti-Tumor necrosis factor receptor superfamily member 18, Monoclonal Antibody to Mouse CD357 (GITR) NALE(TM) Purified (Clone: DTA-1)
Supplier: Abeomics
Supplier-Nr: 43-1076

Properties

Application: IHC/IF
Antibody Type: Monoclonal
Clone: DTA-1
Conjugate: No
Host: Rat
Species reactivity: mouse
Format: Affinity Purified

Handling & Safety

Storage: +4°C
Shipping: +4°C (International: +4°C)
Caution
Our products are for laboratory research use only: Not for administration to humans!
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