Product Description
CD357 Antibody [DTA-1] (FITC) | 76-985 | ProSci
Host: Rat
Reactivity: Mouse
Homology: N/A
Immunogen: N/A
Research Area: Immunology
Tested Application: Flow
Application: N/A
Specificiy: 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.
Positive Control 1: N/A
Positive Control 2: N/A
Positive Control 3: N/A
Positive Control 4: N/A
Positive Control 5: N/A
Positive Control 6: N/A
Molecular Weight: N/A
Validation: N/A
Isoform: N/A
Purification: The monoclonal antibody was purified utilizing affinity chromatography and unreacted dye was removed from the product.
Clonality: Monoclonal
Clone: DTA-1
Isotype: Rat IgG2b
Conjugate: FITC
Physical State: liquid
Buffer: Phosphate-buffered aqueous solution, ≤0.09% Sodium azide, may contain carrier protein/stabilizer, ph7.2.
Concentration: batch dependent
Storage Condition: The product should be stored undiluted at 4˚C and should be protected from prolonged exposure to light. Do not freeze.
Alternate Name: AITR, Gitr, Tnfrsf18
User Note: Optimal dilutions for each application to be determined by the researcher.
BACKGROUND: 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 naïve 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.