TNFRSF18 antibody (PE-Cy7)

Catalog No. ABIN2659499

Product Details anti-TNFRSF18 Antibody (PE-Cy7)

Target: TNFRSF18 (Tumor Necrosis Factor Receptor Superfamily, Member 18 (TNFRSF18))

Reactivity: Mouse

Host: Rat

Clonality: Monoclonal

Conjugate: This TNFRSF18 antibody is conjugated to PE-Cy7

Application: Flow Cytometry (FACS), Intracellular Flow Cytometry (ICFC)

Purification: The antibody was purified by affinity chromatography, and conjugated with PE/Cy7 under optimal conditions. The solution is free of unconjugated PE/Cy7 and unconjugated antibody.

Clone: YGITR 765

Isotype: IgG2b kappa

Application Details

Application Notes: Optimal working dilution should be determined by the investigator.

Restrictions: For Research Use only

Handling

Concentration: 0.2 mg/mL

Buffer: Phosphate-buffered solution, pH 7.2, containing 0.09 % sodium azide.

Preservative: Sodium azide

Precaution of Use: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Handling Advice: Protect from prolonged exposure to light. Do not freeze.

Storage: 4 °C

Storage Comment: The antibody solution should be stored undiluted between 2°C and 8°C.

Target Details for TNFRSF18

Target: TNFRSF18 (Tumor Necrosis Factor Receptor Superfamily, Member 18 (TNFRSF18))

Alternative Name: CD357 (TNFRSF18 Products)

Synonyms: GITR antibody, TNFRSF18 antibody, AITR antibody, Gitr antibody, CD357 antibody, GITR-D antibody, TNF receptor superfamily member 18 antibody, tumor necrosis factor receptor superfamily, member 18 antibody, TNFRSF18 antibody, Tnfrsf18 antibody

Background: GITR, Glucocorticoid-induced TNFR-related gene, is a member of the TNF receptor superfamily, also known as TNFRSF18, and AITR (in humans). It is expressed at low levels on resting T lymphocytes and at high levels on CD4+ CD25+ T regulatory (Treg) cells. The expression of GITR on T cells can be upregulated upon activation. Interaction of GITR with its ligand (GITRL) has been demonstrated to augment T cell activation, proliferation, cytokine production, as well as MAPKs and NF-κB activation, and abrogate the inhibitory functions of CD4+CD25+ Treg cells. In vivo activation GITR causes development of autoimmune diseases and restores the suppressed immune responses.

Pathways: Cancer Immune Checkpoints