TNFRSF18 anticorps (PE-Cy7)

N° du produit ABIN2659499

Détail du produit anti-TNFRSF18 anticorps (PE-Cy7)

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

Reactivité: Souris

Hôte: Rat

Clonalité: Monoclonal

Conjugué: Cet anticorp TNFRSF18 est conjugé à/à la 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

Information d'application

Indications d'application: Optimal working dilution should be determined by the investigator.

Restrictions: For Research Use only

Stockage

Concentration: 0.2 mg/mL

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

Agent conservateur: Sodium azide

Précaution d'utilisation: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Conseil sur la manipulation: Protect from prolonged exposure to light. Do not freeze.

Stock: 4 °C

Stockage commentaire: The antibody solution should be stored undiluted between 2°C and 8°C.

Détails sur TNFRSF18

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

Autre désignation: CD357 (TNFRSF18 Produits)

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

Sujet: 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