TNFSF18 anticorps (PE)

N° du produit ABIN2663705

Détail du produit anti-TNFSF18 anticorps (PE)

Antigène: TNFSF18 (Tumor Necrosis Factor (Ligand) Superfamily, Member 18 (TNFSF18))

Reactivité: Souris

Hôte: Rat

Clonalité: Monoclonal

Conjugué: Cet anticorp TNFSF18 est conjugé à/à la PE

Application: Flow Cytometry (FACS), Blocking Reagent (BR)

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

Clone: YGL 386

Isotype: IgG1 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 TNFSF18

Antigène: TNFSF18 (Tumor Necrosis Factor (Ligand) Superfamily, Member 18 (TNFSF18))

Autre désignation: GITR Ligand (TNFSF18 Produits)

Synonymes: anticorps Gitrl, anticorps AITRL, anticorps GITRL, anticorps TL6, anticorps hGITRL, anticorps TNLG2A, anticorps tumor necrosis factor (ligand) superfamily, member 18, anticorps TNF superfamily member 18, anticorps Tnfsf18, anticorps TNFSF18

Sujet: GITR ligand (GITRL) is a member of the TNF superfamily, also known as TNFSF18 or TL6. It is expressed on B cells, macrophages, dendritic cells and endothelial cells. The expression of GITRL on dendritic cell surface can be transiently up-regulated and then rapidly down-regulated by LPS stimulation. GITRL binds to its receptor, GITR, to co-stimulate T cell activation, proliferation, and cytokine production, and inhibit the suppressive functions of CD4+CD25+ Treg cells, as well as induce macrophages activation. GITR-GITRL interaction has been implicated as an essential regulator of immune response to self antigens and phathogens.