TNFSF18 antibody (PE)

Catalog No. ABIN2663705

Product Details anti-TNFSF18 Antibody (PE)

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

Reactivity: Mouse

Host: Rat

Clonality: Monoclonal

Conjugate: This TNFSF18 antibody is conjugated to 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

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 TNFSF18

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

Alternative Name: GITR Ligand (TNFSF18 Products)

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

Background: 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.