FASL Antikörper

Produktnummer ABIN187307

Produktdetails anti-FASL Antikörper

Target: FASL (Fas Ligand (TNF Superfamily, Member 6) (FASL))

Reaktivität: Human

Wirt: Maus

Klonalität: Monoklonal

Konjugat: Dieser FASL Antikörper ist unkonjugiert

Applikation: Flow Cytometry (FACS), Immunoprecipitation (IP), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p)), Functional Studies (Func), Enzyme Immunoassay (EIA), Immunohistochemistry (Frozen Sections) (IHC (fro))

Spezifität: This antibody is specific for the extracellular domain of human Fas Ligand. Species Reactivity: Human. Others not tested.

Immunogen: Recombinant human FasL (extracellular domain)

Klon: 2C101

Isotyp: IgG1

Anwendungsinformationen

Applikationshinweise: Functional Activity: Inhibits apoptosis in anti-CD3 stimulated Jurkat T-cells ( 0.5 ~ 5 µg/mL) suitable. Excellent for neutralization. Flow cytometry: 1 x 106 H9 T-cells stained with 1 µg/mL antibody, followed by biotinylated goat anti-mouse IgG and streptavidin-PE. Immunocytochemistry Suggested starting dilution is >1:100 The optimal dilution for a specific application should be determined by the researcher.

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Buffer: 100 µg of 1 mg/mL affinity-purified monoclonal antibody. Prepared in 0.15M PBS, pH 7.2 with protein stabilizer. Purity 95% by SDS-PAGE.

Lagerung: 4 °C

Details zu FASL

Target: FASL (Fas Ligand (TNF Superfamily, Member 6) (FASL))

Andere Bezeichnung: CD178 / Fas Ligand (FASL Produkte)

Hintergrund: Fas (CD95/APO-1) Ligand (FasL) is a 43 kDa type II membrane protein and member of the tumor necrosis factor family. Human FasL can be released from cells as a 26 kDa soluble protein upon cleavage by metalloproteinases. FasL is expressed on various cells including T cells, NK cells, Monocytes, Sertoli cells and tumor cells. Interaction of FasL with its receptor triggers rapid apoptosis. FasL-induced apoptosis is involved in T cell receptor/anti-CD3 induced cell death, cytotoxic T cell activity, maintainence of immune privilege, immune escape of tumor cells and viral hepatitis. Malfunction of the Fas system causes hyperplasia.

Pathways: Apoptose, EGFR Signaling Pathway, Production of Molecular Mediator of Immune Response, Positive Regulation of Endopeptidase Activity