Not available outside of the UK & Ireland.

Application

Fas ligand human has been used to induce apoptosis in T-cell lymphoma-derived HuT78 cells and jurkat cells.

Biochem/physiol Actions

Binding of Fas Ligand (FasL) to Fas receptor triggers apoptosis in Fas-bearing cells. FasL has the ability to kill T cells and activated B cells which leads to down-regulation of the immune response. The mechanism of Fas induced apoptosis involves recruitment of pro-caspase 8 through an adaptor molecule called FADD (Fas-Associated protein with death domain) followed by processing of the pro-enzyme to active forms. These active caspases then cleave various cellular substrates leading to the eventual cell death. FasL is also involved in AGE (advanced glycation end-product)-mediated apoptosis in human retinal ARPE-19 cells, suggesting its role in diabetic retinopathy. Changes in the activity of FasL suppresses normal apoptosis, leading to abnormal survival and growth of tumor cells. Mutations in the FasL gene causes autoimmune lymphoproliferative syndrome.

General description

Fas Ligand (FasL) is a member of the TNF (tumor necrosis factor) superfamily that is expressed on the cell surface of activated T cells. It can be present as soluble form in the circulation or membrane bound form in cells. Recombinant human soluble Fas Ligand is a 17.9kDa protein comprising the TNF homologous region of FasL and contains an 8 residue N-terminal His-Tag. Both human and murine sFasL are fully active on human and murine cells.

Physical form

Lyophilized with no additives.

Reconstitution

Centrifuge the vial prior to opening. Reconstitute in water to a concentration of 0.1-1.0 mg/ml. Do not vortex. This solution can be stored at 2-8°C for up to 1 week. For extended storage, it is recommended to further dilute in a buffer containing a carrier protein (example 0.1% BSA) and store in working aliquots at -20°C to -80°C.

Sequence

HHHHHHHHPS PPPEKKELRK VAHLTGKSNS RSMPLEWEDT YGIVLLSGVK YKKGGLVINE TGLYFVYSKV YFRGQSCNNL PLSHKVYMRN SKYPQDLVMM EGKMMSYCTT GQMWARSSYL GAVFNLTSAD HLYVNVSELS LVNFEESQTF FGLYKL