Catalog # or name ...
soluble Fas Ligand is a protein (156 amino acid residues) with a N-teminal
His-Tag. It is expressed in CHO cells.
Fas ligand (FasL)
is a type II transmembrane protein that belongs to the tumor
necrosis factor (TNF) family. Fas ligand is a homotrimeric protein
and signals through trimerization of FasR, which spans the membrane
of the "target" cell. This trimerization usually leads to apoptosis,
or cell death. Soluble Fas ligand is generated by cleaving
membrane-bound FasL at a conserved cleavage site by the external
serine matrix metalloproteinase MMP-7. Soluble FasL is less active
than their membrane-bound counterparts and do not induce receptor
trimerization and DISC formation. FasL is regarded as a potential
target for immunotherapy.
Greater than 95%
(determined by SDS-PAGE and HPLC analysis).
< 0.1 ng per μg
(1EU/μg) of rHu sFasL.
Determined by it"s ability to induce
cytotoxicity in Jurkat cells in the absence of any cross-linking.
The ED50 for this effect is < 10.0 ng/ml,
corresponding to a specific activity of > 1 x 105
Lyophilized from a
sterile-filtered solution with no additives.
Please Note: Always
centrifuge product briefly before opening the vial. Reconstitute in
sterile, ultra-pure water to a concentration of 0.1-1.0 mg/ml. This
solution can be diluted into other aqueous buffers and stored at
-20oC for future use.
powder, though stable at room temperature for up to 3 weeks, is best
stored desiccated at -20oC. Reconstituted sFasL should be used
immediately or stored in undiluted working aliquots at -20oC. Avoid
repeated freeze / thaw cycles.
FASLG Fas ligand (TNF superfamily, member 6) [ Homo sapiens ]
ligand (TNF superfamily, member 6); FASL; CD178; CD95L; TNFSF6;
APT1LG1; fas ligand; CD95 ligand; apoptosis (APO-1) antigen
ligand 1; tumor necrosis factor (ligand) superfamily, member 6;
CD95L protein; APTL; CD_antigen; Tumor necrosis factor ligand
superfamily member 6, membrane form; Tumor necrosis factor
ligand superfamily member 6, soluble form
rejection; Apoptosis; Autoimmune thyroid disease; Cytokine-cytokine
receptor interaction; MAPK signaling pathway; Natural killer cell
mediated cytotoxicity; Neurotrophin signaling pathway; Pathways in
cancer; Type I diabetes mellitus
tumor necrosis factor receptor binding
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