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Recombinant Human sFas Ligand

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Produktdetails

Katalognummer: 310-03H
Beschreibung:
Recombinant Human sFas Ligand

Fas Ligand (FasL) is a member of the TNF superfamily that is expressed on the cell surface of activated T cells. Binding of 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, followed by processing of the pro-enzyme into active forms. These active caspases then cleave various cellular substrates, leading to the eventual cell death. Both human and murine sFasL are fully active on human and murine cells. Recombinant Human soluble Fas Ligand is a 17.9 kDa protein comprising the TNF-homologous region of FasL and contains an 8-residue N-terminal His-Tag.

Source: CHO cells

Synonyms: soluble Fas Ligand (sFasL), TNFSF6, CD95L, Apo I Ligand, APTL

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

Purity: ≥ 95% by SDS-PAGE gel and HPLC analyses.

Biological Activity: Determined by its 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 units/mg.

Recombinant Human sFas Ligand Biological Activity Graph

Calculated Molecular Weight: 17.9 kDa

Accession Number: P48023

Gene ID: 356

Endotoxin: Endotoxin level is < 0.1 ng/ug of protein (< 1 EU/ug)

crossreactivity:
Country Of Origin: USA

Not for human use.

Research Interest

product.subtitle.recentcitations

Erstautor
Tello-Lafoz, M
Titel
Cytotoxic lymphocytes target characteristic biophysical vulnerabilities in cancer.
Literaturstelle
Immunity; 54(5) pg1037-1054.e7
PubMed ID
Erstautor
Gorbea, C
Titel
A viral Sm-class RNA base-pairs with mRNAs and recruits microRNAs to inhibit apoptosis.
Literaturstelle
Nature; 550(7675) pg275-279
PubMed ID
Erstautor
Lim, M C
Titel
Pathogen-induced ubiquitin-editing enzyme A20 bifunctionally shuts off NF-κB and caspase-8-dependent apoptotic cell death.
Literaturstelle
Cell Death and Differentiation; 24(9) pg1621-1631
PubMed ID