• Purity

  >90%, by SDS-PAGE under reducing conditions and visualized by silver stain

• Endotoxin Level

  <0.10 EU per 1 μg of the protein by the LAL method.  

• Activity

  Measured by its ability to inhibit Fas Ligand-induced apoptosis of Jurkat human acute T cell leukemia cells. Cheng, J.     et al. (1994) Science     263:1759. The ED    ₅₀ for this effect is 0.05-0.25 μg/mL in the presence of 100 ng/mL recombinant rat Fas Ligand.

• Source

  Mouse myeloma cell line, NS0-derived

  Rat Fas (Gln22 - Lys170) Accession # NP_631933	IEGRMD	Human IgG1 (Pro100 - Lys330)
  N-terminus		C-terminus

• Accession #

• N-terminal Sequence    
  Analysis

  No results obtained: Gln22 predicted

• Structure / Form

  Disulfide-linked homodimer

• Predicted Molecular Mass

  43.3 kDa (monomer)

• SDS-PAGE

  60-65 kDa, reducing conditions

Background: Fas/TNFRSF6/CD95

Fas, also known as APO-1 or CD95, belongs to the death receptor subfamily of the TNF receptor superfamily and is designated TNFRSF6 (1 ? 3). Rat Fas cDNA encodes 324 amino acids (aa) that include a 21 aa signal peptide, a 150 aa extracellular domain (ECD) that contains three cysteine-rich TNFR repeats, a 17 aa transmembrane sequence, and a 136 aa cytoplasmic domain containing a death domain (DD), which is required for transducing apoptotic signals (4). Mature rat Fas ECD shares 68% aa sequence identity with mouse Fas, and 56 ? 58% with human, feline, bovine and porcine Fas. A 114 aa potential rat Fas isoform contains an alternate start site at aa 211, thus lacking all three TNFR repeats (5). The Fas ligand (FasL, TNFSF6) is a type II transmembrane protein of the TNF family that can be expressed on activated T-lymphocytes, NK cells and cells in immune privileged sites, or shed in soluble form (2). Engagement of FAS induces oligomerization of preformed Fas trimers (1, 2). The activated receptor recruits the adaptor molecule FADD to form the Death-Inducing Signaling Complex (DISC). Upon activation, caspases in the DISC initiate the apoptotic signaling cascade (6). Fas is prominent in epithelial cells, hepatocytes, activated mature lymphocytes, virus-transformed lymphocytes and tumor cells. It is an essential mediator in the activation-induced death of T lymphocytes that terminates the immune reaction (1, 2, 7). In immune-privileged tissues, infiltrating Fas-bearing lymphocytes and inflammatory cells are killed by FasL engagement (8). Both humans and mice with genetic defects in Fas accumulate abnormal lymphocytes and develop systemic autoimmunity (1 ? 3). The Fas pathway also appears to cross-communicate with the BIM (mitochondrial/intrinsic) apoptosis pathway (1).

• References:

1. Bouillet, P. and L.A. O’Reilly (2009) Nat. Rev. Immunol. 9:514.

2. Strasser, A. et al. (2009) Immunity 30:180.

3. Ashkenazi, A. and V. Dixit (1999) Curr. Opin. Cell Biol. 11:255.

4. SwissProt accession Q63199.

5. GenBank protein accession EDM13159.

6. Thorburn, A. (2003) Cellular Signaling 16:139.

7. Barreiro, R. et al. (2004) J. Immunol. 173:1519.

8. Ferguson, T.A. and T.S Griffith (2006) Immunol. Rev. 213:228.

• Long Name:

  Fibroblast-associated

• Entrez Gene IDs:

  355 (Human); 14102 (Mouse); 246097 (Rat); 493881 (Feline)

• Alternate Names:

  Apo-1 antigen; Apo-1; apoptosis antigen 1; Apoptosis-mediating surface antigen FAS; APT1; APT1FASTM; CD95 antigen; CD95; CD95ALPS1A; Fas (TNF receptor superfamily, member 6); Fas AMA; Fas antigen; Fas; FAS1; FASLG receptor; TNFRSF6; TNFRSF6member 6; tumor necrosis factor receptor superfamily member 6