Fas Ligand Protein, Mouse (P.pastoris, His)

Fas Ligand (CD178; APTL) is a ligand to TNFRSF6/FAS, transduces the apoptotic signal to regulate cytotoxic T-cell-mediated apoptosis, natural killer cell-mediated apoptosis and in T-cell development^[1]. Mouse Fas Ligand has a total length of 279 amino acids (M1-L279), with a TNF_2 domain (144-279 a.a.). Fas Ligand Protein, Mouse (P.pastoris, His) is a recombinant protein expressed in P.pastoris cells with N-terminal His-tag.

Fas Ligand (FasL; FASLG; CD95L), is a ligand for TNFRSF6/FAS belonging to the tumor necrosis factor (TNF). FasL is a type II transmembrane protein, riggering apoptosis of lymphocytes^[1].
FasL is expressed on a variety of cell types, including T cells, natural killer (NK) cells, monocytes, neutrophils, breast epithelial cells, and vascular endothelial cells^[2].
FasL exerts different biological activity by cleaved into 4 isoforms including membrane form, soluble form, ADAM10-processed FasL form (APL) and SPPL2A-processed FasL form (SPA). Among them, the membrane-bound form and a soluble form generated by proteolytic action of matrix metalloproteinases (MMP)^[2].
FasL or soluble FasL binding to Fas results in receptor aggregation and in the interaction of a protein called Fas-associated death domain with the Fas cytoplasmic tail. The interaction triggers a cascade of intracellular events, including the activation of the IL-1-converting enzyme-like cysteine protease (caspase 8), that ultimately leads to nucleoprotein cleavage, DNA fragmentation, and cell apoptosis^[4].
The loss of function due to mutations in murine FasL, murine Fas, human Fas, or human FasL leads to lymphoproliferation, lymphadenopathy, and autoimmune diseases^[1][3].
Meanwhile, defective activation-induced cell death (AICD) results in spontaneous mutation of Fas and FasL genes in mice with lupus-like autoimmune disease^[3].
Human Fas Ligand also involves in Jurkat cell apoptosis and binds TNFRSF6B/DcR3 to bolck apoptosis, which is a decoy receptor of apoptosis termination^[2].
FasL is widely found in different animals, while the sequence in Mouse is highly similar to Rat (91.37%), but very different from Human with similarity of 78.06%.

Recombinant mouse soluble FasL (WX1) (4 units/mL; 18 hr) fails to induce IL-1β release from inflammatory cells, suggests that the IL-1β enhances neutrophil infiltration^[6].

Mouse

P. pastoris

N-His

Q544E9 (P132-L279)

14103  [NCBI]

Approximately 18.2 kDa

Greater than 90% as determined by reducing SDS-PAGE.

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• [1]. Schneider P, et al. Characterization of Fas (Apo-1, CD95)-Fas ligand interaction. J Biol Chem. 1997 Jul 25;272(30):18827-33.  [Content Brief]

  [2]. Liu W, et al. Crystal Structure of the Complex of Human FasL and Its Decoy Receptor DcR3. Structure. 2016 Nov 1;24(11):2016-2023.  [Content Brief]

  [3]. Martínez-Lorenzo MJ, et al. Release of preformed Fas ligand in soluble form is the major factor for activation-induced death of Jurkat T cells. Immunology. 1996 Dec;89(4):511-7.  [Content Brief]

  [4]. Puppo F, et al. Fas, Fas ligand, and transfusion immunomodulation. Transfusion. 2001 Mar;41(3):416-8.  [Content Brief]

  [5]. Miwa K, et al. Caspase 1-independent IL-1beta release and inflammation induced by the apoptosis inducer Fas ligand. Nat Med. 1998 Nov;4(11):1287-92.  [Content Brief]

  [6]. Shudo K, et al. The membrane-bound but not the soluble form of human Fas ligand is responsible for its inflammatory activity. Eur J Immunol. 2001 Aug;31(8):2504-11.  [Content Brief]