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

Fas Ligand (CD178; APTL) is a ligand to TNFRSF6/FAS/CD95, transduces the apoptotic signal to regulate cytotoxic T-cell-mediated apoptosis, natural killer cell-mediated apoptosis and in T-cell development^[1]. Rat Fas Ligand exhibits 4 isoforms, the soluble form (127-278 a.a.) involves in germ cell apoptosis in testis of rats undergoing autoimmune orchitis^[4]. Fas Ligand Protein, Rat (P.pastoris, His) has a total length of 175 amino acids (L104-L278), is 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^[3].
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)^[3].
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^[5].
Fas-Fas Ligand system in rat is one of the main mediators of apoptosis in experimental autoimmune orchitis (EAO), involves in germ cell (GC) death induction^[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^[3].
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%.
FasL is widely found in different animals, while the sequence in Rat is highly similar to Mouse (91.37%), but very different from Human with similarity of 77.26%.

Rat

P. pastoris

N-His

P36940 (L104-L278)

25385  [NCBI]

Approximately 21.3 kDa

Greater than 95% as determined by reducing SDS-PAGE.

<1 EU/μg, determined by LAL method.

• [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]. Jacobo PV, et al. Involvement of soluble Fas Ligand in germ cell apoptosis in testis of rats undergoing autoimmune orchitis. Cytokine. 2012 Nov;60(2):385-92.  [Content Brief]

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