Fas Ligand Protein, Human (148a.a, 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. Human Fas Ligand exhibits 4 isoforms, the soluble form (130-281 a.a.) of which plays an important role in the activation-induced cell death (AICD) of T lymphocytes Jurkat cells. However the membrane-bound isoform could be responsible for its inflammatory activity. Fas Ligand Protein, Human (148a.a, P.pastoris, His) has a total length of 148 amino acids (P134-L281), with a TNF_2 domain (146-281 a.a.). It is a recombinant protein expressed in P.pastoris cells with N-terminal His-tag.
- Species: Human
- Source: P. pastoris
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Storage:Stored at -20°C for 2 years from date of receipt. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.
Biological Activity
Description
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]. Human Fas Ligand exhibits 4 isoforms, the soluble form (130-281 a.a.) of which plays an important role in the activation-induced cell death (AICD) of T lymphocytes Jurkat cells[3]. However the membrane-bound isoform could be responsible for its inflammatory activity[4]. Fas Ligand Protein, Human (148a.a, P.pastoris, His) has a total length of 148 amino acids (P134-L281), with a TNF_2 domain (146-281 a.a.). It is a recombinant protein expressed in P.pastoris cells with N-terminal His-tag.
Background
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[6].
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 Human is different from Rat and Mouse with similarity of 77.26% and 78.06%, respectively.
In Vitro
Human soluble FasL (4 units/mL; 18 hr) induces neutrophil infiltration[4].
Human membrane-bound FasL (4 units/mL; 18 hr) is found to induce IL-1β release in plastic adherent macrophages separated from 4-day PEC instead of recombinant mouse soluble FasL (WX1)[4].
Soluble FasL (.1-1 nM) of human induces chemotaxis of mouse neutrophils in vitro at concentrations incapable of inducing cell apoptosis.[6].
Technical Parameters
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Species Human
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Source P. pastoris
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Tag N-His
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Accession
Q53ZZ1 (P134-L281)
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Molecular Construction
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N-term
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His
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Fas Ligand (P134-L281)
Accession # Q53ZZ1 -
C-term
-
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Protein Length
Partial
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Synonyms
FASLG; TNLG1A; Prev. APT1LG1; CD95L; Prev. TNFSF6; APTL; FasL; Tumor Necrosis Factor (Ligand) Superfamily, Member 6; Tumor Necrosis Factor Ligand Superfamily Member 6; Mutant Tumor Necrosis Factor Family Member 6; Fas Antigen Ligand; Apoptosis (APO-1) Ant
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AA Sequence
PSPPPEKKELRKVAHLTGKSNSRSMPLEWEDTYGIVLLSGVKYKKGGLVINETGLYFVYSKVYFRGQSCNNLPLSHKVYMRNSKYPQDLVMMEGKMMSYCTTGQMWARSSYLGAVFNLTSADHLYVNVSELSLVNFEESQTFFGLYKL
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Predicted Molecular Mass
19.3 kDa
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Molecular Weight
Approximately 26 kDa, based on SDS-PAGE under reducing conditions.
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Purity
≥ 90%, as determined by reducing SDS-PAGE.
Product Properties
Lyophilized powder.
<1 EU/μg, determined by LAL method.
It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH2O.
Stored at -20°C for 2 years from date of receipt. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.
Room temperature in continental US; may vary elsewhere.
Documentation
References
[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]. 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]
[5]. Puppo F, et al. Fas, Fas ligand, and transfusion immunomodulation. Transfusion. 2001 Mar;41(3):416-8. [Content Brief]
[6]. Ottonello L, et al. Soluble Fas ligand is chemotactic for human neutrophilic polymorphonuclear leukocytes. J Immunol. 1999 Mar 15;162(6):3601-6. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)