FASLG Proteins

FASLG (Fas Ligand) is a Protein Coding gene. Diseases associated with FASLG include Autoimmune Lymphoproliferative Syndrome and Lung Cancer. Among its related pathways are Apoptosis and survival Caspase cascade and CDK-mediated phosphorylation and removal of Cdc6. Gene Ontology (GO) annotations related to this gene include signaling receptor binding and tumor necrosis factor receptor binding. An important paralog of this gene is TNFSF15.

CUSABIO has five systems (E. coli, In vitro E.coli, Yeast, Insect Baculovirus, Mammalian) from prokaryotic to eukaryotic to express the recombinant protein, and a very strict QC system so that the quality can be guaranteed. And the following FASLG proteins are produced under the system.
FASLG proteins produced by CUSABIO are featured with high purity, low endotoxin, multi-Sources & tags, animal-free, etc. And you will have many choices on sizes from μg to mg. In addition, FASLG custom service is also available for research with more specific needs.

FASLG Proteins Catalog

FASLG Proteins for Homo sapiens (Human)

FASLG Proteins for Macaca mulatta (Rhesus macaque)

FASLG Proteins for Felis catus (Cat) (Felis silvestris catus)

FASLG Proteins for Sus scrofa (Pig)

FASLG Proteins for Cercocebus atys (Sooty mangabey) (Cercocebus torquatus atys)

FASLG Proteins for Rattus norvegicus (Rat)

FASLG Proteins for Mus musculus (Mouse)

FASLG Proteins for Macaca nemestrina (Pig-tailed macaque)

FASLG Proteins for Macaca fascicularis (Crab-eating macaque) (Cynomolgus monkey)

FASLG Background

FASLG gene encodes FAS ligand, a homotrimeric type II transmembrane protein belonging to the tumor necrosis factor (TNF) family [1]. FASLG is also called FASL, CD95L, or TNFSF6 (Tumor necrosis factor ligand superfamily member 6). FASL is mainly expressed in activated T lymphocytes and Natural Killer (NK) cells [2][3] and also has constitutive expression in immune-privileged sites such as the eyes and testis [4][5]. Bossi G and Griffiths GM found that FasL is stored in specialized secretory lysosomes in T cells and NK cells after synthesis, and the delivery of FasL to the cell surface may be associated with activation of these cells [6]. It has been reported that the cytoplasmic tail of FasL transduces the proliferation signal in CD8-T cells [7] and propagates a signal to arrest the cell cycle in CD4-T cells [8]. In the Fas-mediated apoptotic pathway, binding of FasL drives Fas clustering and binding of Fas to FADD. FADD recruits caspase-8 and caspase-10 to form the death-inducing signaling complex (DISC), triggering the cleavage of several pro-caspases and eventually inducing apoptosis [9]. In addition to its role in apoptosis, FASL is involved in immune privilege [5] and a cytotoxic T lymphocyte (CTL)-induced tissue destruction [10]. Significantly increased levels of FASL is detected in numerous diseases such as hemophagocytic syndrome [11], Diamond-Blackfan anemia [11], rheumatoid arthritis [13], myocarditis [12], and acute GvHD (graft-versus-host disease) [14].

[1] Suda T, Takahashi T, et al. Molecular cloning and expression of the Fas ligand: a novel member of the tumor necrosis factor family [J]. Cell 1993, 75: 1169– 78.
[2] Oshimi Y, Oda S, et al. Involvement of Fas ligand- and Fas-mediated pathway in the cytotoxicity of human natural killer cells [J]. J. Immunol. 1996, 157: 2909– 15.
[3] Suda T, Okazaki T, et al. Expression of the Fas ligand in T-cell-lineage [J]. J. Immunol. 1995, 154: 3806– 1.
[4] Griffith TS, Brunner T, et al. Fas ligand-induced apoptosis as a mechanism of immune privilege [J]. Science 1995, 270: 1189– 92.
[5] Green DR, Ferguson TA. The role of Fas ligand in immune privilege [J]. Nat Rev Mol Cell Biol 2001, 2:917–24.
[6] Bossi G, Griffiths GM. Degranulation plays an essential part in regulating cell surface expression of Fas ligand in T cells and natural killer cells [J]. Nat. Med. 1999, 5: 90– 96.
[7] Suzuki I, Fink PJ. Maximal proliferation of cytotoxic T lymphocytes requires reverse signaling through Fas ligand [J]. J. Exp. Med. 1998, 187:123–28.
[8] Alnemri ES, Livingston DJ, et al. Human ICE/CED-3 protease nomenclature [J]. Cell 1996, 87:171.
[9] Nagata S. Fas ligand-induced apoptosis [J]. Annu Rev Genet 1999, 33:29–55.
[10] Nagata S, Golstein P. The Fas death factor [J]. Science 1995, 267: 1449– 56.
[11] Hasegawa D, Kojima S, et al. Elevation of the serum Fas ligand in patients with hemophagocytic syndrome and Diamond-Blackfan anemia [J]. Blood 1998, 91: 2793– 99.
[12] Toyozaki T, Hiroe M, et al. Levels of soluble Fas ligand in myocarditis [J]. Am. J. Cardiol. 1998, 82: 246– 48.
[13] Nozawa K, Kayagaki N, et al. Soluble Fas (APO-1, CD95) and soluble Fas ligand in rheumatic diseases [J]. Arthritis Rheum. 1997, 40: 1126– 29.
[14] Kanda Y, Tanaka Y, et al. Increased soluble Fas-ligand in sera of bone marrow transplant recipients with acute graft-versus-host disease [J]. Bone Marrow Transplant. 1998, 22: 751– 54.

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