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Fas Ligand / FASLG / CD95L  Protein, Antibody, ELISA Kit, cDNA Clone

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Fas Ligand / FASLG / CD95L Summary & Protein Information

Fas Ligand / FASLG / CD95L Background

Subunit structure: Homotrimer (Probable). Interacts with ARHGAP9, BAIAP2L1, BTK, CACNB3, CACNB4, CRK, DLG2, DNMBP, DOCK4, EPS8L3, FGR, FYB, FYN, HCK, ITK, ITSN2, KALRN, LYN, MACC1, MIA, MPP4, MYO15A, NCF1, NCK1, NCK2, NCKIPSD, OSTF1, PIK3R1, PSTPIP1, RIMBP3C, SAMSN1, SH3GL3, SH3PXD2B, SH3PXD2A, SH3RF2, SKAP2, SNX33, SNX9, SORBS3, SPTA1, SRC, SRGAP1, SRGAP2, SRGAP3, TEC, TJP3 and YES1. {ECO:0000269|PubMed:17164290, ECO:0000269|PubMed:19807924, ECO:0000305}.
Subcellular location: Cell membrane; Single-pass type II membrane protein. Cytoplasmic vesicle lumen. Lysosome lumen. Note=Is internalized into multivesicular bodies of secretory lysosomes after phosphorylation by FGR and monoubiquitination. Colocalizes with the SPPL2A protease at the cell membrane.; Tumor necrosis factor ligand superfamily member 6, soluble form: Secreted {ECO:0000250}. Note=May be released into the extracellular fluid, probably by cleavage form the cell surface. {ECO:0000250}.; FasL intracellular domain: Nucleus. Note=The FasL ICD cytoplasmic form is translocated into the nucleus.
Post-translational: The soluble form derives from the membrane form by proteolytic processing. The membrane-bound form undergoes two successive intramembrane proteolytic cleavages. The first one is processed by ADAM10 producing an N-terminal fragment, which lacks the receptor-binding extracellular domain. This ADAM10-processed FasL (FasL APL) remnant form is still membrane anchored and further processed by SPPL2A that liberates the FasL intracellular domain (FasL ICD). FasL shedding by ADAM10 is a prerequisite for subsequent intramembrane cleavage by SPPL2A in T-cells. {ECO:0000269|PubMed:17557115, ECO:0000269|PubMed:9427603}.; N-glycosylated.; Phosphorylated by FGR on tyrosine residues; this is required for ubiquitination and subsequent internalization. {ECO:0000269|PubMed:17164290}.; Monoubiquitinated.
Involvement in disease: DISEASE: Autoimmune lymphoproliferative syndrome 1B (ALPS1B) [MIM:601859]: A disorder of apoptosis that manifests in early childhood and results in the accumulation of autoreactive lymphocytes. It is characterized by non-malignant lymphadenopathy with hepatosplenomegaly, and autoimmune hemolytic anemia, thrombocytopenia and neutropenia. {ECO:0000269|PubMed:8787672}. Note=The disease is caused by mutations affecting the gene represented in this entry.
Sequence similarity: Belongs to the tumor necrosis factor family. {ECO:0000305}.
General information above from UniProt

Fas Ligand, also known as FASLG and CD95L, is the ligand for FAS. It is a transmembrane protein which binds to TNFRSF6/FAS. Interaction of FAS with fas Ligand is critical in triggering apoptosis of some types of cells such as lymphocytes. Fas Ligand may be involved in cytotoxic T-cell mediated apoptosis and in T-cell development. TNFRSF6/FAS-mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both.

Fas Ligand / FASLG / CD95L Alternative Name

Fas ligand (TNF superfamily, member 6),FASLG,ALPS1B,APT1LG1,APTL,CD178,CD95-L,CD95L,FASL,TNFSF6,CD95 ligand,apoptosis (APO-1) antigen ligand 1,apoptosis antigen ligand,fas antigen ligand,tumor necrosis factor (ligand) superfamily, member 6,tumor necrosis factor ligand superfamily member 6, [human]

Fas Ligand / FASLG / CD95L Related Studies

  • Pitti R M. et al., 1998, Nature. 396 (6712): 699-703.
  • Hane M. et al., 1995, FEBS Lett. 373 (3): 265-8.
  • Schneider P. et al., 1997, J Biol Chem. 272 (30): 18827-33.
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