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FLASH GENE
Symbol FASLG contributors: mct/np - updated : 14-12-2013
HGNC name Fas ligand (TNF superfamily, member 6)
HGNC id 11936
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • an extracellular C terminus, which binds to the Fas receptor, triggering apoptosis via activation of a caspase cascade
  • an intracellular domain (ICD) consistent with its ability to transduce signals, including a 26 AA proline-rich region that interacts with proteins containing Src homology 3 (SH3) and WW domains
    • conjugated GlycoP
    mono polymer homomer , trimer
    HOMOLOGY
    interspecies ortholog to rattus Tnfsf6
    ortholog to murine Fasl
    Homologene
    FAMILY
  • tumor necrosis factor (ligand) superfamily
    • CATEGORY adaptor , antigen , signaling cytokine , receptor
    SUBCELLULAR LOCALIZATION extracellular
        plasma membrane
    text
  • may be released into the extracellular fluid, probably by cleavage form the cell surface
  • integral to plasma membrane
  • predominantly retained inside the cell, presumably to limit cell surface expression and extracellular release of this pro-apoptotic ligand
  • type II membrane protein
    • basic FUNCTION
  • FAS ligand, a pro-apoptotic protein induced by DNA damage
  • major effector molecule of cytotoxic T lymphocytes
  • critical skin homeostasis, not major contributing factor in the systemic lupus erythematosus
  • plays a pivotal role in the regulation of apoptosis within and outside the immune system
  • involved in the downregulation of immune reactions by activation-induced cell death (AICD) as well as in T cell-mediated cytotoxicity
  • essential for the growth of many tumour cells
  • FAS/FASLG system plays a central role in maintaining peripheral immune tolerance
  • rotative stress has a significant effect on CA2, FAS, FASLG, OSCAR, and TRAP gene expression in osteoclasts
  • both ADAM10 and ADAM17 are associated with FASLG-containing secretory lysosomes
  • is a cell death-promoting member of the tumor necrosis factor family with important functions in the regulation of T-cell homeostasis and cytotoxicity
    • CELLULAR PROCESS cell life, cell death/apoptosis
    PHYSIOLOGICAL PROCESS immunity/defense
    PATHWAY
    metabolism
    signaling signal transduction
    positive regulation of I-kappaB kinase/NF-kappaB cascade
    a component
  • trimerization may be dependent of FASLG or independent
  • N-glycosylated
  • FAS/FASLG induces erythroblast apoptosis
    • INTERACTION
    DNA
    RNA
    small molecule
    protein
  • interaction with ADAM10 may be of critical importance for the tight regulation of induced cell death in health and disease
  • interacting with GRB2 (promotes sorting of FASLG to the cell surface, and, dynamic regulation of its cell surface localization is critical for controlling local tissue remodeling and inflammation)
  • CCL2 modulate macrophage cytotoxicity by increasing the level of membrane bound FASLG
  • NR5A2 regulates FASLG transcription and associated T-cell effector functions
    • cell & other
    REGULATION
    activated by THY1 (THY1 up-regulates FASLG expression in lung myofibroblasts via Src family kinases)
    Other regulated by ADAM10 (ADAM10 is critically involved in the shedding of FASLG)
    ASSOCIATED DISORDERS
    corresponding disease(s) CSS2
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS