Aliases for FASLG Gene
External Ids for FASLG Gene
Previous HGNC Symbols for FASLG Gene
Previous GeneCards Identifiers for FASLG Gene
This gene is a member of the tumor necrosis factor superfamily. The primary function of the encoded transmembrane protein is the induction of apoptosis triggered by binding to FAS. The FAS/FASLG signaling pathway is essential for immune system regulation, including activation-induced cell death (AICD) of T cells and cytotoxic T lymphocyte induced cell death. It has also been implicated in the progression of several cancers. Defects in this gene may be related to some cases of systemic lupus erythematosus (SLE). Alternatively spliced transcript variants have been described. [provided by RefSeq, Nov 2014]
GeneCards Summary for FASLG Gene
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 Modulation and Signaling and Proteoglycans in cancer. 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 TNFSF14.
UniProtKB/Swiss-Prot Summary for FASLG Gene
Cytokine that binds to TNFRSF6/FAS, a receptor that transduces the apoptotic signal into cells (PubMed:26334989, PubMed:9228058). Involved in cytotoxic T-cell-mediated apoptosis, natural killer cell-mediated apoptosis and in T-cell development (PubMed:9228058, PubMed:7528780, PubMed:9427603). Initiates fratricidal/suicidal activation-induced cell death (AICD) in antigen-activated T-cells contributing to the termination of immune responses (By similarity). TNFRSF6/FAS-mediated apoptosis has also a role in the induction of peripheral tolerance (By similarity). Binds to TNFRSF6B/DcR3, a decoy receptor that blocks apoptosis (PubMed:27806260).
[Tumor necrosis factor ligand superfamily member 6, soluble form]: Induces FAS-mediated activation of NF-kappa-B, initiating non-apoptotic signaling pathways (By similarity). Can induce apoptosis but does not appear to be essential for this process (PubMed:27806260).
[FasL intracellular domain]: Cytoplasmic form induces gene transcription inhibition.