Cytokine that binds to TNFRSF6/FAS, a receptor that transduces the apoptotic signal into cells. 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. Binding to the decoy receptor TNFRSF6B/DcR3 modulates its effects. 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. Belongs to the tumor necrosis factor family. 2 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Protein type: Apoptosis; Membrane protein, integral; Cytokine
Cellular Component: lysosomal lumen; extracellular space; integral to plasma membrane; perinuclear region of cytoplasm; extracellular region; caveola; nucleus; external side of plasma membrane
Biological Process: caspase activation; positive regulation of I-kappaB kinase/NF-kappaB cascade; transcription, DNA-dependent; positive regulation of apoptosis; apoptosis; response to lipopolysaccharide; negative regulation of transcription from RNA polymerase II promoter; signal transduction; cellular chloride ion homeostasis; endosomal lumen acidification; inflammatory cell apoptosis; negative regulation of angiogenesis; induction of apoptosis via death domain receptors; cell-cell signaling; positive regulation of neuron apoptosis; positive regulation of epidermal growth factor receptor signaling pathway; positive regulation of cell proliferation; immune response; retinal cell programmed cell death
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.