TNFSF6 Antibody – Rat Monoclonal

Function: 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

By similarity.The FasL intracellular domain (FasL ICD) cytoplasmic form induces gene transcription inhibition

By similarity.

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

By similarity.

Subcellular location: Isoform FasL: Cell membrane; Single-pass type II membrane protein. Cytoplasmic vesicle lumen

By similarity. Lysosome lumen

By similarity. Note: Is internalized into multivesicular bodies of secretory lysosomes after phosphorylation by FGR and monoubiquitination. Colocalizes with the SPPL2A protease at the cell membrane

By similarity.Isoform FasLS: Secreted. Tumor necrosis factor ligand superfamily member 6, soluble form: Secreted. Note: May be released into the extracellular fluid, probably by cleavage form the cell surface.FasL intracellular domain: Nucleus

By similarity. Note: The FasL ICD cytoplasmic form is translocated into the nucleus

By similarity.

Post-translational modification: 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

By similarity.Phosphorylated by FGR on tyrosine residues; this is required for ubiquitination and subsequent internalization

By similarity.N-glycosylated

By similarity.Monoubiquitinated

By similarity.

Involvement in disease: A deficiency in this protein is the cause of generalized lymphoproliferation disease phenotype (gld). Gld mice present lymphadenopathy and autoantibody production. The phenotype is recessively inherited.

Sequence similarities: Belongs to the tumor necrosis factor family.