Anti-Fas Ligand Antibody, Non-Fucosylated (CAT#: BioBet-858ZP) Datasheet

FASLG

Fas ligand (TNF superfamily, member 6)

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.

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

Plasma membrane, Extracellular region or secreted, Nucleus, Lysosome

Diseases associated with FASLG include Autoimmune Lymphoproliferative Syndrome and Lung Cancer.

Its related pathways are Apoptosis Modulation and Signaling and Signal transduction_JNK pathway.

A cytokine that binds to TNFRSF6/FAS. This receptor transmits apoptotic signals into the cell. Participate in cytotoxic T cell-mediated apoptosis, natural killer cell-mediated apoptosis and T cell development. Initiation of sibling/suicide activation-induced cell death (AICD) in antigen-activated t cells, leading to the termination of the immune response (through similarity). TNFRSF6/fas-mediated apoptosis also plays a role in inducing peripheral tolerance (similar). Combined with TNFRSF6B/DcR3, a decoy receptor that prevents apoptosis. [Tumor necrosis factor ligand superfamily member 6, soluble form]: Induces fas-mediated activation of nf-kpa-b, and initiates non-apoptotic signaling pathways (through similarity). It can induce apoptosis, but it does not seem to be essential for this process.

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. N-glycosylated (PubMed:9228058). Glycosylation enhances apoptotic activity (PubMed:27806260). Phosphorylated by FGR on tyrosine residues; this is required for ubiquitination and subsequent internalization. Monoubiquitinated.

Protein Based Therapies
Monoclonal antibody (mAb)

IgG

NOK2

Humanized

Human

The humanized antibody directed against human Fas ligands (also named CD95L or Apo1L and hereinafter abbreviated as FasL) for the prevention and/or treatment of skin diseases associated with keratinocytes acantholysis, particularly for the prevention and/or treatment of pemphigus.

Skin Diseases

Skin Diseases