Fas

Fas

Fas Informations sur la molécule

Molecule Name
Apoptosis-mediating surface antigen FAS
Alias de la molécule
FAS,ALPS1A,APO1,APT1,CD95,FAS1,FASTM,TNFRSF6,FasR
Drug Development Progress
Nombre de médicaments cliniques1
Nombre de médicaments commercialisés1
Phase de R&D la plus avancéeApproved
Alias de la cible
Tumor Necrosis Factor Receptor Superfamily, Member 6,Apo-1 antigen,CD95,APT1,FAS1,TNFRSF6,FAS,Fas Cell Surface Death Receptor,Fas (TNF Receptor Superfamily, Member 6),Apoptosis-Mediating Surface Antigen FAS,TNF Receptor Superfamily Member 6,FASLG Receptor,CD95 Antigen,Mutant Tumor Necrosis Receptor Superfamily Member 6,Tumor Necrosis Factor Receptor Superfamily Member 6,Apoptosis Signaling Receptor FAS,APO-1 Cell Surface Antigen,Apoptosis Antigen 1,Fas AMA,ALPS1A,APO-1,FASTM,fas Receptor
Contexte de la molécule
The Fas is also known as FAS receptor (FasR), apoptosis antigen 1 (APO-1 or APT), cluster of differentiation 95 (CD95) or tumor necrosis factor receptor superfamily member 6 (TNFRSF6). is a death receptor on the surface of cells that leads to programmed cell death (apoptosis). It is one of two apoptosis pathways, the other being the mitochondrial pathway. FasR is located on chromosome 10 in humans and 19 in mice. Similar sequences related by evolution (orthologs) are found in most mammals. Fas forms the death-inducing signaling complex (DISC) upon ligand binding. Membrane-anchored Fas ligand trimer on the surface of an adjacent cell causes trimerization of Fas receptor. This event is also mimicked by binding of an agonistic Fas antibody, though some evidence suggests that the apoptotic signal induced by the antibody is unreliable in the study of Fas signaling. To this end, several clever ways of trimerizing the antibody for in vitro research have been employed.Upon ensuing death domain (DD) aggregation, the receptor complex is internalized via the cellular endosomal machinery. This allows the adaptor molecule FADD to bind the death domain of Fas through its own death domain. Recently, Fas has also been shown to promote tumor growth, since during tumor progression, it is frequently downregulated or cells are rendered apoptosis resistant. Cancer cells in general, regardless of their Fas apoptosis sensitivity, depend on constitutive activity of Fas. This is stimulated by cancer-produced Fas ligand for optimal growth.

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