human FAS shRNA silencing Adenovirus

ALPS1A; APO-1; Apo-1 antigen; APO-1 cell surface antigen; apoptosis antigen 1; apoptosis signaling receptor FAS; apoptosis-mediating surface antigen FAS; APT1; CD antigen CD95; CD95; CD95 antigen; Fas (TNF receptor superfamily, member 6); Fas AMA; FAS1; FASLG receptor; FASTM; mutant tumor necrosis receptor superfamily member 6; TNF receptor superfamily member 6; TNFRSF6; tumor necrosis factor receptor superfamily member 6; tumor necrosis factor receptor superfamily, member 6

Tumor necrosis factor receptor superfamily member 6, FAS, functions as the receptor for TNFSF6/FASLG. The adapter molecule FADD recruits caspase-8 to the activated FAS receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) which mediate apoptosis. FAS-mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both [taken from the Universal Protein Resource (UniProt) www.uniprot.org/uniprot/ P25445].

FAS is a member of the TNF-receptor superfamily. This receptor contains a death domain. It has been shown to play a central role in the physiological regulation of programmed cell death, and has been implicated in the pathogenesis of various malignancies and diseases of the immune system. The interaction of this receptor with its ligand allows the formation of a death-inducing signaling complex that includes Fas-associated death domain protein (FADD), caspase 8, and caspase 10. The autoproteolytic processing of the caspases in the complex triggers a downstream caspase cascade, and leads to apoptosis. This receptor has been also shown to activate NF-kappaB, MAPK3/ERK1, and MAPK8/JNK, and is found to be involved in transducing the proliferating signals in normal diploid fibroblast and T cells. Several alternatively spliced transcript variants have been described, some of which are candidates for nonsense-mediated mRNA decay (NMD). The isoforms lacking the transmembrane domain may negatively regulate the apoptosis mediated by the full length isoform.

355

Fas cell surface death receptor

Fas cell surface death receptor

FAS

HGNC:11920

9606.0

1008

1008 bp

Tumor necrosis factor receptor superfamily member 6

NM_000043

NM_152872, NM_152871, NM_001320619, NM_000043, BC012479,

Aging,Alzheimer's Disease,Apoptosis,Cancer,CD95/FAS Signaling,DNA Damage/Repair,Estrogen Signaling,Gene Expression,Host-Virus Interactions,Hypoxia,Immunology,Interleukin Signaling,Lung Cancer,MAPK Signaling,Neurobiology,Neurodegeneration,Neurodevelopment,p53 Signaling,Parkinson's Disease,Signal Transduction,Spermatogenesis,T-cell Receptor Signaling,TNF Signaling

cancer,cell_biology,developmental_biology,genetics,immunology,infectious_disease,neurobiology,signal_transduction,transcription_translation

human

Tumor necrosis factor receptor superfamily member 6, FAS, functions as the receptor for TNFSF6/FASLG. The adapter molecule FADD recruits caspase-8 to the activated FAS receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) which mediate apoptosis. FAS-mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both [taken from the Universal Protein Resource (UniProt) www.uniprot.org/uniprot/ P25445].

Hs.244139

P25445