Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Fas triggers an alternative, caspase-8-independent cell death pathway using the kinase RIP as effector molecule.
Caspase-10 is recruited to and activated at the native TRAIL and CD95 death-inducing signalling complexes in a FADD-dependent manner but can not functionally substitute caspase-8.
Mechanisms of nonspecific cytotoxic cell regulation of apoptosis: cytokine-like activity of Fas ligand.
Large-scale identification and characterization of human genes that activate NF-kappaB and MAPK signaling pathways.
Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes.
Regulation of apoptosis by the Ft1 protein, a new modulator of protein kinase B/Akt.
Regulation of FasL expression: a SH3 domain containing protein family involved in the lysosomal association of FasL.
The role of receptor internalization in CD95 signaling.
The adaptor protein Nck interacts with Fas ligand: Guiding the death factor to the cytotoxic immunological synapse.
Specific isolation of placenta-derived exosomes from the circulation of pregnant women and their immunoregulatory consequences.
The Fas ligand intracellular domain is released by ADAM10 and SPPL2a cleavage in T-cells.
A proteomic screen reveals novel Fas ligand interacting proteins within nervous system Schwann cells.
Peroxisome proliferator-activated receptor gamma activates fas ligand gene promoter inducing apoptosis in human breast cancer cells.
Plasminogen activator inhibitor-1 protects endothelial cells from FasL-mediated apoptosis.
Identification of SH3 domain interaction partners of human FasL (CD178) by phage display screening.
Modulation of the CD95-induced apoptosis: the role of CD95 N-glycosylation.
PMLRARα binds to Fas and suppresses Fas-mediated apoptosis through recruiting c-FLIP in vivo.
Vesicles released by activated T cells induce both Fas-mediated RIP-dependent apoptotic and Fas-independent nonapoptotic cell deaths.
A type III effector antagonizes death receptor signalling during bacterial gut infection.
Caspase-mediated cleavage of phospholipid flippase for apoptotic phosphatidylserine exposure.
Using an in situ proximity ligation assay to systematically profile endogenous protein-protein interactions in a pathway network.
A proteome-scale map of the human interactome network.
TNFα sensitizes neuroblastoma cells to FasL-, cisplatin- and etoposide-induced cell death by NF-κB-mediated expression of Fas.
Lifeguard Inhibits Fas Ligand-mediated Endoplasmic Reticulum-Calcium Release Mandatory for Apoptosis in Type II Apoptotic Cells.
Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing.
Architecture of the human interactome defines protein communities and disease networks.
A reference map of the human binary protein interactome.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
A physical wiring diagram for the human immune system.
Multimodal cell maps as a foundation for structural and functional genomics.
Human Fas ligand: gene structure, chromosomal location and species specificity.
Fas ligand mutation in a patient with systemic lupus erythematosus and lymphoproliferative disease.
Characterization of Fas (Apo-1, CD95)-Fas ligand interaction.
Fas and Fas ligand interaction is necessary for human osteoblast apoptosis.
Caspase-8 processing in the DISC
FASL:FAS Receptor Trimer:FADD complex binds procaspase-10
FLIP(S) and procaspase-8 form heterodimer
Caspase-8 and FLIP(L) processing at DISC
FLIP(L) and procaspase-8 form heterodimer in FasL/CD95 signaling
FLIP(L) and procaspase-8 form heterodimer
Trimerization of the FASL:FAS receptor complex
FAS-mediated dimerization of procaspase-8
FASL:FAS Receptor Trimer:FADD complex binds pro-Caspase-8
FASLG (FasL) gene expression
FASLG gene expression is stimulated by FOXO1,FOXO3,(FOXO4)