Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic assignment of GO terms using logical inference, based on on inter-ontology links
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
p38 protects human melanoma cells from UV-induced apoptosis through down-regulation of NF-kappaB activity and Fas expression.
Fas preassociation required for apoptosis signaling and dominant inhibition by pathogenic mutations.
Negative regulation of Fas-mediated apoptosis by FAP-1 in human cancer cells.
Inhibition of Daxx-mediated apoptosis by heat shock protein 27.
Glutamine-dependent antiapoptotic interaction of human glutaminyl-tRNA synthetase with apoptosis signal-regulating kinase 1.
Fas triggers an alternative, caspase-8-independent cell death pathway using the kinase RIP as effector molecule.
Apoptosis signal-regulating kinase 1 controls the proapoptotic function of death-associated protein (Daxx) in the cytoplasm.
Apoptosis-linked gene 2 binds to the death domain of Fas and dissociates from Fas during Fas-mediated apoptosis in Jurkat cells.
Caspase-10 is an initiator caspase in death receptor signaling.
Glutathione peroxidase-1 protects from CD95-induced apoptosis.
FAP-1 association with Fas (Apo-1) inhibits Fas expression on the cell surface.
Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes.
Purification and molecular cloning of the APO-1 cell surface antigen, a member of the tumor necrosis factor/nerve growth factor receptor superfamily. Sequence identity with the Fas antigen.
A death receptor-associated anti-apoptotic protein, BRE, inhibits mitochondrial apoptotic pathway.
CD47 augments Fas/CD95-mediated apoptosis.
The role of receptor internalization in CD95 signaling.
Inhibition of ADP/ATP exchange in receptor-interacting protein-mediated necrosis.
Caspase-8 prevents sustained activation of NF-kappaB in monocytes undergoing macrophagic differentiation.
Palmitoylation of CD95 facilitates formation of SDS-stable receptor aggregates that initiate apoptosis signaling.
Yes and PI3K bind CD95 to signal invasion of glioblastoma.
Identification of an antiapoptotic protein complex at death receptors.
Expression of the Bcl-2 protein BAD promotes prostate cancer growth.
MHC class II-associated proteins in B-cell exosomes and potential functional implications for exosome biogenesis.
The Fas-FADD death domain complex structure reveals the basis of DISC assembly and disease mutations.
Whole-exome-sequencing-based discovery of human FADD deficiency.
Caveolin-1 mediates Fas-BID signaling in hyperoxia-induced apoptosis.
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.
Structural insights into the mechanism of calmodulin binding to death receptors.
Using an in situ proximity ligation assay to systematically profile endogenous protein-protein interactions in a pathway network.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
A physical wiring diagram for the human immune system.
Protection from Fas-mediated apoptosis by a soluble form of the Fas molecule.
Three functional soluble forms of the human apoptosis-inducing Fas molecule are produced by alternative splicing.
A novel protein that interacts with the death domain of Fas/APO1 contains a sequence motif related to the death domain.
FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis.
RIP: a novel protein containing a death domain that interacts with Fas/APO-1 (CD95) in yeast and causes cell death.
Fas and Fas ligand interaction is necessary for human osteoblast apoptosis.
Requirement for the CD95 receptor-ligand pathway in c-Myc-induced apoptosis.
Effect of age and apoptosis on the mouse homologue of the huWRN gene.
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
TP53 family members stimulate FAS gene expression
Trimerization of the FASL:FAS receptor complex
FAS-mediated dimerization of procaspase-8
FASL:FAS Receptor Trimer:FADD complex binds pro-Caspase-8
Deep research report on FAS
Falcon deep research report on FAS (CD95/APO-1) functional annotation and translational landscape
The Crosstalk of Apoptotic and Non-Apoptotic Signaling in CD95 System.
FAS mediates apoptosis, inflammation, and treatment of pathogen infection.
Genetic Testing in Patients with Autoimmune Lymphoproliferative Syndrome: Experience of 802 Patients at Cincinnati Children's Hospital Medical Center.
CAN008 prolongs overall survival in patients with newly diagnosed GBM characterized by high tumor mutational burden.
Treatment with the apoptosis inhibitor Asunercept reduces clone sizes in patients with lower risk myelodysplastic neoplasms.