Gene Ontology annotation through association of InterPro records with GO terms
Gene Ontology annotation by the MGI curatorial staff, curated orthology
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
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
Automated transfer of experimentally-verified manual GO annotation data to mouse-rat orthologs
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Automated transfer of experimentally-verified manual GO annotation data to mouse-human orthologs
Combined Automated Annotation using Multiple IEA Methods
The phosphoprotein protein PEA-15 inhibits Fas- but increases TNF-R1-mediated caspase-8 activity and apoptosis.
Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta.
Activation of pro-death Bcl-2 family proteins and mitochondria apoptosis pathway in tumor necrosis factor-alpha-induced liver injury.
C/EBPbeta phosphorylation by RSK creates a functional XEXD caspase inhibitory box critical for cell survival.
Relief of extrinsic pathway inhibition by the Bid-dependent mitochondrial release of Smac in Fas-mediated hepatocyte apoptosis.
Active caspase-8 translocates into the nucleus of apoptotic cells to inactivate poly(ADP-ribose) polymerase-2.
Ex vivo whole-embryo culture of caspase-8-deficient embryos normalize their aberrant phenotypes in the developing neural tube and heart.
Transcriptional activation of known and novel apoptotic pathways by Nur77 orphan steroid receptor.
Caspase-8 serves both apoptotic and nonapoptotic roles.
Inhibition of both the extrinsic and intrinsic death pathways through nonhomotypic death-fold interactions.
Vhlh gene deletion induces Hif-1-mediated cell death in thymocytes.
Apoptosis caused by p53-induced protein with death domain (PIDD) depends on the death adapter protein RAIDD.
The E3 ubiquitin ligase itch couples JNK activation to TNFalpha-induced cell death by inducing c-FLIP(L) turnover.
The apoptosome activates caspase-9 by dimerization.
Palmitoylation is required for efficient Fas cell death signaling.
A novel function of caspase-8 in the regulation of androgen-receptor-driven gene expression.
No death without life: vital functions of apoptotic effectors.
TIPE2, a negative regulator of innate and adaptive immunity that maintains immune homeostasis.
A mitochondrial protein compendium elucidates complex I disease biology.
FADD and caspase-8 control the outcome of autophagic signaling in proliferating T cells.
RIP3 mediates the embryonic lethality of caspase-8-deficient mice.
Catalytic activity of the caspase-8-FLIP(L) complex inhibits RIPK3-dependent necrosis.
Caveolin-1 mediates Fas-BID signaling in hyperoxia-induced apoptosis.
Mechanisms of necroptosis in T cells.
Caspase 8 inhibits programmed necrosis by processing CYLD.
TNF-induced necroptosis in L929 cells is tightly regulated by multiple TNFR1 complex I and II members.
Survival function of the FADD-CASPASE-8-cFLIP(L) complex.
Pellino3 targets RIP1 and regulates the pro-apoptotic effects of TNF-α.
Activity of protein kinase RIPK3 determines whether cells die by necroptosis or apoptosis.
RIPK1 regulates RIPK3-MLKL-driven systemic inflammation and emergency hematopoiesis.
RIPK1 blocks early postnatal lethality mediated by caspase-8 and RIPK3.
NEMO Prevents Steatohepatitis and Hepatocellular Carcinoma by Inhibiting RIPK1 Kinase Activity-Mediated Hepatocyte Apoptosis.
Phosphorylation and linear ubiquitin direct A20 inhibition of inflammation.
MOMP, cell suicide as a BCL-2 family business.
Death-domain dimerization-mediated activation of RIPK1 controls necroptosis and RIPK1-dependent apoptosis.
Pathogen blockade of TAK1 triggers caspase-8-dependent cleavage of gasdermin D and cell death.
Cleavage of RIPK1 by caspase-8 is crucial for limiting apoptosis and necroptosis.
K63-linked ubiquitination regulates RIPK1 kinase activity to prevent cell death during embryogenesis and inflammation.
Caspase-8 is the molecular switch for apoptosis, necroptosis and pyroptosis.
Mutations that prevent caspase cleavage of RIPK1 cause autoinflammatory disease.
Integration of innate immune signalling by caspase-8 cleavage of N4BP1.
Molecular cloning and characterization of mouse caspase-8.
Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors.
Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis.
Targeted disruption of the mouse Caspase 8 gene ablates cell death induction by the TNF receptors, Fas/Apo1, and DR3 and is lethal prenatally.
Molecular cloning and identification of murine caspase-8.
cIAPs block Ripoptosome formation, a RIP1/caspase-8 containing intracellular cell death complex differentially regulated by cFLIP isoforms.