Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
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
DNA damage-induced neural precursor cell apoptosis requires p53 and caspase 9 but neither Bax nor caspase 3.
Bcl-X(L)-caspase-9 interactions in the developing nervous system: evidence for multiple death pathways.
Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9.
Differential requirement for caspase 9 in apoptotic pathways in vivo.
An endoplasmic reticulum stress-specific caspase cascade in apoptosis. Cytochrome c-independent activation of caspase-9 by caspase-12.
Comparative analysis of apoptosis and inflammation genes of mice and humans.
Bax and Bak can localize to the endoplasmic reticulum to initiate apoptosis.
Molecular components of a cell death pathway activated by endoplasmic reticulum stress.
Nucling recruits Apaf-1/pro-caspase-9 complex for the induction of stress-induced apoptosis.
Regulation of the expression of caspase-9 by the transcription factor activator protein-4 in glucocorticoid-induced apoptosis.
Apoptosis caused by p53-induced protein with death domain (PIDD) depends on the death adapter protein RAIDD.
Caspases 3 and 7: key mediators of mitochondrial events of apoptosis.
Estrogen suppresses uterine epithelial apoptosis by inducing birc1 expression.