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
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
Bax-dependent caspase-3 activation is a key determinant in p53-induced apoptosis in neurons.
Epistatic and independent functions of caspase-3 and Bcl-X(L) in developmental programmed cell death.
DNA damage-induced neural precursor cell apoptosis requires p53 and caspase 9 but neither Bax nor caspase 3.
Deafness due to degeneration of cochlear neurons in caspase-3-deficient mice.
Caspase 3 deficiency rescues peripheral nervous system defect in retinoblastoma nullizygous mice.
An endoplasmic reticulum stress-specific caspase cascade in apoptosis. Cytochrome c-independent activation of caspase-9 by caspase-12.
The role of Asp-462 in regulating Akt activity.
p73 is required for survival and maintenance of CNS neurons.
Role of prodomain in importin-mediated nuclear localization and activation of caspase-2.
Comparative analysis of apoptosis and inflammation genes of mice and humans.
Bax and Bak can localize to the endoplasmic reticulum to initiate apoptosis.
Ischemic preconditioning by caspase cleavage of poly(ADP-ribose) polymerase-1.
Caspase-3 regulates cell cycle in B cells: a consequence of substrate specificity.
Roles of MGMT and MLH1 proteins in alkylation-induced apoptosis and mutagenesis.
Enhanced oligodendrocyte survival after spinal cord injury in Bax-deficient mice and mice with delayed Wallerian degeneration.
Molecular components of a cell death pathway activated by endoplasmic reticulum stress.
Transcriptional activation of known and novel apoptotic pathways by Nur77 orphan steroid receptor.
High commitment of embryonic keratinocytes to terminal differentiation through a Notch1-caspase 3 regulatory mechanism.
BAD is a pro-survival factor prior to activation of its pro-apoptotic function.
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.
Caspases 3 and 7: key mediators of mitochondrial events of apoptosis.
Huntingtin inhibits caspase-3 activation.
Targeted disruption of the murine large nuclear KIAA1440/Ints1 protein causes growth arrest in early blastocyst stage embryos and eventual apoptotic cell death.
Estrogen suppresses uterine epithelial apoptosis by inducing birc1 expression.
Ronin is essential for embryogenesis and the pluripotency of mouse embryonic stem cells.
Proteome-wide substrate analysis indicates substrate exclusion as a mechanism to generate caspase-7 versus caspase-3 specificity.
Caspase-3 triggers early synaptic dysfunction in a mouse model of Alzheimer's disease.
Focusing forward genetics: a tripartite ENU screen for neurodevelopmental mutations in the mouse.
Cyclooxygenase-2-dependent phosphorylation of the pro-apoptotic protein Bad inhibits tonicity-induced apoptosis in renal medullary cells.
Maintenance of muscle stem-cell quiescence by microRNA-489.
Nek5, a novel substrate for caspase-3, promotes skeletal muscle differentiation by up-regulating caspase activity.
Loss of Usp9x disrupts cortical architecture, hippocampal development and TGFβ-mediated axonogenesis.
Dok5 is involved in the signaling pathway of neurotrophin-3 against TrkC-induced apoptosis.
BDNF and NT4 play interchangeable roles in gustatory development.
Local pruning of dendrites and spines by caspase-3-dependent and proteasome-limited mechanisms.
Mammalian target of rapamycin is essential for cardiomyocyte survival and heart development in mice.
Exposure of phosphatidylserine by Xk-related protein family members during apoptosis.
The BAD-BAX-Caspase-3 Cascade Modulates Synaptic Vesicle Pools via Autophagy.
Gasdermin D licenses MHCII induction to maintain food tolerance in small intestine.
Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice.
Essential contribution of caspase 3/CPP32 to apoptosis and its associated nuclear changes.
Caspase cleavage of Unc5h1
E-cadherin strand dimer degradation by Casp3
UniProt record for mouse Casp3
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Casp3 is the major effector caspase in the execution phase of apoptosis.
"Thiol protease that acts as a major effector caspase involved in the execution phase of apoptosis...mediates execution of apoptosis by catalyzing cleavage of many proteins"
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The active Casp3 enzyme is a heterotetramer with p17 and p12 subunits.
"Heterotetramer that consists of two anti-parallel arranged heterodimers, each one formed by a 17 kDa (p17) and a 12 kDa (p12) subunit."
Manual deep research synthesis for mouse Casp3
Falcon deep research report on mouse Casp3
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Falcon synthesis identifies mouse Casp3 as a cysteine-aspartate executioner protease in apoptotic proteolysis, with context-specific pyroptotic and non-apoptotic outputs.
"Caspase-3 is a cysteine-aspartate protease functioning as a principal executioner protease in apoptotic cell death."