EC Number   |
General Information |
Reference |
|---|
   3.4.22.B66 | malfunction |
carbon tetrachloride-induced apoptosis and liver damage is markedly reduced in caspase-12-deficient mice |
732979 |
| 3.4.22.B66 | physiological function |
apoptosis is elevated when myoblasts are subjected to cyclic mechanical stretch for 12, 24, and 36 hr. Cyclic mechanical stretch triggers the endoplasmic reticulum stress and caspase-12 cleavage. Endoplasmic reticulum stress inhibitor GSK 2606414 suppresses the cyclic mechanical stretch-induced cleavage of caspase-12 and myoblast apoptosis. Silencing of caspase-12 attenuates the apoptosis of myoblasts. Cells overexpressing a truncated caspase-12 segment which starts from Asp94 and ends at Asn419, undergo apoptosis under both static and stretched conditions |
754246 |
| 3.4.22.B66 | physiological function |
caspase-12 is an important upstream messenger in POX-induced apoptosis in EL-4 cells |
718428 |
| 3.4.22.B66 | physiological function |
caspase-12 knockout mice also lack caspase-11 expression. Caspase-12 deficiency in both ex vivo-stimulated bone-marrow-derived macrophages and in in vivo-challenged mice fails to increase caspase-1 activation. Release of mature IL-1beta and IL-18 by both the canonical and noncanonical inflammasome pathways is consequently also not enhanced by deletion of caspase-12 |
754887 |
| 3.4.22.B66 | physiological function |
caspase-12 plays a pivotal role in carbon tetrachloride-induced hepatic apoptosis through the activation of the downstream effector caspase-3 directly and/or indirectly via capase-9 activation |
732979 |
| 3.4.22.B66 | physiological function |
caspase-12 plays a role in controlling West Nile virus viral infection via the pattern recognition receptor RIG-I. Caspase-12 positively modulates the production of type I interferon by regulating E3 ubiquitin ligase TRIM25-mediated ubiquitination of RIG-I |
718146 |
| 3.4.22.B66 | physiological function |
cyclic stretch leads to apoptosis in myoblast. GRP78 mRNA and protein are significantly increased and ER chaperone CHOP and caspase-12 are activated in myoblast exposed to cyclic stretch. Caspase-12 inhibition reduces stretch-induced apoptosis, and caspase-12 activates caspase-3 to induce apoptosis |
752520 |
| 3.4.22.B66 | physiological function |
in mice with experimental autoimmune encephalomyelitis, expression of chaperone CHOP, caspase-12, and protein disulfide isomerase is upregulated in the brain. Elevated levels of caspase-12/CHOP are observed in astrocytes, oligodendrocytes, and microglia in the hippocampus section of experimental autoimmune encephalomyelitis mice |
753123 |
| 3.4.22.B66 | physiological function |
loss of caspase-12 in mouse strains predisposes mice to develop obesity, metabolic inflammation, and insulin resistance, whereas loss of caspase-11 has no effect. The Nlrp3 inflammasome pathway mediates the metabolic syndrome of caspase-12 deficient mice |
754325 |
| 3.4.22.B66 | physiological function |
overexpression of Casp12 mediates IkappaBalpha degradation and significantly increases NFkappaB activity. Exposure of human nasopharyngeal carcinoma cells to phorbol-12-myristate-13-acetate increases the levels of Casp12 and MMP-9 resulting in nasopharyngeal carcinoma cells invasion. Suppression of Casp12 or an inhibitor of Casp12 markedly decreases the level of phorbol-12-myristate-13-acetate-induced MMP-9 protein and cell invasion. Suppression of Casp12 significantly inhibits the basal activity of NFkappaB and decreases the phorbol-12-myristate-13-acetate-induced NFkappaB reporter activity |
754963 |
