EC Number   |
General Information |
Reference |
|---|
   3.4.22.55 | evolution |
caspase-2 is an evolutionarily conserved caspase with features of both initiator and executioner caspases |
718112 |
| 3.4.22.55 | evolution |
caspase-2 is the most evolutionarily conserved member in the human caspase family |
717846 |
| 3.4.22.55 | malfunction |
both pharmacological inhibition and shRNA-mediated knockdown of caspase-2 suppresses myogenic differentiation and dramatically impaired myotube formation |
752842 |
| 3.4.22.55 | malfunction |
Casp2-null animals develop normally, and thymocytes and neurons derived from them seem to undergo similar levels of apoptosis to those from wild-type littermates. Nevertheless, several subtle phenotypes are associated with the Casp2-knockout mice: Casp2-knockout females have a slight increase in the number of oocytes and Casp2/ oocytes show reduced apoptosis in response to treatment with doxorubicin. The neurons derived from Casp2-null mice are resistant to beta-amyloid-mediated death, which suggests a role for caspase 2 in neuronal death. Casp2-deficient mice also show signs of premature ageing, including accumulation of oxidative damage. Mouse embryonic fibroblasts from Casp2-deficient animals show a reduced or delayed apoptotic response to some cytotoxic drugs, have an aberrant DNA damage and cell cycle response and are readily transformed when they are challenged by oncogene expression. |
713092 |
| 3.4.22.55 | malfunction |
caspase-2 deficiency leads to increased cellular stress largely because these mice fail to respond to oxidative stress by upregulating their antioxidant defense mechanism |
754936 |
| 3.4.22.55 | malfunction |
caspase-2 knockout mice do not develop early spontaneous tumors, but loss of caspase-2 in mice is associated with accelerated tumorigenesis driven by transgenic c-Myc on the mu-enhancer, thus caspase-2-deficient embryonic fibroblasts are more efficiently transformed than wild-type cells. Caspase-2-deficient mice have features consistent with accelerated ageing, phenotype, overview |
717458 |
| 3.4.22.55 | malfunction |
cells lacking caspase-2 are protected from cell death induced by Staphylococcus aureus alpha-toxin |
732220 |
| 3.4.22.55 | malfunction |
decreased caspase-2 and RAIDD expression is observed in mantle cell lymphoma tumor samples. In addition, drug resistance in childhood forms of acute lymphoblastic leukemia is correlated with decreased levels of caspase-2. In contrast, increased levels of caspase-2 in acute myelogenous leukemia and adult ALL are associated with decreased patient survival. Possibly inactivation of caspase-2 in tumors occurs through disruption of the pathway through mutation or improper regulation of a protein that regulates caspase-2 activity |
717458 |
| 3.4.22.55 | malfunction |
decreasing the levels of caspase-2 restores long-term memory in mice that have existing deficits |
754859 |
| 3.4.22.55 | malfunction |
depletion of caspase-2 prevents p21 expression and thereby reverts the gamma-IR-induced senescent phenotype of wild-type HCT116 colon carcinoma cells into apoptosis, knockdown of none of the caspase-2-interacting components RAIDD, RIP or DNA-PKcs is able to mimic these processes, but knockdown of caspase-2 specifically impairs DNA damage-induced p21 expression, and silencing of caspase-2 impairs exogenous expression of p21 constructs containing 3'-UTR sequences, whereas overexpression of a caspase-2 mutant increases p21 levels. Silencing of caspase-2 impairs exogenous expression of p21 constructs containing 3'-UTR sequences |
717457 |
