EC Number   |
General Information |
Reference |
|---|
   3.4.22.55 | malfunction |
down-regulation or inactivation of caspase-2 blocks amyloid beta-mediated effects on primary hippocampal cultures |
732560 |
| 3.4.22.55 | malfunction |
loss of caspase-2 leads to an acceleration of tumor onset in the Emü-Myc mouse lymphoma model |
753175 |
| 3.4.22.55 | malfunction |
loss of caspase-2 leads to enhanced tumor proliferation and progression |
753176 |
| 3.4.22.55 | malfunction |
maturation, activation, and cytokine secretion are significantly impaired in Caspase-2 knockout cells infected with Brucella abortus strain RB51 or Salmonella typhimurium strain SL1344 |
732704 |
| 3.4.22.55 | malfunction |
the loss of caspase-2 in mice results in an osteopenic phenotype associated with increased numbers of osteoclasts in vivo. Mitochondrial reactive oxygen species are significantly increased in caspase-deficient precursors after receptor activator of nuclear factor kappa-B ligand administration |
731559 |
| 3.4.22.55 | metabolism |
caspase-2 cleavage of tau at Asp314 impairs cognitive and synaptic function in animal and cellular models of tauopathies by promoting the missorting of tau to dendritic spines. The truncation product, DELTAtau314, resists fibrillation and is present at higher levels in brains from cognitively impaired mice and humans with Alzheimer's disease |
754859 |
| 3.4.22.55 | metabolism |
caspase-2 cleavage of tau at Asp314 impairs cognitive and synaptic function in animal and cellular models of tauopathies by promoting the missorting of tau to dendritic spines. The truncation product, DETAtau314, resists fibrillation and is present at higher levels in brains from cognitively impaired mice and humans with Alzheimer's disease |
754859 |
| 3.4.22.55 | metabolism |
caspase-2 is a critical mediator in the activation of the RhoA/ROCK-II signaling pathway, leading to the collapse of dendritic spines. Inactive RhoA-GDP but not active RhoA-GTP forms a complex with caspase-2 |
732560 |
| 3.4.22.55 | more |
caspase-2 is synthesized as an inactive zymogen. The zymogen sequence includes a long prodomain containing a CARD followed by a large domain, a linker, and a small domain. Caspase-2 undergoes autocatalytic activation to remove the prodomain and linker region to generate a stable dimer consisting of the large subunit p19 and the small subunit p12. This p19/p12 dimer self-associates to form the active caspase-2 |
717846 |
| 3.4.22.55 | physiological function |
apoptosis induced by doxorubicin and 5-fluorouracil is caspase-2-dependent |
710904 |
