Refine search

Search General Information

show results
Don't show organism specific information (fast!)
Search organism in taxonomic tree (slow, choose "exact" as search mode, e.g. "mammalia" for rat,human,monkey,...)
(Not possible to combine with the first option)
Refine your search

Search term:

Results 1 - 10 of 35 > >>
EC Number
General Information
Commentary
Reference
evolution
caspase-2 is an evolutionarily conserved caspase with features of both initiator and executioner caspases
evolution
caspase-2 is the most evolutionarily conserved member in the human caspase family
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.
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
malfunction
cells lacking caspase-2 are protected from cell death induced by Staphylococcus aureus alpha-toxin
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
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
malfunction
down-regulation or inactivation of caspase-2 blocks amyloid beta-mediated effects on primary hippocampal cultures
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
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
Results 1 - 10 of 35 > >>