Activating Compound | Comment | Organism | Structure |
---|---|---|---|
additional information | the topoisomerase-II inhibitor etoposide induces processing of procaspase-2 | Homo sapiens |
Protein Variants | Comment | Organism |
---|---|---|
additional information | knockdown of caspase-2 and overexpression of a caspase-2 mutant | Homo sapiens |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Posttranslational Modification | Comment | Organism |
---|---|---|
proteolytic modification | the topoisomerase-II inhibitor etoposide induces processing of procaspase-2 | Homo sapiens |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
HCT-116 cell | - |
Homo sapiens | - |
General Information | Comment | Organism |
---|---|---|
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 | Homo sapiens |
physiological function | caspase-2 is commonly required for DNA damage-induced p21 expression. Caspase-2 regulates p21 expression at the translational level, independently of its enzymatic activity but also not requiring known caspase-2-activating platforms | Homo sapiens |