| Protein Name: | Caspase-3 (P42574) |
|---|---|
| Gene Name: | CASP3 |
| Description: | Caspase-3 precursor (EC 3 4 22 -) (CASP-3) (Apopain) (Cysteine protease CPP32) (Yama protein) (CPP-32) (SREBP cleavage activity 1) (SCA-1) [Contains: Caspase-3 p17 subunit; Caspase-3 p12 subunit] |
| PDB ID: | 1CP3 |
| Protein Family: | |
| Protein Category: | Enzyme |
This panel provides drug-protein interaction and their ADRs along with references
| Interacting Drugs | Toxicity | Mechanism | Reference |
|---|---|---|---|
| Arsenic trioxide | Cytotoxicity | As(2)O(3) also caused an INCREASE of cytoplasmic cytochrome c@ translocation of antiapoptosis-inducing factor to the nuclei@ and a slight ACTIVATION of caspase 3@suggesting activation of a cytotoxic pathway different from that induced by conventional chemotherapeutic agents. [ ADR Type 2 ] | Arsenic trioxide-induced death of neuroblastoma cells involves activation of Bax and does not require p53 |
| Cidofovir | Apoptosis | Induction of CPP32 (caspase-3) protease activity by cidofovir@which leads to apoptosis [ ADR Type 2 ] | Induction of apoptosis by cidofovir in human papillomavirus (HPV)-positive cells |
| Digoxin | Oncogenesis | DiGOxin induced alteration in intracellular calcium/magnesium ratios and low ubiquinone levels can lead to a mitochondrial dysfunction resulting in increased free radical generation and reduced scavenging & caspase-3 activation producing a P21 defect contributing to oncogenesis [ ADR Type 2 ] | Hypothalamic digoxin mediated model for oncogenesis |
| Docetaxel | Cell Death | Docetaxel is able to activate caspase-3@ induce Bcl-2 phosphorylation and apoptosis in cells that show a prolonged G2/M arrest@ but cells may also die by a caspase-3-independent cell death mechanism [ ADR Type 2 ] | Variation in the kinetics of caspase-3 activation, Bcl-2 phosphorylation and apoptotic morphology in unselected human ovarian cancer cell lines as a response to docetaxel |
| Doxorubicin | Apoptosis | Adriamycin activated caspase-3 before the rise in JNK activity@ while the response to cisplatin occurs hours after JNK activation. [ ADR Type 2 ] | Lack of c-Jun activity increases survival to cisplatin |
| Etoposide | Apoptosis | Association of active caspase 8 with the mitochondrial membrane during apoptosis: potential roles in cleaving BAP31 and caspase 3 and mediating mitochondrion-endoplasmic reticulum cross talk in etoposide-induced cell death. [ ADR Type 2 ] | Association of active caspase 8 with the mitochondrial membrane during apoptosis: potential roles in cleaving BAP31 and caspase 3 and mediating mitochondrion-endoplasmic reticulum cross talk |
| Lovastatin | Apoptosis | Consistent with initiation of apoptosis@ cellular caspase-8@ caspase-9 and caspase-3 activities were elevated in lovastatin-treated cells. [ ADR Type 2 ] | Lovastatin inhibits tumor growth and lung metastasis in mouse mammary carcinoma model: a p53-independent mitochondrial-mediated apoptotic mechanism |
| Mannitol | Apoptosis | Mannitol induces the activation of caspases-3 and -9 in a time course similar to the dephosphorylation and degradation of FAK@which may lead to apoptosis [ ADR Type 2 ] | Insulin-like growth factor I prevents mannitol-induced degradation of focal adhesion kinase and Akt |
This panel provides information on drug category
| Toxicity | Source |
|---|---|
| Apoptosis | Cisplatin (CDDP) specifically induces apoptosis via sequential activation of caspase-8, -3 and -6 in osteosarcoma |