| Protein Name: | Cytochrome c oxidase subunit 4 (P13073) |
|---|---|
| Gene Name: | COX4I1 |
| Description: | Cytochrome c oxidase subunit 4 isoform 1, mitochondrial precursor (EC 1 9 3 1) (Cytochrome c oxidase subunit IV isoform 1) (COX IV-1) (Cytochrome c oxidase polypeptide IV) |
| PDB ID: | |
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This panel provides drug-protein interaction and their ADRs along with references
| Interacting Drugs | Toxicity | Mechanism | Reference |
|---|---|---|---|
| Didanosine | Cytotoxicity | Increase lactate production and decrease activities of COX (complex IV) and SDH (part of complex II)@are the most potent inhibitors of mitochondrial function@thus AZT@ ddI and ddC all exert Cytotoxicity on human muscle cells and induce functional alterations of mitochondria possibly due to mechanisms other than the sole mtDNA depletion [ ADR Type 1 ] | Cellular and mitochondrial toxicity of zidovudine (AZT), didanosine (ddI) and zalcitabine (ddC) on cultured human muscle cells |
| Zalcitabine | Cytotoxicity | Increase lactate production and decrease activities of COX (complex IV) and SDH (part of complex II)@are the most potent inhibitors of mitochondrial function@thus AZT@ ddI and ddC all exert Cytotoxicity on human muscle cells and induce functional alterations of mitochondria possibly due to mechanisms other than the sole mtDNA depletion [ ADR Type 1 ] | Cellular and mitochondrial toxicity of zidovudine (AZT), didanosine (ddI) and zalcitabine (ddC) on cultured human muscle cells |
| Zidovudine | Cytotoxicity | Increase lactate production and decrease activities of COX (complex IV) and SDH (part of complex II)@are the most potent inhibitors of mitochondrial function@thus AZT@ ddI and ddC all exert Cytotoxicity on human muscle cells and induce functional alterations of mitochondria possibly due to mechanisms other than the sole mtDNA depletion [ ADR Type 1 ] | Cellular and mitochondrial toxicity of zidovudine (AZT), didanosine (ddI) and zalcitabine (ddC) on cultured human muscle cells |
This panel provides information on drug category
| Toxicity | Source |
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