Protein Variants | Comment | Organism |
---|---|---|
additional information | replication-deficient human adenovirus containing rat GPX4 cDNA (adenovirus GPX4 [Ad-GPX4]) is used to overexpress GPX4 in rats by injection into the right lateral ventricle of the brain of male Sprague-Dawley rats | Rattus norvegicus |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
2 glutathione + a hydroperoxy-fatty-acyl-[lipid] | Rattus norvegicus | - |
glutathione disulfide + a hydroxy-fatty-acyl-[lipid] + H2O | - |
? | |
2 glutathione + a hydroperoxy-fatty-acyl-[lipid] | Rattus norvegicus Sprague-Dawley | - |
glutathione disulfide + a hydroxy-fatty-acyl-[lipid] + H2O | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Rattus norvegicus | P36970 | male rats | - |
Rattus norvegicus Sprague-Dawley | P36970 | male rats | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
brain | - |
Rattus norvegicus | - |
cerebral cortex | - |
Rattus norvegicus | - |
neuron | endogenous GPX4 is mainly expressed in neurons, usage of primary cultured cortical neurons | Rattus norvegicus | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
2 glutathione + a hydroperoxy-fatty-acyl-[lipid] | - |
Rattus norvegicus | glutathione disulfide + a hydroxy-fatty-acyl-[lipid] + H2O | - |
? | |
2 glutathione + a hydroperoxy-fatty-acyl-[lipid] | - |
Rattus norvegicus Sprague-Dawley | glutathione disulfide + a hydroxy-fatty-acyl-[lipid] + H2O | - |
? |
Synonyms | Comment | Organism |
---|---|---|
glutathione peroxidase 4 | - |
Rattus norvegicus |
Organism | Comment | Expression |
---|---|---|
Rattus norvegicus | subarachnoid hemorrhage (SAH) reduces enzyme expression | down |
General Information | Comment | Organism |
---|---|---|
malfunction | decrease of GPX4 expression potentially plays an important role in ferroptosis during early brain injury after SAH. Overexpression of GPX4 significantly reduces lipid peroxidation and cell death in the experimental SAH models both in vivo. Overexpression of GPX4 has a neuroprotective effect after SAH. Overexpression of GPX4 ameliorates brain edema and neurological deficits at 24 h after SAH | Rattus norvegicus |
physiological function | early brain injury is an essential pathological process after subarachnoid hemorrhage (SAH), with many cell death modalities. Ferroptosis is a regulated cell death caused by the iron-dependent accumulation of lipid peroxidation, which can be prevented by glutathione peroxidase 4 (GPX4), role of GPX4 in neuronal cell death, overview. Among the various mechanisms of early brain injury, lipid peroxidation is an important mechanism and is closely related to a poor clinical outcome. The generation of oxidized phospholipid (oxPL) species plays a crucial role in ferroptosis13. Glutathione peroxidase 4 (GPX4) inhibits ferroptosis by acting as the sole enzyme to convert hydroperoxides into nontoxic lipid alcohols | Rattus norvegicus |