Application | Comment | Organism |
---|---|---|
medicine | activation of glycogen synthase kinase 3beta is a key mediator of the initial phase of acetaminophen-induced liver injury through modulating GCL and Mcl-1 degradation, as well as JNK activation in liver. The silencing of glycogen synthase kinase 3beta decreases the loss of hepatic GCL, and promotes greater GSH recovery in liver following acetaminophen treatment | Mus musculus |
Inhibitors | Comment | Organism | Structure |
---|---|---|---|
acetaminophen | treatment promotes the loss of glutamate cysteine ligase in liver. Activation of glycogen synthase kinase 3beta is a key mediator of the initial phase of acetaminophen-induced liver injury through modulating GCL and Mcl-1 degradation, as well as JNK activation in liver. The silencing of glycogen synthase kinase 3beta decreases the loss of hepatic GCL, and promotes greater GSH recovery in liver following acetaminophen treatment | Mus musculus |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
hepatocyte | - |
Mus musculus | - |
liver | - |
Mus musculus | - |
primary cell | - |
Mus musculus | - |