EC Number | Application | Comment | Organism |
---|---|---|---|
6.3.2.2 | 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 |
EC Number | Inhibitors | Comment | Organism | Structure |
---|---|---|---|---|
6.3.2.2 | 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 |
EC Number | Organism | UniProt | Comment | Textmining |
---|---|---|---|---|
6.3.2.2 | Mus musculus | - |
- |
- |
EC Number | Source Tissue | Comment | Organism | Textmining |
---|---|---|---|---|
6.3.2.2 | hepatocyte | - |
Mus musculus | - |
6.3.2.2 | liver | - |
Mus musculus | - |
6.3.2.2 | primary cell | - |
Mus musculus | - |