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Literature summary for 6.3.2.2 extracted from

  • Shinohara, M.; Ybanez, M.D.; Win, S.; Than, T.A.; Jain, S.; Gaarde, W.A.; Han, D.; Kaplowitz, N.
    Silencing glycogen synthase kinase-3beta inhibits acetaminophen hepatotoxicity and attenuates JNK activation and loss of glutamate cysteine ligase and myeloid cell leukemia sequence 1 (2010), J. Biol. Chem., 285, 8244-8255.
    View publication on PubMedView publication on EuropePMC
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Application

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

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

Organism UniProt Comment Textmining
Mus musculus
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-
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Source Tissue

Source Tissue Comment Organism Textmining
hepatocyte
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 Mus musculus
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liver
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 Mus musculus
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primary cell
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 Mus musculus
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