[HTML][HTML] Silencing glycogen synthase kinase-3β inhibits acetaminophen hepatotoxicity and attenuates JNK activation and loss of glutamate cysteine ligase and …
M Shinohara, MD Ybanez, S Win, TA Than… - Journal of biological …, 2010 - ASBMB
Previously we demonstrated that c-Jun N-terminal kinase (JNK) plays a central role in
acetaminophen (APAP)-induced liver injury. In the current work, we examined other possible
signaling pathways that may also contribute to APAP hepatotoxicity. APAP treatment to mice
caused glycogen synthase kinase-3β (GSK-3β) activation and translocation to mitochondria
during the initial phase of APAP-induced liver injury (∼ 1 h). The silencing of GSK-3β, but
not Akt-2 (protein kinase B) or glycogen synthase kinase-3α (GSK-3α), using antisense …
acetaminophen (APAP)-induced liver injury. In the current work, we examined other possible
signaling pathways that may also contribute to APAP hepatotoxicity. APAP treatment to mice
caused glycogen synthase kinase-3β (GSK-3β) activation and translocation to mitochondria
during the initial phase of APAP-induced liver injury (∼ 1 h). The silencing of GSK-3β, but
not Akt-2 (protein kinase B) or glycogen synthase kinase-3α (GSK-3α), using antisense …