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c-jun-n-terminal kinase month download article/chapter amp-activated protein kinase high-molecular-weight phosphoprotein phosphatase glycogenolysis-related gene expression fatty acid beta-oxidation protein serine/threonine phosphatases acetaminophen-induced liver injury drug-induced liver injury dna damage-inducible 45α acetaminophen-evoked liver injury glucose-upregulated molecular chaperone repair-mediated dna demethylation virus-induced immune tolerance liquid chromatography–mass spectrometry foxo–smad synexpression group interferon-alpha therapeutic response immunostimulatory 3p-hbx-sirnas apap-induced liver injury rat-liver phosphoprotein phosphatase p53-regulated protein gadd45 gadd45-mediated growth suppression ampk-mediated gsk3beta inhibition jnk/sapk-dependent apoptosis gadd45-gamma utilize p38 iron-catalyzed oxidative stress related subjects full article pdf acetaminophen-induced hepatotoxicity drug-induced hepatotoxicity hep-g2 hepatoma cells apap-injured mouse livers primary human hepatocytes protein phosphatase 2a cell cycle checkpoint tricarboxylic acid cycle ancient energy gauge apap-treated hepatocytes apap-induced damage drug-induced toxicity basic medical sciences privacy choices/manage cookies gadd45α ampk access cdc2 kinase correlates clinical research center acute liver failure intact rat liver nonalcoholic steatohepatitis induced nuclear dna fragmentation amp triggers phosphorylation

Questions {❓}

• Hoyer-Hansen M, Jaattela M (2007) AMP-activated protein kinase: a universal regulator of autophagy?

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         headline:GADD45α alleviates acetaminophen-induced hepatotoxicity by promoting AMPK activation
         description:As an analgesic and antipyretic drug, acetaminophen (APAP) is commonly used and known to be safe at therapeutic doses. In many countries, the overuse of APAP provokes acute liver injury and even liver failure. APAP-induced liver injury (AILI) is the most used experimental model of drug-induced liver injury (DILI). Here, we have demonstrated elevated levels of growth arrest and DNA damage-inducible 45α (GADD45α) in the livers of patients with DILI/AILI, in APAP-injured mouse livers and in APAP-treated hepatocytes. GADD45α exhibited a protective effect against APAP-induced liver injury and alleviated the accumulation of small lipid droplets in vitro and in vivo. We found that GADD45α promoted the activation of AMP-activated protein kinase α and induced fatty acid beta-oxidation, tricarboxylic acid cycle (TCA) and glycogenolysis-related gene expression after APAP exposure. Liquid chromatography–mass spectrometry (LC–MS) analysis showed that GADD45α increased the levels of TCA cycle metabolites. Co-immunoprecipitation analysis showed that Ppp2cb, a catalytic subunit of protein phosphatase 2A, could interact directly with GADD45α. Our results indicate that hepatocyte GADD45α might represent a therapeutic target to prevent and rescue liver injury caused by APAP.
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      headline:GADD45α alleviates acetaminophen-induced hepatotoxicity by promoting AMPK activation
      description:As an analgesic and antipyretic drug, acetaminophen (APAP) is commonly used and known to be safe at therapeutic doses. In many countries, the overuse of APAP provokes acute liver injury and even liver failure. APAP-induced liver injury (AILI) is the most used experimental model of drug-induced liver injury (DILI). Here, we have demonstrated elevated levels of growth arrest and DNA damage-inducible 45α (GADD45α) in the livers of patients with DILI/AILI, in APAP-injured mouse livers and in APAP-treated hepatocytes. GADD45α exhibited a protective effect against APAP-induced liver injury and alleviated the accumulation of small lipid droplets in vitro and in vivo. We found that GADD45α promoted the activation of AMP-activated protein kinase α and induced fatty acid beta-oxidation, tricarboxylic acid cycle (TCA) and glycogenolysis-related gene expression after APAP exposure. Liquid chromatography–mass spectrometry (LC–MS) analysis showed that GADD45α increased the levels of TCA cycle metabolites. Co-immunoprecipitation analysis showed that Ppp2cb, a catalytic subunit of protein phosphatase 2A, could interact directly with GADD45α. Our results indicate that hepatocyte GADD45α might represent a therapeutic target to prevent and rescue liver injury caused by APAP.
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         Drug-induced liver injury (DILI)
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         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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