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  2. Matching Content Categories
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  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
  6. Keywords
  7. Topics
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We began analyzing https://link.springer.com/article/10.1007/s00018-018-2912-y, but it redirected us to https://link.springer.com/article/10.1007/s00018-018-2912-y. The analysis below is for the second page.

Title[redir]:
GADD45α alleviates acetaminophen-induced hepatotoxicity by promoting AMPK activation | Cellular and Molecular Life Sciences
Description:
Abstract 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. Graphical abstract

Matching Content Categories {📚}

  • Education
  • Health & Fitness
  • Science

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


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How Does Doi.org Make Money? {💸}

We don’t know how the website earns money.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Doi.org could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

article, google, scholar, pubmed, cas, liver, wang, cell, protein, kinase, central, injury, biol, gadd, zhang, activation, acetaminopheninduced, hepatotoxicity, ampk, ampactivated, gaddα, chen, signaling, hardie, druginduced, growth, dna, cycle, fornace, biochem, acetaminophen, acid, phosphatase, access, protects, hepatology, mechanism, inhibition, chem, med, yang, zhan, energy, kim, shanghai, university, privacy, cookies, content, publish,

Topics {✒️}

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?

Schema {🗺️}

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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
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         Drug-induced liver injury (DILI)
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         Biomedicine
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         Biochemistry
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      name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China
      name:Division of Gastroenterology and Hepatology, School of Medicine, Shanghai Institute of Digestive Disease, Renji Hospital, Shanghai Jiao Tong University, Shanghai, China
      name:Division of Gastroenterology and Hepatology, School of Medicine, Shanghai Institute of Digestive Disease, Renji Hospital, Shanghai Jiao Tong University, Shanghai, China
      name:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China
      name:Division of Gastroenterology and Hepatology, School of Medicine, Shanghai Institute of Digestive Disease, Renji Hospital, Shanghai Jiao Tong University, Shanghai, China
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