ArticleThe Journal of cell biology1998
Mutation of a major keratin phosphorylation site predisposes to hepatotoxic injury in transgenic mice.
Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 98 citations in OpenAlex.
- Microcystin-LR and its health impacts: Chemistry, transmission routes, mechanisms of toxicity and target organs.Toxicology reports · 2025Review
- Posttranslational modifications of the cytoskeleton.Cytoskeleton (Hoboken, N.J.) · 2021Review
- KRT8 phosphorylation regulates the epithelial-mesenchymal transition in retinal pigment epithelial cells through autophagy modulation.Journal of cellular and molecular medicine · 2020Article
- The role of keratins in the digestive system: lessons from transgenic mouse models.Histochemistry and cell biology · 2018Review
- The application of post-translational modification oriented serum proteomics to assess experimental diabetes with complications.PloS one · 2018Article
- Intermediate Filaments and the Regulation of Cell Motility during Regeneration and Wound Healing.Cold Spring Harbor perspectives in biology · 2017Review
- Microcystin-LR induced liver injury in mice and in primary human hepatocytes is caused by oncotic necrosis.Toxicon : official journal of the International Society on Toxinology · 2017Article
- Keratins: Biomarkers and modulators of apoptotic and necrotic cell death in the liver.Hepatology (Baltimore, Md.) · 2016Review
- Functional Implications of O-GlcNAcylation-dependent Phosphorylation at a Proximal Site on Keratin 18.The Journal of biological chemistry · 2016Article
- Post-translational modifications of intermediate filament proteins: mechanisms and functions.Nature reviews. Molecular cell biology · 2014Review
- Type I keratin 17 protein is phosphorylated on serine 44 by p90 ribosomal protein S6 kinase 1 (RSK1) in a growth- and stress-dependent fashion.The Journal of biological chemistry · 2011Article
- Keratin hypersumoylation alters filament dynamics and is a marker for human liver disease and keratin mutation.The Journal of biological chemistry · 2011Article
- p38 MAP kinase and MAPKAP kinases MK2/3 cooperatively phosphorylate epithelial keratins.The Journal of biological chemistry · 2010Article
- Cytoskeletal keratin glycosylation protects epithelial tissue from injury.Nature cell biology · 2010Article
- Keratin 18 phosphorylation as a progression marker of chronic hepatitis B.Virology journal · 2010Article
- Toward unraveling the complexity of simple epithelial keratins in human disease.The Journal of clinical investigation · 2009Review
- Introducing intermediate filaments: from discovery to disease.The Journal of clinical investigation · 2009Review
- Gastrointestinal differentiation marker Cytokeratin 20 is regulated by homeobox gene CDX1.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Intermediate filament cytoskeleton of the liver in health and disease.Histochemistry and cell biology · 2008Review
- Keratin mutation predisposes to mouse liver fibrosis and unmasks differential effects of the carbon tetrachloride and thioacetamide models.Gastroenterology · 2008Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Simple epithelia express keratins 8 (K8) and 18 (K18) as their major intermediate filament (IF) proteins. One important physiologic function of K8/18 is to protect hepatocytes from drug-induced liver injury. Although the mechanism of this protection is unknown, marked K8/18 hyperphosphorylation occurs in association with a variety of cell stresses and during mitosis. This increase in keratin phosphorylation involves multiple sites including human K18 serine-(ser)52, which is a major K18 phosphorylation site. We studied the significance of keratin hyperphosphorylation and focused on K18 ser52 by generating transgenic mice that overexpress a human genomic K18 ser52--> ala mutant (S52A) and compared them with mice that overexpress, at similar levels, wild-type (WT) human K18. Abrogation of K18 ser52 phosphorylation did not affect filament organization after partial hepatectomy nor the ability of mouse livers to regenerate. However, exposure of S52A-expressing mice to the hepatotoxins, griseofulvin or microcystin, which are associated with K18 ser52 and other keratin phosphorylation changes, resulted in more dramatic hepatotoxicity as compared with WT K18-expressing mice. Our results demonstrate that K18 ser52 phosphorylation plays a physiologic role in protecting hepatocytes from stress-induced liver injury. Since hepatotoxins are associated with increased keratin phosphorylation at multiple sites, it is likely that unique sites aside from K18 ser52, and phosphorylation sites on other IF proteins, also participate in protection from cell stress.
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