ArticleVirology journal2010
Keratin 18 phosphorylation as a progression marker of chronic hepatitis B.
Article in Virology journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Targeting RANKL-independent osteoclastogenesis overcomes denosumab resistance in models of ER+ breast cancer bone metastasis.The Journal of clinical investigation · 2026Article
- Leukamenin E Induces K8/18 Phosphorylation and Blocks the Assembly of Keratin Filament Networks Through ERK Activation.International journal of molecular sciences · 2020Article
- Serum Cytokeratin 18 M30 Levels in Chronic Hepatitis B Reflect Both Phase and Histological Activities of Disease.Mediators of inflammation · 2017Article
- Review
- Clinical values of elevated serum cytokeratin-18 levels in hepatitis: a meta-analysis.Hepatitis monthly · 2015Article
- The Clinical Significance of Serum Apoptotic Cytokeratin 18 Neoepitope M30 (CK-18 M30) and Matrix Metalloproteinase 2 (MMP-2) Levels in Chronic Hepatitis B Patients with Cirrhosis.Hepatitis monthly · 2013Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe intermediate filament proteins keratins 18 (K18) and 8 (K8) polymerize to form the cytoskeletal network in the mature hepatocytes. It has been shown that the phosphorylation of K18 at two serine residues, 33 and 52, correlates with the progression of hepatitis C, but little is known of chronic hepatitis B (CHB). In this study, we examined K18 phosphorylation in relation to CHB.
resultsSite-specific phosphorylation of K18 was determined in livers of twelve healthy donors, and non-cirrhosis (n = 40) and cirrhosis (n = 21) patients. On average, progressively higher level of Ser52 phosphorylation was observed in non-cirrhotic and cirrhotic livers, while elevated Ser33 phosphorylation was detected in both livers but no significant difference. Progressive increase of Ser33 and Ser52 phosphorylation correlated with the elevation of both histological lesions and enzymatic activities of alanine aminotransferase in non-cirrhotic livers. In the hepatocytes of an inactive HBV carrier, strong signals of Ser33 phosphorylation were co-localized with viral infection, while only basal level of Ser52 phosphorylation was detected in infected cells.
conclusionAssuming all obtained data, our data suggest that K18 phosphorylation is a progression marker for CHB.
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Registered trials
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