ArticleExperimental and molecular pathology2010
SAMe prevents the induction of the immunoproteasome and preserves the 26S proteasome in the DDC-induced MDB mouse model.
Article in Experimental and molecular pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- NUB1 and FAT10 Proteins as Potential Novel Biomarkers in Cancer: A Translational Perspective.Cells · 2021Review
- The Role of FAT10 in Alcoholic Hepatitis Pathogenesis.Biomedicines · 2020Review
- UBA6 and Its Bispecific Pathways for Ubiquitin and FAT10.International journal of molecular sciences · 2019Review
- Article
- Proteasome and Organs Ischemia-Reperfusion Injury.International journal of molecular sciences · 2017Review
- Proteasomes in corneal epithelial cells and cultured autologous oral mucosal epithelial cell sheet (CAOMECS) graft used for the ocular surface regeneration.The ocular surface · 2017Article
- Role of Protein Quality Control Failure in Alcoholic Hepatitis Pathogenesis.Biomolecules · 2017Review
- The mechanisms of Mallory-Denk body formation are similar to the formation of aggresomes in Alzheimer's disease and other neurodegenerative disorders.Experimental and molecular pathology · 2016Review
- Mallory-Denk Body (MDB) formation modulates Ufmylation expression epigenetically in alcoholic hepatitis (AH) and non-alcoholic steatohepatitis (NASH).Experimental and molecular pathology · 2014Article
- Ufmylation and FATylation pathways are downregulated in human alcoholic and nonalcoholic steatohepatitis, and mice fed DDC, where Mallory-Denk bodies (MDBs) form.Experimental and molecular pathology · 2014Article
- Article
- Impact of altered methylation in cytokine signaling and proteasome function in alcohol and viral-mediated diseases.Alcoholism, clinical and experimental research · 2013Review
- FAT10 knock out mice livers fail to develop Mallory-Denk bodies in the DDC mouse model.Experimental and molecular pathology · 2012Article
- Emerging roles of immunoproteasomes beyond MHC class I antigen processing.Cellular and molecular life sciences : CMLS · 2012Review
- Oxidative stress, Nrf2 and keratin up-regulation associate with Mallory-Denk body formation in mouse erythropoietic protoporphyria.Hepatology (Baltimore, Md.) · 2012Article
- The role of innate immunity in the pathogenesis of preneoplasia in drug-induced chronic hepatitis based on a mouse model.Experimental and molecular pathology · 2011Review
- The immunoproteasome in steatohepatitis: its role in Mallory-Denk body formation.Experimental and molecular pathology · 2011Article
- Increased expression of FAT10 in colon benign, premalignant and malignant epithelial neoplasms.Experimental and molecular pathology · 2011Article
- Mallory-Denk body pathogenesis revisited.World journal of hepatology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Mallory-Denk bodies (MDBs) form in the liver of alcoholic patients. This occurs because of the accumulation and aggregation of ubiquitinated cytokeratins, which hypothetically is due to the ubiquitin-proteasome pathway's (UPP) failure to degrade the cytokeratins. The experimental model of MDB formation was used in which MDBs were induced by refeeding DDC to drug-primed mice. The gene expression and protein levels of LMP2, LMP7 and MECL-1, the catalytic subunits in the immunoproteasome, as well as FAT10, were increased in the liver cells forming MDBs but not in the intervening normal hepatocytes. Chymotrypsin-like activity of the UPP was decreased by DDC refeeding, indicating that a switch from the UPP to the immunoproteasome had occurred at the expense of the 26S proteasome. The failure of the UPP to digest cytokeratins would explain MDB aggregate formation. SAMe prevented the decrease in UPP activity, the increase in LMP2, LMP7, and MECL-1 protein levels and MDB formation induced by DDC. DDC refeeding also induced the TNFalpha and IFNgamma receptors. SAMe prevented the increase in the TNFalpha and IFNgamma receptors, supporting the idea that TNFalpha and IFNgamma were responsible for the up regulation of LMP2, LPM7, and FAT10. These results support the conclusion that MDBs form in FAT10 over-expressing hepatocytes where the up regulation of the immunoproteasome occurs at the expense of the 26S proteasome.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.