ArticleBMC medical genomics2013
ChIP-seq in steatohepatitis and normal liver tissue identifies candidate disease mechanisms related to progression to cancer.
Article in BMC medical genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 9 citations in OpenAlex.
- Review
- Epigenetics of Hepatic Insulin Resistance.Frontiers in endocrinology · 2021Review
- Deregulation of obesity-relevant genes is associated with progression in BMI and the amount of adipose tissue in pigs.Molecular genetics and genomics : MGG · 2018Article
- Epigenetics and Liver Fibrosis.Cellular and molecular gastroenterology and hepatology · 2017Review
- PATZ1 down-regulates FADS1 by binding to rs174557 and is opposed by SP1/SREBP1c.Nucleic acids research · 2017Article
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSteatohepatitis occurs in alcoholic liver disease and may progress to liver cirrhosis and hepatocellular carcinoma. Its molecular pathogenesis is to a large degree unknown. Histone modifications play a key role in transcriptional regulations as marks for silencing and activation of gene expression and as marks for functional elements. Many transcription factors (TFs) are crucial for the control of the genes involved in metabolism, and abnormality in their function may lead to disease.
methodsWe performed ChIP-seq of the histone modifications H3K4me1, H3K4me3 and H3K27ac and a candidate transcription factor (USF1) in liver tissue from patients with steatohepatitis and normal livers and correlated results to mRNA-expression and genotypes.
resultsWe found several regions that are differentially enriched for histone modifications between disease and normal tissue, and qRT-PCR results indicated that the expression of the tested genes strongly correlated with differential enrichment of histone modifications but is independent of USF1 enrichment. By gene ontology analysis of differentially modified genes we found many disease associated genes, some of which had previously been implicated in the etiology of steatohepatitis. Importantly, the genes associated to the strongest histone peaks in the patient were over-represented in cancer specific pathways suggesting that the tissue was on a path to develop to cancer, a common complication to the disease. We also found several novel SNPs and GWAS catalogue SNPs that are candidates to be functional and therefore needs further study.
conclusionIn summary we find that analysis of chromatin features in tissue samples provides insight into disease mechanisms.
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