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Updated: May 28, 2026
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Cell Type-specific Gene Expression Profiling in the Mouse Liver
Published on: September 17, 2019
Identification of high-copper-responsive target pathways in Atp7b knockout mouse liver by GSEA on microarray data
Kan He1, Zhenliang Chen, Yufang Ma
1School of Agriculture and Biology, Department of Animal Sciences, Shanghai Jiao Tong University, Shanghai, Peoples' Republic of China. hekan@sjtu.edu.cn
Summary
Wilson's disease protein ATP7B mutations cause high hepatic copper accumulation. This study identified novel high-copper-responsive pathways and coexpression networks in mouse liver, advancing understanding of Wilson's disease pathology.
Area of Science:
- Genomics
- Molecular Biology
- Hepatology
Background:
- Wilson's disease is linked to ATP7B mutations and hepatic copper accumulation.
- Previous studies identified key genes but lacked focus on pathway involvement and coexpression patterns.
Purpose of the Study:
- To investigate high-copper-responsive pathways and coexpression networks in the early stages of Wilson's disease.
- To identify candidate transcription factors involved in copper accumulation-induced liver pathology.
Main Methods:
- Utilized microarray data from an Atp7b knockout mouse model of Wilson's disease.
- Applied Gene Set Enrichment Analysis (GSEA) to identify affected pathways.
- Constructed coexpression networks using significant core genes and transcription factors.
Main Results:
- Identified 16 upregulated pathways (e.g., tryptophan metabolism, cell cycle) and 15 downregulated pathways (e.g., TCA cycle, PPAR signaling).
- Most identified pathways were previously unreported in the context of high copper.
- Constructed coexpression networks highlighting key transcription factors like SREBP1 and PPARG.
Conclusions:
- This study provides a genome-wide understanding of molecular mechanisms underlying high copper effects in mouse liver.
- Findings offer insights into the pathogenesis of Wilson's disease and potential therapeutic targets.