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Fig. 2 | Cell & Bioscience

Fig. 2

From: Knocking out Fkbp51 decreases CCl4-induced liver injury through enhancement of mitochondrial function and Parkin activity

Fig. 2

RNA-Seq reveals differentially expressed genes (DEGs), downstream effects, and upstream regulators in Control and CCl4-treated Fkbp51 KO and WT liver samples. A Venn Diagram shows differentially expressed genes (DEGs) between CCl4-treated Fkbp51 KO and WT, between vehicle control-treated Fkbp51 KO and WT, and in common of both conditions. Statistical significance was set as the adjusted p-value (adj p) < 0.05 and fold change >  = 2. B The bar-chart represents downstream effects, and the most significant canonical pathways are plotted by their statistical significance (-log p-value) when unique CCl4-responsive DEGs served as the input for IPA pathway analysis. C Regulator effects analysis featuring the top predicted upstream regulators were plotted by their activation Z-score. Immuno-responsive substances (LPS, TGF-β1, IL-6, and IL-1B), hormone regulators (Medrol, DHT, and LEP), d-glucose, and CCl4 are inhibited, while functional enzymes related to fatty acid β-oxidation (ACOX1), ligand-binding receptors (AHR), and nuclear factors (PPARγ) are activated. D STRING analysis identified clusters of down- and upregulated genes with log2FC KO/WT higher than 2 involved in several critical functions of liver fibrosis formation. Arrows indicate up- and downregulation and the fold changes are listed. (Abbreviations: ACOX1, Acyl-CoA Oxidase 1; AHR, Aryl Hydrocarbon Receptor; DHT, dihydrotestosterone; LEP, leptin; LPS, lipopolysaccharide; Medrol, methylprednisolone. Key: WT, wild type; KO, Fkbp51 KO

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