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Fig. 3 | Cell & Bioscience

Fig. 3

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

Fig. 3

Loss of Fkbp51 increases ATP production by enhanced mitochondrial function. A DEG between Fkbp51 KO and WT after CCl4 treatment functionally-related to mitochondria are interconnected based on STRING analysis. Figure was modified from STRING analysis, red-colored gene names indicate upregulation in KO, blue-colored gene names indicate downregulation in KO, and black-colored gene names indicate similar expression between KO and WT (added to identify more interactions). Log2 fold-change (FC) of DEG are included. B ATP production of WT and KO MEF cells as determined by PhosphoWork Luminometric ATP Assay. C Mitochondrial respiration reflected by OCR was detected in Fkbp51 KO and WT MEFs during the course of the Seahorse XF Cell Stress Test. The arrow indicates the sequential addition of oligomycin, FCCP, and rotenone (Rot). The OCR profile is normalized to total cultured cell protein. D Graph demonstrating increases in KO MEF OCR during basal mitochondrial respiration, ATP production, H+ (Proton) leak, maximal respiration, spare respiration capacity, and non-mitochondrial respiration relative to WT. Graphs represent mean values ± SEM from 3 independent experiments. p values were determined by student’s unpaired t-test with the statistical significance labeled as follows: ** as p < 0.01; *** as p < 0.001 and **** as p < 0.0001; NS, not statistically significant. Key: WT, wild type; KO, Fkbp51 KO

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