Fig. 3: CdtB-induced mitochondrial damage through the interaction with ATP5A1 along with the decreased activity of mitochondrial respiratory complex V. | Nature Communications

Fig. 3: CdtB-induced mitochondrial damage through the interaction with ATP5A1 along with the decreased activity of mitochondrial respiratory complex V.

From: Helicobacter hepaticus promotes hepatic steatosis through CdtB-induced mitochondrial stress and lipid metabolism reprogramming

Fig. 3

a Live cell images of Hep3B cells transfected with pBIFC-COX8A-VN173, pBIFC-CdtB-VC155 and pBIFC-C. j-CdtB-VC155 along with their corresponding reverse validation plasmids. b Western blot analysis of CdtB content in mitochondrial fractions. Hep3B cells were transfected with either pCMV-Myc-EGFP or pCMV-Myc-EGFP-CdtB for 24 h. Whole-cell lysates (cell), cytoplasmic (cyto), and mitochondrial components (mito) were probed with CTCF, β-actin, and TOM20 antibody, respectively. c Co-immunoprecipitation (Co-IP) assay of the interaction between CdtB and ATP5A1 in Hep3B cells transfected with pCMV-Myc-EGFP or pCMV-Myc-EGFP-CdtB. d Immunofluorescence images of the subcellular localization of CdtB (green) and ATP5A1 (red) in Hep3B cells transfected with pCMV-vector or pCMV-CdtB for 24 h. e The activity of mitochondrial respiratory complex V in Hep3B cells transfected with pCMV-vector or pCMV-CdtB for 24 h (n = 3 independent experiments). Scale bars: 10 µm (d) or 50 µm (a). Statistical analysis was performed using unpaired, two-tailed Student’s t test (e). Source data are provided as a Source Data file.

Back to article page