Skip to main content
Fig. 5 | Journal of Translational Medicine

Fig. 5

From: GCN5L1-mediated TFAM acetylation at K76 participates in mitochondrial biogenesis in acute kidney injury

Fig. 5

GCN5L1-induced TFAM K76 acetylation inhibits the binding of TFAM to translocase TOM70. A, B Electron microscopy analysis of kidney for mitochondrial number and morphology with semi-quantification of mitochondrial abundance. C mtDNA copy number in GCN5L1 knockdown mice kidney treated with I/R. D, E Protein levels of ND1, COXII, CYTB and ATP6 were detected by western blot in GCN5L1 knockdown mice kidney treated with I/R. F Oxygen consumption was recorded by clark-type electrode in GCN5L1-KD mice kidney treated with I/R. G, H Electron microscopy analysis of TECs for mitochondrial number and morphology with semi-quantification of mitochondrial abundance. I mtDNA copy number in H/R induced TECs. J, K Protein levels of ND1, COXII, CYTB and ATP6 were detected by western blot in hypoxia-reoxygenation induced TECs. L, M Mitochondrial OXPHOS were analyzed with basal respiration, maximal respiration, ATP production and spare respiratory capacity in GCN5L1 knockdown TECs under H/R treatment respectively. *P < 0.05, **P < 0.01, and ***P < 0.001

Back to article page