HIGHLIGHTS
SUMMARY
The authors investigated the role of SLC25A46 in the control of mitochondrial morphology and lipid homeostasis by first knocking out SLC25A46 in fibroblasts and subsequently expressing the WT cDNA or the cDNA of three different pathogenic variants spanning the range of protein stability and disease severity (Fig 1B and C). Mitochondrial fragmentation in SLC25A46 knock-out cells and hyperfusion in pathogenic variants To investigate the molecular basis for SLC25A46 pathogenicity, the authors first established a knock-out in a control immortalized human fibroblast cell line using CRISPR/Cas9 editing (Fig 1B). (A) Mitochondrial morphology . . .
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