Fig_6.tif (3.5 MB)
The abundance of the mitochondrial deoxynucleotide (di- and tri- phosphate) transporters is increased in the absence of MPV17.
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posted on 2016-01-18, 15:33 authored by Ilaria Dalla Rosa, Yolanda Cámara, Romina Durigon, Chloe F. Moss, Sara Vidoni, Gokhan Akman, Lilian Hunt, Mark A. Johnson, Sarah Grocott, Liya Wang, David R. Thorburn, Michio Hirano, Joanna Poulton, Robert W. Taylor, Greg Elgar, Ramon Martí, Peter Voshol, Ian J. Holt, Antonella SpinazzolaRepresentative immunoblot of the equilibrative nucleoside transporter (ENT1) in (A) control and MPV17-mutant fibroblasts in dividing and quiescent cells, and (B) in the liver of wild-type (WT) and knockout (KO) mice. (C) Steady state levels of the mitochondrial deoxynucleotide transporters 1 and 2 (PNC1 and PNC2) in control and MPV17 deficient fibroblasts in proliferating and quiescent conditions. (D) Pnc1 and Pnc2 steady state levels in the liver, of type (WT) and knockout (KO) mice. Vinculin (VCL), and Tom20 were used as loading control.
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dNTP levelsMitochondria MPV 17mitochondrial DNA lossMPV 17 deficiencymitochondrial DNA depletiondysfunction causes mitochondrial DNA abnormalitiesMPV 17 Loss Causes Deoxynucleotide Insufficiencydeoxynucleoside supplementationSlow DNA Replicationmitochondrial deoxynucleotide homeostasismitochondrial genomic instabilityDNA copy numberMPV 17 disease models
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