Interaction of oncoprotein transcription factor MYC with chromatin-associated protein host cell factor–1 controls expression of genes important for ribosome biogenesis and mitochondrial vigor, loss of which promotes tumor regression.
Transcription factors KLF2 and ETV1 repress the transcriptional program of mitochondrial biogenesis, resulting in impaired mitochondrial function in lysosomal storage diseases.
The essential function of ACP is not related to mitochondrial fatty acid and lipoic acid synthesis, but rather an evolutionarily-conserved role in iron sulfur cluster biogenesis.
An insulin-Myc feed-forward loop triggered by transient JNK boosts transcription of genes essential for mitochondrial respiration and biogenesis during early oogenesis to support massive mtDNA replication and inheritance in Drosophila.
The convergent evolution of yeast Mim1/2 and trypanosomal pATOM36 enable the first demonstration of reciprocal functional rescue of two evolutionary unrelated mitochondrial biogenesis complexes belonging to two different eukaryotic supergroups.
The optimal macronutrient composition, macronutrient space, varies strongly between closely related species and is determined by genetic changes in regulatory genes that globally reprogram gene expression profiles of metabolic pathways.
Two GAP proteins bound to mitochondria regulate the enyzme Rab7, and thereby the expansion of the isolation membrane during mitophagy, downstream of PINK1 and Parkin, two proteins that are mutated in familial Parkinson's disease.
Systemic hypoxia model reveals the detrimental effect of hypoxia on mitochondrial biogenesis in activated T-cells and points at a new approach for improving viral resistance in patients with respiratory diseases.
Biochemical analyses show that mitochondrial COX16 assists in the process of copper insertion into COX2 and reveal a second COX16 function in linking assembly routes of the redox center-containing COX1 and COX2 subunits.
Mitochondrial proteins Nfu1 and BolA3 mediate the transfer of preformed [4Fe-4S] clusters within the mitochondria to recipient proteins to shield clusters from oxidative damage during transfer.
