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Mutations affecting a nuclear encoded metalloprotease cause of a new form of mitochondriopathy, highlighting the importance of this protease for mitochondrial function in humans.

Defective mitochondrial protein import results in protein aggregation and a specific chaperone response in the cytosol, causatively linking mitochondrial function and cellular protein homeostasis disturbances observed in neurodegeneration.

Stable isotope labeling reveals that NAD crosses the inner membrane of mammalian mitochondria via an unknown transporter.

The MondoA transcription factor localizes to the outer mitochondrial membrane where it coordinates an adaptive transcriptional response to elevated cellular energy represented by high cytoplasmic glucose and high mitochondrial ATP.

Current models of Alzheimer's disease that put mitochondria as an endpoint of disease should be reconsidered because genetic defects affecting mitochondria by themselves can also regulate Alzheimer’s disease risk factor apolipoprotein E (APOE) expression and secretion.

One minute biotinylation with APEX2 peroxidase in living cells identifies established and new components of mitochondrial and ER membranes; dataset intersection and overexpression screen identifies SYNJ2BP overexpression as inducing mitochondria-rough ER contacts.

Tom70 connects the mitochondrial import to the nuclear transcriptional activity of mitochondrial proteins and controls mitochondrial biogenesis defects during aging.

RSV's unique ability to co-opt host cell mitochondria to facilitate viral infection reveals the RSV-mitochondrial interface as a viable target for therapeutic intervention.

Removal of spurious poly(A) tails by the PDE12 exoribonuclease is required to maintain the integrity of human mitochondrial tRNAs and rRNAs and their availability for efficient mitochondrial translation.

SIT4 deletion and phosphate starvation increase mitochondrial membrane potential via electron transport chain dependent and independent manners, and the increased membrane potential induced by phosphate depletion is conserved between yeast, flies, and humans.