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In vivo studies reveal that mitochondrial Complex I deficiencies induce iron misregulation and liver iron overload that may contribute to neurodegeneration in mitochondrial disease mice, and that iron restriction is effective in reducing disease progression.

The first atomic resolution structure of a mitochondrial respiratory complex from plants provides insight into the assembly and evolution of respiration in autotrophic eukaryotes.

BUD23 links ribosome function with mitochondrial protein expression and efficient oxidative phosphorylation by promoting selective mRNA translation and is therefore critical to mouse development and postnatal cardiac function.

Common nuclear genetic variants are associated with fundamental biological processes occurring in human mitochondria and potentially point to novel roles for nuclear genes in transcriptional regulation of the mitochondrial genome.

Drosophila HNF4 directs a developmental switch at the onset of adulthood that suppresses diabetes by promoting mitochondrial function and supporting glucose-stimulated insulin secretion.

Transferred mitochondria do not always regulate cell behavior by simply restoring mitochondrial function, but rather, transferred mitochondria are dysfunctional, initiating downstream signaling and proliferation in response to reactive oxygen species.

A mitochondria-based 'priming' of stemness happens by fine-tuned repression of the level or activity of the master regulator of mitochondrial fission, Drp1, which supports carcinogen-induced transformation in a keratinocyte model.

A new mitochondrial protein degradation pathway selectively sorts and destroys a subset of the mitochondrial membrane proteome to protect mitochondria in times of stress.

Correlated light and electron microscopy of cortical neurons reveals a local organization of mitochondria near dendritic spines with diverse functional properties.

An aorta smooth muscle-on-a-chip model indicated that NOTCH1 insufficiency in HAoSMCs induced phenotypic switching from a contractile to a synthetic phenotype accompanied by an impairment of mitochondrial fusion, implying its potential role as a therapeutic target for BAV-TAA.