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.
Stress-induced alternative translation of an otherwise common gap junction protein generates an isoform that orchestrates protective mitochondrial fission and organ protection during anticipated ischemia.
Latest advances in biological timing studies substantiate an emerging concept of autonomous clocks that are normally entrained by the cell cycle and/or the circadian clock to run in synchrony, but have evolved to run independently to regulate different cellular events.
Although cellular organelles show a functional deterioration in aging, genetic loci associated with common age-associated disease instead nominate nuclear transcription factors across several age-related diseases.
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.
In vivo dopamine neuron imaging-based neuroprotective small molecule screen in larval zebrafish and mechanistic investigation using conditional CRISPR knockout and cell-type-specific RNA-seq analysis, coupled with cross-species analyses including human clinical data interrogation, uncover potential disease-modifying therapeutics for Parkinson's disease (PD).
The crystal structure of human WIPI2 bound to the ATG16L1 WIPI2-interacting region, combined with in vitro reconstitution and cellular autophagy assays, shows how the LC3 lipidation machinery is recruited in autophagy initiation.