Phillip Andrew Frankino

This study shows heat stress activates UPRER through XBP-1 and HSF-1 in C. elegans, with cross-talk to cytosolic HSR and inter-tissue stress communication enhancing thermotolerance.

This study identifies SKN-1 as a metabolic surveillance factor that responds to amino acid catabolism to influence stress resistance in C. elegans.

This paper shows that glia in C. elegans can induce a heat shock response in peripheral cells, increasing lifespan and stress resistance, independent of neurons and neurotransmitters.

This study shows that DNA double-strand breaks cause ribosome remodeling and translational shutdown, independent of p53 and preceding transcriptional changes.